Scholarships SINGA 2023-06-21-BMS

Research Institute Course Category Focus Area
A*STAR Infectious Diseases

Biomedical Sciences (BMS) Infectious Diseases
Labs (ID Labs)

Labs (ID Labs)

Labs (ID Labs)

Labs (ID Labs)

Labs (ID Labs)
A*STAR Infectious Diseases Bioengineering &

Biomedical Sciences (BMS)
Labs (ID Labs) Bionanosystem
Bioinformatics Institute (BII) Biomedical Sciences (BMS) Gene Therapy/ Therapeutics
Bioinformatics Institute (BII) Biomedical Sciences (BMS) Molecular Biosciences
Bioengineering &
Bioinformatics Institute (BII) Biomedical Sciences (BMS)
Bionanosystem
Bioinformatics Institute (BII) Biomedical Sciences (BMS) Gene Therapy/ Therapeutics

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Diseases
All of the above. Computing,

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Engineering, Biophysics,
Biomedical
All of the above: Computing,

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Engineering, Biophysics,
Biomedical Sci
Bioinformatics Institute (BII) Biomedical Sciences (BMS) Chemical Biology
Bioinformatics Institute (BII) Biomedical Sciences (BMS) Infectious Diseases
Bioinformatics Institute (BII) Biomedical Sciences (BMS) Health & Nutrition
Bioinformatics Institute (BII) Biomedical Sciences (BMS) Genetics/ Genomics

Bioprocessing Technology
Biomedical Sciences (BMS) Molecular Biosciences
Institute (BTI)
Biomedical Sciences (BMS) Gene Therapy/ Therapeutics
Institute (BTI)
Institute (BTI)
Centre For Frontier AI Research Bioengineering &

(CFAR) Bionanosystem
Genome Institute of Singapore

Biomedical Sciences (BMS) Genetics/ Genomics
(GIS)

(GIS)

(GIS)
(GIS)

(GIS)
Genome Institute of Singapore Biostatistics, Diseases,

(GIS) Genetics/Genomics

Biomedical Sciences (BMS) Health & Nutrition
(GIS)

(GIS)

(GIS)

(GIS)
(GIS)

Biomedical Sciences (BMS) Diseases
(GIS)

(GIS)

(GIS)
Institute of Molecular & Cell

Biology (IMCB)

Biology (IMCB)

(GIS)
Biomedical Sciences (BMS) Other - Cancer Biology
(GIS)

(GIS)

(GIS)

(GIS)

(GIS)

(GIS)

(GIS)
(GIS)

(GIS)

(GIS)
Infectious Disease Labs (ID

Labs)

Labs)

Labs)

Labs)
Labs)

Labs)

Labs)

Labs)
Singapore Institute for Clinical Interdisciplinary (Biomedical

Sciences (SICS) Imaging and Health
Singapore Institute for Clinical Interdisciplinary (Biomedical

Sciences (SICS) Imaging and Health
Bioprocessing Technology Bioengineering &

Institute (BTI) Bionanosystem
Biomedical Sciences (BMS) Bioengineering or Therapeutics
Institute (BTI)

(GIS)

(GIS)
Biomedical Sciences (BMS) Translational bioengineering
Institute (BTI)




Institure of Sustainability for

Bioengineering &
Chemicals, Energy and Biomedical Sciences (BMS)
Bionanosystem
Environment (ISCE2)
Institute of Materials Research Bioengineering &

and Engineering (IMRE) Bionanosystem

Biomedical Sciences (BMS) Neuroscience
Biology (IMCB)

Biomedical Sciences (BMS) Behavioral Genetics
Biology (IMCB)
Biology (IMCB)

Biomedical Sciences (BMS) Behavioral Genetics
Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)
Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)
Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biomedical Sciences (BMS) Immunology
Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)
Biology (IMCB)

Biomedical Sciences (BMS) Molecular biosciences, diseases
Biology (IMCB)

Biology (IMCB)

Biology (IMCB)
Inter-disciplinary: Cancer
Biomedical Sciences (BMS) biology + Chemical Biology + AI
Biology (IMCB)
& data Science

Biology (IMCB)

Biology (IMCB)
Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)
Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)

Biology (IMCB)
Biology (IMCB)

Biomedical Sciences (BMS) Diseases/immunology
Biology (IMCB)

Biomedical Sciences (BMS) Genetics/Genomics
Biology (IMCB)

Biomedical Sciences (BMS) Genes therapy/therapeutics
Biology (IMCB)
Other - Cancer Cell Signalling &

Biology, Non-Coding RNAs,
Novel anti-cancer strategies,
Institute of Molecular & Cell Oncology drug development,
Biology (IMCB) Small Molecules,
Peptide/siRNA therapeutics,
Patient Derived xenografts,
Orphan disease models.
Other - Cancer Cell Signalling &
Biology, Non-Coding RNAs,
Novel anti-cancer strategies,
Institute of Molecular & Cell Oncology drug development,
Biology (IMCB) Small Molecules,
Peptide/siRNA therapeutics,
Patient Derived xenografts,
Orphan disease models.

Biology (IMCB)
Biology (IMCB)

Biology (IMCB)

Biology (IMCB)
Singapore Immunology Bioengineering &

Network (SIgN) Bionanosystem
Singapore Immunology
Network (SIgN)
Network (SIgN)
Singapore Immunology Bioengineering &

Network (SIgN) Bionanosystem
Network (SIgN)
Network (SIgN)
Singapore Institute for Clinical

Sciences (SICS)

Sciences (SICS)

Sciences (SICS)

Sciences (SICS)

Biomedical Sciences (BMS) Biostatistics
Sciences (SICS)
Biomedical Sciences (BMS) Biostatistics
Sciences (SICS)
Singapore Institute for Clinical Other - Development and

Sciences (SICS) human potential
Singapore Institute of Food and

Biotechnology Innovation Biomedical Sciences (BMS) Food Process Engineering
(SIFBI)

Biocatalysis, microalage
Biotechnology Innovation Biomedical Sciences (BMS)
fermentation and extraction
(SIFBI)

Biotransformation and
downstream process
(SIFBI)

Food, Nutrition and
Biotechnology
(SIFBI)

Biotechnology Innovation Biomedical Sciences (BMS) Food ingredients
(SIFBI)
Biotechnology Innovation Biomedical Sciences (BMS) Food ingredients
(SIFBI)

Biotechnology Innovation Biomedical Sciences (BMS) Health & Nutrition
(SIFBI)

Biotechnology Innovation Biomedical Sciences (BMS) Health & Nutrition
(SIFBI)

Food, Nutrition and
Biotechnology
(SIFBI)

Biotechnology Innovation Biomedical Sciences (BMS) Molecular Biosciences
(SIFBI)

Food, Nutrition and
Biotechnology
(SIFBI)

Biotechnology Innovation Biomedical Sciences (BMS) Shared Analytics Platform
(SIFBI)
Synthetic biology, metabolic
engineering
(SIFBI)
Singapore Institute of
Bioengineering &
Manufacturing Technology Biomedical Sciences (BMS)
Bionanosystem
(SIMTech)
Manufacturing Technology Biomedical Sciences (BMS) Diseases
(SIMTech)
Bioengineering &
Bionanosystem
(SIMTech)
Bioengineering &
Bionanosystem
(SIMTech)
Skin Research Labs (A*SRL) Biomedical Sciences (BMS) Skin (cross-disciplinary)
Bioengineering &
Skin Research Labs (A*SRL) Biomedical Sciences (BMS)
Bionanosystem
Other - Ageing and wound
Skin Research Labs (A*SRL) Biomedical Sciences (BMS)
healing
Skin Research Labs (A*SRL) Biomedical Sciences (BMS) Molecular Biosciences
Skin Research Labs (A*SRL) Biomedical Sciences (BMS) Diseases
Skin Research Labs (A*SRL) Biomedical Sciences (BMS) Molecular Biosciences
Skin Research Labs (A*SRL) Biomedical Sciences (BMS) Gene Therapy/ Therapeutics

Immune cells effector function are intimately linked
to the cellular metabolic pathways, which can dictate
the disease immunopathology. Recent studies have
revealed that along with transcription factors some
Project Title metabolites (signaling Project intermediates)
Description are crucial for
immune regulatory elements that are key to control
microbial infections and the maintenance of immune
homeostasis. This project aim to investigate the the
molecular mechanisms underlying host immune-
metabolic framework including immune cell signaling
Identifying protective immune
pathways, metabolic regulators, host metabolic
pathways that can be Recent studies have
reprogramming, andrevealed
immune that genes along transcription
expression
harnessed to control infection factors some metabolites
during bacterial infection. (signaling
Some of the intermediates)
experimental
and drug resistance. are crucial for
techniques andimmune
research regulatory
methods elements
that would that
be are
used
key to controlthe
in executing microbial
proposed infections
work includeand the
maintenance
metabolomics,ofproteomics,
immune homeostasis. gene cloning, In this
PCRproject,
we aim tocell
analysis, explore
culture, theexpression
molecularand mechanisms
purification of
underlying
recombinant host immune-metabolic
proteins, RNA sequencing, framework
flow
including
cytometry, immune
SDS-PAGE, cell signaling
Western blot, pathways, metabolic
etc. These
Investigating crosstalk between regulators,
findings would hosthelpmetabolic reprogramming,
in uncovering the dynamics and of
immunity and metabolism immune genes interactions
host-pathogen expression during and thusbacterial infections.
may lead to new
during bacterial/viral infection. Some
avenues of the experimentaltherapeutics
of host-targeted techniques and research
to treat
methods
infections.that would be used in executing the
proposed work include metabolomics, proteomics,
gene
The PhDcloning,
Bacteriophages
project PCR analysis,
(phages)
will aim to arecell culture,
widely
characterize expression
distributed
host-
and purification
viruses
alphavirus of
thatinteractions recombinant
infect and replicate
both in vitro proteins,
and inRNA
in bacteria. Phage
vivo in
sequencing,
have
animal been flowMulti-Omics
cytometry,
instrumental
models. SDS-PAGE,
in landmark
approaches, Western
protein-inblot,
discoveries
etc. These
molecular
protein findingsand
biology
interactions, would were
crispr help towill
used
cas9 device
as be newto
antimicrobial
used
Host-Alphavirus interactions therapeutic regimens (host-directed therapies)
agents priorviral
investigate to the discovery
hijacking of theof antibiotics.
cellular andThe thefor
during replication and impact microbial
advent infections.
of bacterial drug resistance has emerging
re-ignitedand the
immunological response for epidemic,
on immunopathogenesis interest in phage as potential therapeutic, sterilizing
re-emerging arboviruses (i.e. Chikungunya virus). The
agent
projectandwilldiagnostic
aim to identify tools and in infection control.
characterize Here,
cellular
we are interested
pathways for antiviralin phage for the purpose of
and immune-modulatory
treatment of Gram negative infections, either as a
therapy strategies.
cocktail or in combination with existing
antimicrobials.
Applied bacteriophage biology Klebsiella pneumoniae (Kp) is a Gram-negative
We aim to build
opportunistic a collection
member of environmental phage
of Enterobacteriaceae. It is
with focus on diagnostics and
with therapeutic and
commonly found as a part of humandiagnostic potentials.
gut, skinTheand
therapy
identified phage will
mouth microbiota butfirst be characterized
it also accounts for 11.8% of
phenotypically (including
hospital-acquired infections forandspecificity
50% ofagainst
bacteremiaa
panel of clinical isolates) and genotypically.
cases worldwide, affecting especially elderly and Selected
phage will then be molecularly
immunocompromised individuals. modified in order to
Acinetobacter
delete genes involved in recombination,
baumanii, another Gram -negative opportunistic rendering
them strictly
organism canlytic and pathogenic
be associated to the target
with urinary tract
Therapeutic interventions for organisms. Finally, these phage will beasevaluated in
infections, bacteraemia, pneumoniae well as skin
Klebsiella pneumoniae and cocktails and/or in combination with existing
and soft tissue infections. Both of these organisms
Acinetobacter baumanii antimicrobials
are associated for withantimicrobial
increased multidrug efficacy in vitro and in
resistance
infections. vivo. With the alarming increase in multidrug
and underline the critical need for the development
resistant organisms, phage
of novel therapeutics therapy present a viable
strategies.
and valuable strategy in
Here, we are interested in developing infection control.
pathophysiologically relevant pre-clinical small animal
models for Klebsiella
The project will involve pneumoniae and Acinetobacter
the novel development of
Development of microfluidic baumanii to study virulence
high-throughput droplet-based bioassays for and evaluate new
systems for high-throughput therapeutic strategies,asincluding
biological exploration small therapeutics
well as direct molecules as
bioassays for disease well as phage therapy.
discovery. Mixed expertise in biology, chemistry (in
intervention particular water-in-fluorinated-oil emulsions), and
bioengineering will be developed.
p53, the guardian of the genome is found to be
mutated in several cancers. While there is abundant
data on p53, yet therapeutic modulation is still
Viral control of p53:
lacking. This project will explore the interactions of
development of novel
viruses that inactivate p53 and use the understanding
therapeutics
to derive novel antivirals using a combination of
Bioinformatics, Design, Molecular simulations and
machine
Peptides learning techniques.
offer a third class of medicines along with
small molecules and antibodies. They offer many
distinct advantages over the other two and yet suffer
limitations of stability and cell permeability.
Constraining peptides with linkers such as staples has
How do peptides enter cells:
made them robust to degradation and even makes
computational models
some peptides cell permeable. Yet a comprehensive
model
There isofincreasing
how they evidence
enter cellsthat
is still
phaselacking. This
separations
project will apply physics based models (atomistic
(LLPS) occur across multiple length scales in biology
and
and coarse
is one of grained),
the mostsimulations, machine learning
exciting developments in to
develop a rigorous model of how peptides
understanding biomolecular interactions. This project enter cells.
will explore intermolecular interactions regulating
LLPS at the atomic level using multiscale molecular
Unravelling the properties of
dynamics simulations. The work will draw upon
condensates (LLPS) for use in
experimental explorations in the laboratory of Prof
food, cosmetic and pharma
Miserez using proteins from marine organisms.
Lessons learnt will be directed towards understanding
characteristics of proteins such as aggregation,
gellation, solubility, liquid-liquid
Enzyme engineering plays a centralphaseroletransitions to
in developing
develop machine learning methods for use
efficient biocatalysts for biotechnology, biomedicine, in the
food, cosmetic,
and life sciences.pharma industry.
The student will learn to use
computational methods such as protein structure
AI-guided computational
modeling, protein-ligand docking, and machine
enzyme engineering
learning to suggest useful mutants and substrates for
selected enzymes involved in diseases and
biosynthesis. The predictions will be tested in
collaborator's lab.
Covalent kinase inhibitor (CKIs) is one of the best
strategies to solve drug-resistance dilemma in kinase
drug discovery. The student will learn to use
Structure-based ligand
computational methods such as protein structure
discovery and design for cancer
modeling, protein-ligand docking, molecular
drug development
dynamics simulations, and machine learning to
suggest new generations of CKIs. The predictions will
be tested in collaborator's lab.
GPCRs are involved in nearly every physiological
process, including mediating the cellular responses to
most hormones, metabolites, cytokines, and
GPCR structure-function neurotransmitters. The student will
Cancer cells are self-organizing, highly build structure-AI
variable and
mechanism and ligand model for GPCRs based on available GPCR
largely resistant even to modern state-of-the-art structural,
regulation functional,
therapeuticand ligand information,
intervention. In order toand apply thissuch
understand
model
complex behaviors and to determine a more on
for novel ligand discovery and design, holistic
biased
treatmentsignaling andcross-disciplinary
strategy, allosteric regulation. The
efforts
predictions will be tested
combining theoretical, in collaborator's
computational and lab.
wet
experimental methods are imminent. In this project,
the student will undertake a systems biology strategy
to investigate the resistance mechanisms for a drug
Sensitizing Cancer Cell
treatment. By first measuring the intracellular
Resistance to Treatment by
signaling molecules dynamic response to a given drug
Systems Biology
perturbation in a chosen cancer cell type, the student
will subsequently use the data to create a dynamic
computational model using differential equations.
The model will simulate the differential signaling
kinetics between untreated and treated conditions,
and identify areas that possibly causes resistance
during treatment. The predictive capacity will be
tested experimentally to observe the downregulation
of resistance mechanisms by co-targeting strategy.
the neo-adjuvant setting is one of the important
therapeutic strategies for management of both early
stage and locally advanced cancers. Nevertheless,
resistance to chemotherapy remains a significant
problem. A large majority of human genome encodes
for non-coding (nc) RNAs, and these are broadly
classified into small ncRNAs, long ncRNAs and
pseudogenes. Recent findings indicate several of
Multi-dimensional Data these are dysregulated in cancer. Targeting ncRNAs
Analytics to Identify Key could
Cancerbeaffects
an effective approach
one-quarter of our forpopulation.
the development With
ncRNAs Regulating of novel therapeutics to overcome
advances in treatment, cancer patients chemoresistance.
are living
Chemoresistance in Cancer In this project,
longer, even forthe student
several will explore
decades. Henceand thecompare
focus in
time-series RNA-Sequencing data
cancer patients has begin to shift towards how of cancer cellsto
unstimulated
manage them(control)better and and stimulated
allowing to undergo
patients to live cell
proliferation (test). By utilizing
well. As an example case study, lung infectiona number of dataand
analytic tools, the student will
inflammation are common and potentially fatalnarrow down a set of
ncRNAs that are
complications in crucial
cancer for cancerundergoing
patients chemoresistance.
Artificial Intelligence These will be ranked according to their predictive
treatment. These conditions present similarly but
Applications for clinical importance and, subsequently, experimentally
require different treatment. A misdiagnosis leads to
management of cancer verified in cellular mechanisms underlying resistance
inappropriate treatment, unnecessary
patients to cancer treatments.
discontinuation of critical anti-cancer agents and
worse quality of life. We can use Artificial Intelligence
The emergence
(AI) to distinguish of between
Artificial Intelligence (AI) has led to
these conditions.Through
the develop
use of bigofdatadisruptive
and AI,technologies
this project aims in thetoclinical
settings. In particular,invasive
reduces unnecessary in the area of digital shortens
procedures, pathology,
AI will play increasing
hospitalization duration, roleleads
in the todiagnosis
appropriate of biopsies
Artificial Intelligence as well as resection
treatment
Dysfunction andof cost patients
savings,
nucleotide samples.
helping
binding tomanyCombinations
proteinscancer
is the
Applications in Digital of AI with
patients tothe
live development
better and to of
cause of several diseases (e.g. cancers and high
live throughput
well. slide
Pathology scanner will lead of big changes in clinical
Parkinson's), and the ability to track the amounts of workflows
in the pathology
nucleotides departments
in living cells wouldofrepresent
hospitals.aThis PhD
project strives to develop cutting-edge
revolution in improved diagnostic and treatment artificial
intelligence technologies that can be translated
strategies. In this project, we will develop biologically into
standard-of-care in the clinics.
inspired fluorescence-based sensors, based on
existing proteins whose normal function in the cell is
to sense ATP. As part of the Multiscale Simulation,
Computational design and
Modelling & Design Group in BII, we will use
experimental development of
computational approaches to model protein
novel nucleotide sensors The ever growing crisis
structure/dynamics andofpredict
bacterial multidrug point
side-directed
resistance
mutations threatens to make existing
to tune nucleotide selectivity, antibiotic
and design
therapies for infectious
novel protein-sensor diseasesAlongside
chimeras. redundant. Asinpart
this, the
of the of
group Multiscale
Prof. ThorstenSimulation,
Wohland Modelling & Design
(Chemistry, NUS),
Group in BII,
molecular a computational
biology approachesmodellingwill be used approach
to will
be used tothe
engineer investigate
designed the molecular
mutants mechanisms
that may be fused by to
which synthetic
fluorescent antimicrobial
constructs, towards peptides interact with
the development of
Computational design and
bacterial membranes
novel in vitro and in vivo to induce
biosensors bacterial
with cell
broadlysis
development of novel
and/or aggregation.
therapeutic This will
and diagnostic be performed in order to
potential.
antimicrobial peptides
understand how different sequences in a library of
peptides influence such interactions, and to design
new peptides. This will be iteratively validated via wet
lab experiments in the group of Prof. EE Pui Lai Rachel
(Pharmacy, NUS) towards the development of new
molecules with optimized antimicrobial properties for
Computational sequence and Computational sequence and
use against drug-resistant structure
bacterial analysis to
pathogens.
structure analysis to study study protein allergenicity in novel food => use
protein allergenicity in novel and develop tools to predict protein allergenicity in
food novel food from the sequence and structure
Computational sequence and structure analysis using

Computational sequence and AI for evaluating genetic variants in human diseases
structure analysis using AI for => Apply and develop workflows of computational
evaluating genetic variants in methods inlcuding AI to predict effects of mutations
human diseases on protein structure and function relevant for human
diseases
To meet the huge demand for quality and cost-
effective biologics with tight timelines through
discovery, development, and manufacturing,
biopharma industries, we are focusing on
understanding the process fundamentals of the
platform through quality by design (QbD) strategy at
all production scales via process analytical technology
Application of mass (PAT) for at-line/real-time monitoring of product
spectrometry digitized quality attributes. Mass spectrometry (MS) is one of
proteomic mapping to identify the core components with high sensitivity and
optimal conditions for robustness,
There is a wideandusage
the reliable high-performance
of lentiviral vector (LV) asDIA a
biotherapeutic products SWATH-MS can play an important
gene delivery vehicle in clinical gene role in the
therapy.
characterization
Potential bottlenecks of process and productinclude
in LV production criticalviral
quality
RNA export, viral gRNA encapsidation, RNAonline
attributes (CQAs) monitoring in an real-
stability
time manner.
and transgene expression. By screening for and
identifying beneficial Institute
cis-acting DNA(BTI) has for the
elements
established a full value chain of CHO based
above-mentioned processes, a set of plasmids for the
Engineering lentiviral vectors biotherapeutics manufacturing, process
improved production of lentiviral vectors can be
for improved production and development, and product analytics, comprehensive
engineered. Upon successful expression, purified LVs
utility CHO proteome spectral library, the proposed project
will undergo transduction and response studies in T-
is to develop innovative and streamlined sample
cells. It is very vital for successful transduction in gene
preparation
therapy as itandhelps apply DIA-MS
to ensure technologies
DNA for real-
is stably integrated.
time biologics product multiple quality attributes
In addition, the response by T-cells after integration
characterization and processing
would help to determine profilingand
the infectivity during
mortality
upstream and
of the host cells. downstream processing before final
Development of platform product release testing.
technology for bispecific Development of platform technology for bispecific
antibody purification and antibody purification and developability assessment
developability assessment
New optical imaging platforms have broad

New Optical Platforms for Non- applications from 3D culture development to pre-
Destructive Biological Imaging clinical cancer models. The student will explore new
and Spatial Characterization applications and hypotheses in biology supported by
new technologies developed in house.
Spatially-resolved
Spatially-resolved Transcriptomics with MERFISH and
Transcriptomics with MERFISH
Split-FISH
The project will revolve around the development of
and Split-FISH
new technologies in gene editing, synthetic biology,
and immunology. Our broad and long-term goal is to
bring nucleic acid therapeutics into the clinic. In doing
this, the technologies we build will need to enable
new biological functions, unprecedented efficiencies,
and new levels of safety profile. In developing these
Nucleic Acid Therapeutics - technologies, the PhD candidate will also explore and
Gene editing and novel enable new biological innovations that go beyond
technologies therapeutics, specifically in biotech and synthetic
biology
A tumorapplications.
is a mixture of cells thus conventional cancer
drugs often lead to incomplete elimination. Single cell
The PhD candidate
genomics will conceive,
is a powerful technology design, and execute
to decode the
his/her thesis project in a very independent
cellular heterogeneity of tumor and its manner,
with guidance and support
microenvironment, frommajor
and reveals the PIvulnerabilities
and the lab
team members. The PhD will be done amidst
to design effective drugs for future therapy. Using a
Discovery of Cancer Therapy vibrant and happy lab culture.
single-cell Perturb-seq experiments, which leverages
based on Single Cell Genomics CRISPR gene editing technology and single cell
genomics, the project aims to identify major
vulnerabilities of tumor, and design Nucleic-Acid
based modalities to target coding and non-coding
RNAs. The project involves both experimental and
computational work, and a chance to work from
bench to translational research.
The project will focus on studying the genetic bases
of complex diseases and developing related genomic
technologies. Besides research efforts on the
discovery of disease loci through GWAS, the group is
also working on large-scale whole genome
sequencing (WGS) analysis, such as the SG10K project
Singapore
where 10,000 already has a successful
Singaporean individuals healthcare
were system
that offers high-quality
sequenced. In addition,care the groupat an affordable
is also exploring price.
Genomics of Complex Diseases However,
electronic the medicalgovernment is projected to
record (EMR)-based devote an
genomic
increasing
There
analysis is whereportion
increasing EMR of its revenue
evidence
information to suggestto healthcare
and that somatic
genomic in
data
years
will betointegrated
mutations come.that The torapidly
occur duringaging
advance thepopulation
post-zygoticunderstanding cellof division
of
Singapore
may
diseasepredisposeand rising
development, chronic
to neurological
progressiondisease disorders.
and burden We
treatment demands
will
that
attemptwe 1)
outcome. toincrease
detect
The public
somatic
project health
mutations
is looking literacy,
for at high 2) helpwho
candidates
clinicians
expected adapt
sensitivity, toand to potential
map
develop related paradigm
cellular
an independent shifts in chronic
phenotypes
research inin
disease
diseased
these areas,screening
brain andusing
tissue
particularly healthcare,
on the latest
developing and 3) new buildanalytical
capabilities
single-cell/spatial
strategies and to empower genomic
methods individuals
for technologies
large-scale to better
at themanage
genomic and
their
Genome ownInstitute
multidimensional health and chronic
of Singapore,
data analysis. conditions.
A*STAR. We Precision
will
Evaluating somatic mosaicism health
analyzeand the prioritization
post-mortem brain tissueof who benefit
from deceasedfrom
in diseased brain tissue screening using data-driven
patients that have previouslyscience been diagnosedholds promises with to
provide
neurological value-based
diseasescare suchfor asthe population.
Parkinson’s disease,
Alzheimer’s disease and Lewy Body Dementia as well
This project
as from healthy aimscontrols.
to solve We issues willrelated to the
ask if recurrently
implementation
disrupted genes are of precision
enrichedhealth at sitesinof the pathology,
Singaporean
and follow uppopulation.these genesAnfunctionally understanding in of the
level of public precision
animal/cell/organoid healthtoliteracy
models probe diseasewill be
established
mechanisms.by both traditional and novel methods
Risk Stratification For Cancer
(Aim 1). Novel knowledge on which risk predictors are
and Chronic Disease Screening
ready
Women to are
be deployed
not “cured” at aafter
population-based
successful primary screening
level will be generated; new methods
treatment, even with full remission. Ongoing physical are developed
to
andincrease
psychologicalthe accuracyneeds of prediction
remain. (Aim 2).
This multi-faceted
Insights from interviews with
PhD project aims to use a variety of approaches, breast specialists
(including those participating
including questionnaire surveys, in afocuspilot group
breast cancer
risk-based screening study)
discussions, national registries, breast cancer will reveal the challenges
in
databases, and large breast cancer cohort healthy
communicating personal disease risk to studies to
Breast Cancer Survivorship in screening
identify gaps participants
and unmet and help in
needs tocaredraftfor guidelines
breast for
Singapore communication
cancer patients transiting of risk results and actionable
to survivors. Biostatistical
interventions (Aim 3). A cost-effectiveness
tools using large breast cancer cohort studies analysis
will beon
the
used to describe the landscape of breast cancer risk
implementation of genetic and non-genetic
stratification for multiple
survivors in Singapore. Usingchronic diseases
qualitative at the we
studies,
same
try time will evaluate whether the proposed
and new
Thistostudy
screening
learnwill from
paradigm
breasttranscriptomic
perform is a
cancer survivors
worthy investment analyses (Aim in4).
We live relevant
caregivers
disease in aonmicrobial
what works
arterial world forwith
wall them.
tissues enormous
Good diversity
science
from Asian
and
We function.
communication
are inartery DNA
thewillmidst sequencing
skills ofisanpreferred.
ageing technologies
Knowledge
population are of deep
the R
coronary
Our findings
revolutionizing
programming
patients
be ability
our
language important
is
(CAD)
to do
highly inpatients
developing
surveillance
encouraged.
through acrisis,
and
with
roadmapmanyasnations,
genome-wide to RNAseq.
which including
TheseSingapore,
conditions data canwould facing
benefit be expected
Metagenomic technologies for harness
massive
to provide this vast
healthcare
validationsbiodiversity.
burdens
of our due In this
recent project,from
to prolonged
findings we will
on
risk
microbial surveillance stratification
develop in
cutting-edge public health
sequencing, screening, culturing and to
and
lifespan
dysfunctional
estimate spent
the healthin poor
immune and health.
and Chronological
lifeinflammatory
savings for the age is an
response in
systems
imprecise
subtypes biology
ofmeasure
CAD techniques
andofprovide
ansystem. to study
individual’s
disease health microbial
pathology status
Singaporean
communities healthcare
and
insights due toand
an increasing leverage
trendexposures
various these capabilities
of premature development
(i.e Type to
2 diabetes of
understand
chronic
status). diseases their
Additionally impact
manifesting on
in the same our
earlierworld.
set in of life is
patients we
observed.
aim to perform We have reported on
genome-wide the strong
germline role of to
genotyping
genetics
perform gene and age-related
expression biomarkersquantitativesuch traitas loci (eQTL)
telomere length dysfunctions
analyses. Overlaying gene expression in relation to future
patterns with
Arterial wall gene expression disease
germlineoutcomes, mortalitiescould
variant information and healthy
highlight ageing
on
and expression quantitative status in thekey
potentially Singapore
genetic loci Chinese population
that control (Dorajoo R
or modulate
trait loci analyses et al, 2019,
arterial wallChang X et al, 2020,
gene expressions fromChang birth.X etThese
al, 2021).
Nevertheless
variants wouldalmost all studies
subsequently bethat have evaluated
followed up in large-
ageing molecular biomarkers
scale longitudinal datasets in Singapore(including our withearlier
work)
phenotypichave evaluated
information these factors in
on incident CAD isolation
and CAD and it
is unclear how
mortalities. Thethese biomarkers
subsequent aim of interact
the study withwouldeach
other
be to useas wellthe as rich with environmental
genomics data on gene exposures expressionto
affect futurevariants
and genetic health outcomes.
to performIncolocalizationthis study, we aim
Ageing hallmarks in predicting at generating
analyses at knownadditional
common ageing genetic hallmarks, i.e
loci previously
prospective health outcomes mitochondrial
identified for CAD dysfunction
risks through usinglarge-scale
a validated qPCR
and mortalities. assay in baseline
international CADsamples from the Singapore
GWAS meta-analysis consortia. Chinese
Health Study incould
These studies up tohelp 25,000 individuals
characterise with CAD
recent
available
GWAS findings baseline andDNA samples.
pin-point likely Subsequently
functional gene we will
develop
dysfunctions strategies,
at the including
disease-relevant machines learning
arterial wall.
approaches and AI technology, to incorporate ageing
hallmarks (mitochondrial dysfunction and telomere
length) with germline genetic variants (common and
rare single-nucleotide variants and copy number
variants) and lifestyle and environmental exposures
(various dietary scores such as DASH, AHEI, alcohol
and smoking status, obesity levels, physical activity
levels) from baseline study samples to predict
subtyping
progesterone patients (ER, PR) based andon age-related
growth factorsrelated(HER2)
immune dysfunctions
receptors BCs are sub-divided into four is conceptually novel.
major Using
bronchiectasis as the
subtypes i.e. ER+/PR+/HER2- (Luminal-A), model respiratory disease, this
study aims at firstly sorting
ER+/PR+/HER2+ (Luminal-B), ER-/PR-/HER2+ (Her2+) and isolating major
immune cell-types from
and ER-/PR-/HER2- sputum (neutrophils,
(triple-negative/basal-like/TNBC).
eosinophils, macrophages
In addition to molecular heterogeneity and CD4+ T-cells) withinof
bronchiectasis
malignant cells, tumors are complex ecosystemthe
patients to specifically pinpoint of
precise
malignant immunecancercell-type/s
cells and the thatnonmalignant
are dysfunctional tumor due
The role of ageing and
to ageing hallmarks (telomere
microenvironment (TME) consisting of endothelial, attrition and
immunosenescence -
mitochondrial
immune and fibroblast dysfunctions). Secondly theof
cells. Composition study
TMEwill and
disentangling dysfucntional
combine ageing hallmarks
reciprocal interactions between various cell-types with multi-omics data
pathways in respiratory
(genetic and gene expression
further contribute towards thedata) in these specific
intratumor
disease.
sputum
heterogeneity (ITH). Once malignant cells age-related
immune cell-types to understand colonize in
dysfunctional
the mammarypathways. Eventually, identified
glands, chemotherapy remains one cell-of
types,
Recent
the most genes
workeffectiveand
from thepathways DasGupta
strategies from this study
lab on generating
to combat will
the tumor. be a
additionally
single
However, evaluated
cell chemotherapy
atlas of human leads using in vitro
HCC identified studies to
a remarkable
to the heterogeneous
confirm
“fetal-like findings
clinical outcomes.or oncofetal” andWedeeply evaluate
reprogramming
hypothesise thatspecific
of the
both immune
HCC-
tumor
Characterizing chemo-therapy dysfunctions
tumor (phagocytic
microenvironment potential, oxygen
cell intrinsic properties, as(TME) well asinto an immuno-
dynamically
induced resistance in ER/PR+ consumption
tolerant rate, glycolysis rates, cytokine
is to a)release)
evolving ecosystem,
OVERALL OBJECTIVES
interactions which
in this
with promotes
theirproposal growth
microenvironment, and
use
HER2- Breast Cancer at single resulting
survival bronchiectasis
ofapproaches
cancer outcomes. This study will be
single
contributecell to drugcells. toMoreover,
response. determine this
theonco-fetal
It is therefore dynamicessential
cell resolution an important
reprogramming
trajectories step
andthe was to better
not
theimpact understand
restricted
molecular to the
HCC-TME.
mechanisms of role of
We
to understand of chemotherapy onthe the
age-related
identified
evolution
diverse and the
of physiological
emergence
individual
reciprocal dysfunctions
cancerof similar
interactions cells under
betweenin
onco-fetal distinct
tumor
bronchiectasis
signatures
selection
cells and their to improve
in cirrhotic
pressures/stress
ecosystem liverthat future
samples
cues patient
as well
(including
may drive as in a
cytotoxic,
tumor
management
mouse
metabolic,
progression.model strategies.
of partial
epigenetic
Notably, and
amongstImportantly,
hepatectomy.
pathway-targeted
the various demonstration
Altogether drugsour
subtypes,
for
and the
findings first
suggest
metastasis);
the hormone time, that
that telomere
and growth-promoting,
b) exploreER/PR+
receptor-positive length dysfunctions
the consequences immune-
HER2- BCs ofin
specific
tolerant
how
respond immune
the microenvironment
tumor stroma,
poorly cell-types
to chemotherapy results in
is established
specifically a human earlier
CAFs, influence
compared disease,
to triple-
TraCER-seq: Mapping will
during enable
liver translation
damage and ofinflammation,
similar studiescells to other
which may the
the evolutionary
negative (TNBC). trajectories
We therefore of propose
cancer to under
trajectories of cancer evolution human
drive thediseases
creation where
of telomere
a tumor-permissive attrition maythat
niche have
that a
different
comprehensively selective pressures.
characterize We hypothesize
response to
under selective stress, one cell functional
can support role (i.e
growth and coronary survivalartery diseases,
of malignant cells.
genomic aberrations
chemotherapy-induced associated
tumor with
progression in the
at-a-time Alzheimer’s disease
However
chemoresistance
ER/PR+ HER2- little andetc).
is known
patients. about
metastasis
In order the are
to mechanisms,
pre-existing
uncover the in
signalling
granularitypathways,
phenotypically and dynamic
heterogeneous
of tumor-TME tumor
interactions, cell-cell weinteractions
mass and can to
propose
that
be
employ underlie
adaptively
scRNA-seq the generation
selected in response
to identify ofcell-types/states
disease associated,
to chemotherapy
immune-tolerant
or metastatic
associated with intra-hepatic
dissemination/colonization.
therapeutic environment
response and We during
also
implement
the
propose
Diseaseprogression
that adaptive
Associated of liver disease
Cellepigenetic
states (DACs) from early
mechanisms steatosis,
as a ‘biomarker’ play a
steato-hepatitis,
central
instead role
of a in the
limited acute set fibrosis,
activation
of genes.of and
specific cirrhosis to HCC.
transcriptional
Simultaneously we
Targeting the developmental
Our
will research
programs
evaluate that objective
theallowcell cellsis therefore
surface to adopt
proteome to generate
distinctof a
(resistant)
the same
origins of liver disease and its
comprehensive, single cell atlas/catalog of The
the
progression to hepatocellular cell
cellsstates.
From
to identify protein-based
an ongoing rare variant
biomarkers.
association analysis of
evolution
overarching of goalfunctional
of this disease
proposal states
is to based
generate on and
carcinoma (HCC) ATTRACT
validate a~2500
alterations in gene
single Singaporean
cellexpression
spatio-temporal heart failure
(transcriptome)
atlas of andchemo-
control
that
whole
define
resistance genomes,
individual
in ER/PR+ we
cellhave
types,
HER2- identified
and by
BCs a Gene
determine
the X as a
the
longitudinal
candidate
regulatory for
effect
tracing of chemo-treated which of thelossenvironment
ofbreast
function tumours.appears
(epigenome) to confer
athat
protective benefit. Whiletrajectories
control evolutionary HF cohortsduring from
elsewhere
longitudinalare soughtprogression
disease for replication, in thewe are liver,
human
proceeding
from normaltoadult generate Gene X knock-out
homeostatsis  liver damage, human
pluripotent
including stem cell
steatosis, lines, and Geneacute
steato-hepatitis, X knockoutfibrosis 
Heart Failure genomics and
mice.
cirrhosisGene  X encodes
HCC. Successful a DNA binding factor,
completion of the and a
project
therapeutics
bona fide binding
will result partner of the
in the identification of important
molecular myogenic
We have established
transcription
mechanisms factor
that that
MEF2.
drive thethe We long-noncoding
are also
evolution liver RNA
ofgenerating
VENTHEART
expression
disease/damage is necessary
constructs to cancer. forThe
of Gene ventricular
Xmolecules
cDNA bearing patient
associated
cardiomyocyte
based
with ormutations
regulating specification
tothese
validate andloss
the
mechanisms maturation.
of function
could in turn and
VENTHEART
test
servefor asGene
novel knockout
cellularhuman
Xprognostic localisation pluripotent
biomarkers and and stem
protein
therapeuticcells
fail to differentiate
interaction.
targets aimed Overall,
as both into cardiomyocytes,
experiments
prevention will
(by establishand divert
blocking
instead
whether
progression towards
Gene into X the
is a neuronal
HCC), novel
as well lineage.
HF related
as treatment VENTHEART
gene, and
knockdown
whether
(especially it is
ininathe cardiomyocytes
target
contextfor disease
of result
therapy.
immuno-therapy). in
Long noncoding RNA in heart Colorectal cancer (CRC) is the third most common
downregulation
Importantly, these of calcium
discoveries regulatory
inform the genes, loss of
disease cancer globally.
sarcomeric
development of Development
organisation and reduced
novel therapeutic of therapeuticcontractility.
and/or treatment
strategies
The VENTHEART
regimens targeting
that locus
target novel
is also
both cell types is the
contains
malignant/diseased a GWAS needhit of the
for
hour for CRC treatment.
non-ischaemic
hepatocytes, anddilated ofThe
cells cardiomyopathy. broad objective
intra-hepatic We are of this
project
therefore is to study experiments
pursing
microenvironment. the role of cancer-associated
to elucidate the
fibroblasts
molecular mechanism(CAFs) in CRC of tumour
action for growth
VENTHEART and and
metastasis
establish whether using a over-expressing
multipronged approach VENTHEART designed
to harnessagainst
mitigates the power heartoffailure.
cutting-edge technology
(MIBI-TOF, Visium, M-FISH). We are looking for
Spatial Multi-Omics in the
graduate students keen on working at the
study of Colorectal Cancer
intersection of cancer biology, imaging, spatial omics
and computational biology to correlate to clinical
outcome. They should be comfortable working in a
highly collaborative, multidisciplinary environment
that includes biologists, imaging technologists,
pathologists and medical oncologists. This will be a
unique opportunity to work on new data types and
ask new questions in the rapidly growing field of
spatial multi-omics.
in the 1920s,
stemness the clinical application
vs differentiation programs, ofepithelial
this concept, vs
i.e., the use of transitions,
mesenchymal 18Fluorine-deoxyglucose treatment resistance positronvs
emission
naïve responses,tomography (FDG-PET)
and localized vsfor tumor imaging,
metastatic
was implemented
phenotypes, underlie onlydiseasein the 1980s.progression In theand lastclinical
decade,
outcomes. metabolic
Such cellular alterations in canceratbecame
heterogeneity the genomic a re-
emerging paradigm,levels
and transcriptomic but the is agapshallmark in knowledge
of tumors. The
remain
heterogeneoussignificant compared
nature of tumors to other may fields.
be driven It is bynow
clear
evolution that ofthedistinct
Warburg clonal effect cellrepresents
populationonly as athe tip
result
Investigating the regulation of of the iceberg pertaining to the wide range of
selection or through inherent phenotypic plasticity.
cellular plasticity in cancer metabolic derangements accompanying
Cellular plasticity may be enabled by cell malignant
state
metastasis and therapy transformation and progression. A deepgene dive into
transitions regulated through complex
resistance principles
expressiongoverning programs.dysregulated Understanding cellular
cellular energetics
affords
pathways novelandinsights
programs intogoverning
the biology of cancer cells
phenotypic
Tumors
and howare
plasticity willcomplex
they inentities
use nutrients
result the more tosurrounded
fuel
precise by stromal
biosynthetic
control of cell
components.
growth,
states and regulate
gene Fibroblasts,
epigenetics,
functions, immune cells,
and maintain
thereby providingadipocytes,new
endothelial
homeostasis.
opportunities cellsto arealterkey
Well-studied theplayers somatic
course that serve toWe
of mutations
disease. (e.g.
promote
One
IDH1/2,
engineerof the cancer
grandprogression
PIK3CA)
vulnerabilities challenges
and reactivation or enable
for
into specific cancer
of gene the acquisition
treatment
expression
populations ofis
of
thatdrug
pathways
aggressive resistance
current (e.g. therapeutic
cancer MYC, following
cellsHIF1A)that cancer
strategies
have
will therapy.
to treat
pinpointed
cause them Cancer
tumor
to gain are
Redefining the nutritional cells have been thought
ineffective
metabolic
susceptibility due
programsto totherapy, thatto
therapy are
and utilize
resistance
generally
rewire nutrients
andadopted
stemness in cell-
tumor by
and
needs of cancer autonomous manner, butin
recurrence
bulk cancerthat
differentiation cells. areIn caused
programs view ofmore
by
tumor
cancer recently,
cancer stem cell-extrinsic
heterogeneity,
cells. Our cells
findings
factors
(CSCs).
however,
have resultedarising
The labin
broad from
addresses the tumor
principles
clinical this
of how
trials tomicroenvironment
importantdistinctchallenge
examine metabolic
how the by
have been
integrating
alterations
control of cellobserved.
thestates
arise fields
fromwith The
of diverse
cancer,
variations
therapeutics inroles
CSC, of
canstromal
targeted
phenotypic affect cell
components
therapy,
states
cancerand and in
mutations
progression providing
disease inmodeling,
have
cancer contextual
not been
patients. signaling
to translate
systematicallybiological
molecules,
findings
defined
The tropical in aespecially
about CSCs
tissue-specific
rain forest cytokines
into ofinnovative,
context.
South-East and growth Asia is factors
targeted one cancerto
promote
therapies. tumor
Advanced growth, resistance
multidisciplinary
home to a highly diverse array of plants many which and metastasis,
approaches
are
To well-established.
(genomics,
areprovide atranscriptomics,
still understudiedcomprehensive The
andnotion viewthat
metabolomics,
provide of stromal and
metabolic
numerous
Systematic identification of tumor cells engage in metabolic exchange (i.e.and
lipidomics,
alterations organoids,
and reveal biophysics)
unique cancer are employed
dependencies, to
therapeutic targets in cancer resources
crosstalk)
for potential food crops, botanicals
is very nascent and only recently observed.
uncover
systematic and interrogate
profiling of the
medicine. The project will seek to capitalize on emerging
cancer paradigms
metabolome in CSC
for
stem cells for disease For instance, lactate
intervention
biology. This
precisely-induced
aspects of thewill diverse cellproduced
reveal facets
states
flora and
and ascollaborative
of a by-product
CSCs
gene that are of will
mutations
fibroblast
amendable
be performed. cells
to can
rationallybe
Integrating used
opportunities to assemble high-quality reference as
designed an
genomics, energy
targeted source
therapies.
flux-tracing, by
lung carcinoma
High-throughput
metabolomics, cells
and to fuel
chemical-genetic
chemical-genetic
genomes to translate into scientific discoveries. Plant their biosynthetic
screens
screens, are needs.
further
the
From
utilized antoopposite
identification
genomes discover
are perspective,
potentially
and mechanistic
described with ideas however,
useful
validation
such asthe
agents manner
that
ofgenome
metabolic can
by
gene which
eradicate nutrients
targets is expected secreted
size, gene content, ploidy and repeats however theof
CSCs. In the long-term,
to by the
illuminate the development
pathways that
microenvironmental
these
are agentsof
amendable
architecture through cells
to therapeutic
their the use
genomic mayof program
AI-powered
intervention
structure metabolic
can in drug
rangetissue-in
addiction
screens
and cell in in
the tumor
state-specificlab cells
will to
provide
contexts.
complexity and size from simple small genomes to induce novel
How therapeutic
therapeutic
metabolites
Targeting tumor- vulnerability
modalities
regulate
large complex which
epigenetichas not
genome been
canprocesses
bethat explored.
employed
havesuch asUnderstanding
various neoadjuvants
methylation
ploidy, (by
microenvironmental crosstalk thefor
SAM) extent
cancer
and and
treatment.
acetylationnature of
(by
heterozygosity and genetic repeats. For instance, such
Current metabolic
key
acetyl-CoA) thematic
of exchanges
gene areas
targetsare:
in cancer between
wheat genome is hexaploid with 7 chromosomes andit
(i)
to Cancer
determine tumor
metabolism;
cell andstatesmicroenvironment
(ii)
willCellalso statebe cells
transitions;
examined. is new;
and
Our
can
(iii)
a size inform
Tumor
findings of have onresulted
niche
16Gb. theinteractions.
use therapeutic
in the identification inhibitors ofto target
novel
metabolic vulnerabilities.
gene targets that led to drug development
effort.
Genome assembly is a process of computationally
Harnessing
decipheringwhole-metabolome
the genetic composition functional withinchemical-
the cell of
genetic screens and our
a target organism. The complexity of plant unique in-house resource
genomeof
patient-derived
assembly depends cancer
on the andtargetstromal speciescells,and we are will
Plant Genome Assembly interrogate their metabolic exchange and induced-
usually presented with challenges due to their
Annotation and Biological dependencies.
Chronic liver Cancer-stromal
disease is a major co-culture health organoid
problem,
underlying genomic architecture. The advent of third-
Studies (under GIS) systems
especially will be adopted to understand how cancer-
generationwith a quartertechnologies,
sequencing of the world population
associated
being affected
instrumentations fibroblasts,
by and macrophages
Non-Alcoholic
scaffolding Fatty and
Liver
techniques T- Disease
are
lymphocytes,
(NAFLD).
crucial to Despite program
plant genome metabolic
the tremendousassembly as addiction
regenerative
they enable in cancer
cells.
capacity
resolutionConversely,
ofinthe liver
complex theand possibility
serial of
regions of cancer
transplantation
these cells
genomes.
secreting
experiments
Completion ofevenmetabolites that
indicating
assembly nourish
a nearly
is usually and infinite aby
sustain
accompanied pro-
tumor microenvironment,
proliferation in contrast to a healthy
genome
Exosomes arecapacity
annotation, extracellular for hepatocytes,
where functional
vesicles that the
studies
contain is
In vivo functional genetics for tissue
usually
proteins
ecology,
regenerative required
and
will
power
nucleic to also
of
lend be
the examined.
liver
phenotypic
acids. These vesicles declines Usingduring
significance. a new
are releasedaging in
dissecting liver biology and vivo
and and
chronicinducible
liver disease.whole-metabolome
Therefore, CRISPR-Cas9
we are
into
gene the extracellular
knockout screening space and enter
platform we circulation.
recently As
identifying new therapeutic conducting
Biological
exosomes in
study
contain vivo then functional
reveals
proteins, hepatocentric
gene
mRNAs, contents
noncoding genetic
that make
RNAs
targets developed
screens and
in amouse our customized
models metabolic
ofassociation
chronic drug
up
as the rich
well
library, as
we
annotation
membrane
will examine
and
derived
howtoare fromliver
stromal their
cells
disease,
between
“mother”
can favor
to
gene
identify
networks
cell, therapeutic
and
they represent clusters targets
which
perfect enhance
important endogenous
for
the
liver expansion
regeneration of cancer cellsbiomarkers.
and counteracting bearing chronic Importantly,
a particular
downstream
exosomes
metabolic canfunctional
phenotype.be found and metabolite
in diverse fluids,liver
body studies.
disease.
includingFurthermore,
Information saliva,fromblood genome we
andare unravelling
assemblies
urine. Almost the
alsoall reduces
cell types
underlying
the gap for mechanism
associative to better
studies
ubiquitously release low levels of extracellular understand
between genotype the and
biology
phenotype. of liver regeneration
vesicles. In normal physiology, most circulating a
Currently, plant and
genomes the mechanisms
are playing
Identification of liquid biopsy driving
huge regenerative
role
extracellular vesiclesdecline.
in agriculture are(Agrigenomics)
derived Our from goal isplatelets
to translate
where and
derived exosome based our findings
genetically to
fortifiednew innovative
plants
endothelial cells. Furthermore, it was shown are therapies.
critical to increase for the
diagnostic biomarker productivity
liver that mesenchymal for traditional stem or cell-derived
high density/open- as well as
space farming. To solve
hepatocyte-derived exosomes can promote the problem of feeding liveran
increasing
regeneration. We have an established pipelinethreats
world population while posed with for
from
isolation global warming and
of exosomes from limited
serumland andresources.
analyzing their
RNA content in our lab. Mouse models of liver cancer
and chronic liver disease as well as human patient
derived samples will be used. Exosome based
biomarker for early disease detection and population
wide screening will be identified. Our goal is to
translate our finding into diagnostic kits for using in
the clinic.
We conduct in vivo and in vitro functional genetic
screens. On one hand mouse models of liver disease
(liver cancer, Non-Alcoholic Fatty Liver Disease ,
chronic liver damage) will be used. Full in vivo RNAi
Functional genetic screens to
screens identify new therapeutic targets for these
identify therapeutic targets for
diseases. Targets will be validated in vivo and in vitro.
liver disease
For validated targets we will generate nucleic acid
based therapeutics for disease interception. The goal
is to unravel novel biology, strong IP and translate the
research results.
Recent developments in single cell technologies have
unveiled an extensive amount of heterogeneity at the
level of gene expression in individual cells. However
Single cell RNA structure how RNA structure could be different in individual
heterogeneity in human cells to result in different functional consequences is
diseases still largely unknown. We aim to develop single cell
strategies to interrogate RNA structures in individual
cells in normal cellular tissues as well as in diseased
states such as cancer.
RNA viruses including Dengue, Zika, SARS-CoV-2 are
of clinical importance around the world. Studying
how they fold and interact with host cellular RNAs is
Studying the genome key to understanding their pathogenesis and being
architecture and virus host able to target them. We will use a variety of
interactions of RNA viruses genomics strategies to interrogate how the viruses
fold, and interact with host RNAs, as well as how the
interactions
Gene expression resultstudies
in functional
on whole consequences
blood from activefor the
virus and the host.
tuberculosis and dengue patients suggest that
alterations in pathways such as interferon signalling,
TB continues toapoptosis
inflammation, be the world’s most important
and pattern recognition
infectious diseases may
receptor signalling claiming more than
contribute to the2 million lives
Role of potassium channels in every year globally. Although current
pathogenesis of these diseases. In thisantibiotic
project we drugs
aim
innate immunity against are effective forthe drug-sensitive TB patients, the
to characterise role of myeloid cell - specific
pathogens treatment
potassium periodchannels is long and the to
in immunity drugs are toxic,
bacterial and viral
making
infection. it difficult
Noteworthy, for patients
potassium to adhere
channels to the
are
regimen
important ininfull compliance.
regulating Moreover,
potassium importtheandtreatment
becomes
homeostasis, extremely
which challenging once thefunction
is crucial to cellular bacteriaat
develop
steady state resistance
and during to thestress.
drugs. This has led to the
emergence of host directed therapies (HDTs) that
Understanding role of Sirtuins involves modulation of host’s immune responses in
in regulating immuno- order to improve pathogen eradication. Recently we
metabolic crosstalk during Current
showed advances
that activating in vaccine
sirtuintechnology,
1, a metabolic in particular
sensor in
bacterial infection mRNA
immune vaccines, havethe
cells, inhibit shortened the time
intracellular growthneeded
of
between
Mycobacterium pathogen identification
tuberculosis (Mtb), to dampen
an FDA approved
disease
product to years versus
immunopathology decades.the
and enhance However,
efficacythisof
technology
conventional still has shortcomings
anti-TB drugs in mice. such as activating
Thus,
immunogenicity,
sirtuin 1 (by natural price and strongactivator)
or synthetic cold chain represent
constrains. This project
a potential TB-HDT that aims to further
can improve TBrefine and
treatment
optimize
outcome.inInhouse developed
this project we willconstructs
decipherfor thedelivery,
Development and optimization The PhD project will aim to characterize host-
efficiency
molecular and immunogenicity.
mechanism(s) underlyingThis the
project will entail
activation of
of a pathogen agnostic vaccine alphavirus interactions
molecular
SIRT1 by naturalbiology toolsboth
activator fori.einresveratrol
vitro and and
construction in
andvivowillin
platform technology animal models. Using aofnovel approach
validation
investigate asthe
well as small
impact animal
resveratrol on of
models viral
such
the and
immune
expressed
mice
benefits selectable
mice. formarker,
andinzebrafish deliverywe identified in
optimization,
multiomic
immunogenicity data ofand pure infected
efficacy cell populations
studies. State of the art
several
immunology proviral host factors.
techniques and inThe PhD
vivo project models
infection will
entail
will beaused
closetocharacterization
characterise theofsafety theseand hostefficacy
factorsof
and their role inConstructs
the constructs. the viral life cycle as well
developed in theas proof
the of
Understanding alphavirus immune
concept stageresponse of small
will target animal
three humanmodel to these
relevant
cellular hijacking for novel viruses.
pathogens In addition
from diverse to multi-Omics
parts of theapproaches,
tree of life.
antiviral and immune protein-protein interactions, microscopy, functional
modulator drug targets genomics, CRISPR Cas9 gene editing will be some of
the tools used to investigate this viral hijacking and
understand the host-viral interplay. Downstream of
characterization we will aim to validate these targets
in small preclinical models for subsequent drug
discovery. Throughout the project, close collaborative
work within A*STAR ID Labs as well as other institutes
throughout Singapore and overseas will be used to
leverage expertise for high impact studies.
This project will aim to establish in vitro and in vivo
tools and small animal models to study Mayaro virus.
Mayaro virus is a reemerging arbovirus currently
circulating in South America. During the course of the
PhD project, the student will aim to establish reverse
genetic systems for Mayaro and study host factors
Characterization of Mayaro
and immune cell populations affecting viral
virus, a reemerging alphavirus
replication and disease. Small animal models such as
with epidemic potential
mice, zebrafish and mosquito vectors will be explored
in an effort to better understand the factors that
could contribute to a widespread pandemic.
Outcomes
This projectofinvolves
these studies
the usewill
of inform potential
cutting-edge
antiviral drug and vaccine development,
microfluidic techniques in developing new ashigh-
well as
treatment and control strategies.
throughput methods for antibody design and
Monoclonal antibody design development. Such monoclonal antibody candidates
against emerging infectious are useful as therapeutics and/or diagnostics.
diseases Generating and analysing diverse functional
antibodies in relevant in vitro and in vivo models
allows downstream structure-function analyses to
enable reverse vaccinology approaches.
Mycobacteria are able to subvert the host immune
response to drive tissue pathology and prevent the
efficient clearance of infection by the immune
Host determinants of
system. This project will study the role of genes and
susceptibility to mycobacterial
molecular pathways that are hijacked during
infection
mycobacterial infection. We will then use genetic
The
toolsmodern pathogenic
to manipulate mycobacterium
the host immune responsefaces an
to
unprecedented numberresponse
modulate the immune of selective pressures
against and
infection.
must respond to maintain evolutionary fitness. In
addition to the host immune system, factors such as
deadly antibiotics, mutagenic cigarette smoke, and
predatory bacteriophages are regularly encountered.
In vivo analysis of
This project will determine how genetic adaptation to
mycobacterial determinants of
stressors affects the pathogenesis of mycobacteria to
pathogenesis
provide insight into mycobacterial virulence and
strategies to counter the damage caused by
mycobacterial infection. We will use genetic
manipulation of multiple species of pathogenic
MRI methods including
mycobacteria and hostsPDFF, perfusion
to study imaging, of
the consequences
relaxometry have been well established
genetic changes in relevant animal models. by our
group and also by other investigators for investigating
Fatty Acid Composition Imaging the liver diseases. In this proposal we will implement
of Body Composition in MRI based novel fatty acid composition imaging
Metabolic Diseases technology to resolve the overall fat content into its
saturated fatty acid (SFA), mono-unsaturated fatty
acid (MUFA), and poly-unsaturated fatty acid (PUFA)
components. We hope to develop this as the new
This project involves development of advanced
imaging methods for investigating skeletal muscle
metabolism using 1H MRI, 1H MRS, 31P MRS and
Musculoskeletal Imaging and Ultrasound imaging in subjects with muscle weakness
Metabolic Health (MRI, MRS, and fat infiltration. The established methods will
NIRS / Ultrasound) then be utilized along with interventions to
investigate subjects with diabetes, muscle weakness
and muscle loss.
Cells are an essential component of many biological
applications, ranging from cell-based therapies (e.g.
adoptive T-cell therapy, regenerative medicine, stem
Optimizing conditions and cell therapy) to cultivated meat. In such applications,
methods for ultra-high density the large number of cells that need to be
cell culture manufactured is often a bottleneck, resulting in high
costs and limiting adoption. Currently, most culture
systems utilize either 2D culture on tissue culture
plastic, or suspension culture on microcarrier beads.
For people suffering from organ failure, an organ
transplant is often their only hope. However, the
chronic shortage of available organs means that
Bioprinting of Organoids to many remain on the waitlist for years, all the while
Recapitulate Organ Functions undergoing treatment that greatly impact their
quality of life. The goal of the project is to make
meaningful gains towards solving this problem. While
it is not possible to recreate whole organs, we may be
able to recapitulate some organ functions within
In recent years, cell therapies have emerged as
potent treatments for cancer, in the form of cellular
immunotherapies such as CAR-T, CAR-NK, TCR
Non-viral delivery of genetic therapies, etc, as well as various genetic conditions.
material for cell manufacturing Currently, the vast majority of treatment options are
manufactured through the use of viruses. Due to the
obvious safety issues associated with the use of
highly-infective viruses to generate these cellular
therapeutics, there are currently very strict
Development of recyclable
Development of recyclable enzymes for diagnostics
enzymes for diagnostics and
and manufacturing
manufacturing
Development of treatment- Effective delivery is the key for success translation of

Development
nucleic acids toofclinic.treatment-responsive
This project is aimed switches for
to develop
responsive switches for control
control
Gene
safe and of
therapygene
effective therapies
holds great
lipid promise forfor
nanoparticles treating
targeted a wide
of gene therapies
range
delivery of of
diseases,
mRNA vaccinesuch as against
cancer and infection.
cancer. In this
According
project, thetostudent
a recentwill report
learnbyhow Grand View Research,
to design and
Inc.,
makethe global
lipids, how gene therapymRNA-loaded
to prepare market size is lipid expected
to grow to US$6.6
nanoparticles usingbillion by 2027microfluidic
an advanced at a Compound device,
Annual Growth Rate (CAGR)
how to functionalize the surface of 16.6%.
of lipidHowever,
nanoparticles the
available FDA- and/or
with a targeting signal EMA-approved
that can recognize geneimmunetherapy
Functional Lipid Nanoparticles products
cells. The are few and
student will faralsobetween.
be trained Most of these
to characterize
for Targeted Delivery of mRNA products employ
the functional lipidviral vectors, which
nanoparticles usingarevarious
inherently
Cancer Vaccine constrained
modern toolsbyfor their limited
particle size,cargo
size size and carry
distribution,
immunogenicity,
surface charge and toxicity and mutagenesis
functionality, nanostucture, risks.
Therefore,
mRNA loading the efficiency
main bottleneck for clinical
and stability. application
Finally, the
of gene therapy
student is the lack
will be trained of available
to evaluate the safe
in vitroandand in
Most of cancer
effective patients
gene delivery
vivo transfection efficiency after of chemotherapy
vectors. The aim
mRNA, andofefficacydevelop
this
resistance
project
against is to anticancer
aimed
tumor to design
challenging. drugs.
and Doctors
Thedevelop have
student biodegradable
will haveto give
the patients
synthetic
opportunities multiple
cationic
to work drugs to mitigateexperts
polymers/polypeptides
with renowned drug as genein
Biodegradable non-viral gene resistance
delivery
bioengineering,and tumor
vectors metastasis,
for vaccine
mRNA biology,against but limited
viral
chemistry, andsuccess
infection and
delivery vectors for vaccine is observed
cancer.
immunology, inand
most
Artificial cases.
intelligence
will develop In (AI)/machine
this project,
skills we aim to
learning
in identifying
against infection and cancer develop
will new
andstrategies
be applied
problems to accelerate
developing based ondevelopment
the
solutions. macromolecular of the
polypeptides,
non-viral genewhich delivery exhibit
vectors. anticancer
Students activity
will bevia
multiple
trained tomechanisms, and overcome drug resistance.
synthesize biodegradable
The polypeptides will beperform
polymers/polypeptides, designedininvitro the way that
they can self-assemble
characterization for gene into nanoparticles
transfection with a and
efficiency
targeting signal on theand
delivery mechanism, surface, which using
cytotoxicity can recognize
state-of-
cancer
the-art cells. Students
equipment. The will be trained
students will to
alsosynthesize
be trained
Drug-free polypeptide
polypeptides
to conduct with varying
animal studies structures
for evaluationandof in vivo
nanoparticles that overcome
compositions,
vaccination efficacyperform andinpotential
vitro characterization
toxicity. The for
drug resistance and tumor
anticancer
students activity,
will be cytotoxicity,
supported and and functional
trained by a world
metastasis
mechanisms using state-of-the-art
leading multidisciplinary and productive equipment.
team with The
students
expertisewill also be trained chemistry,
in bioengineering, to conductbiologyanimal and
studies
medicine. forTheevaluation
studentsofwill in vivo
alsoanticancer efficacy, to
have opportunities
toxicity
work with andlocal
biodistribution
and international etc. The students willand
collaborators, be
supported
most of them andare trained by a worldrenowned
internationally leading scientists
multidisciplinary
in their respectiveand productive
fields. team with
Two to three expertise
new students
in
canbioengineering,
be trained in this chemistry,
researchbiologyarea. and medicine.
The students will also have opportunities to work
with local and international collaborators, and many
of them are internationally renowned scientists in
their respective fields. Two new students can be
imperative to develop safe and effective preventive
measures against the SARS-CoV-2 virus, which are
effective, economical and facile to use in order to
boost public compliance and enhance prevention
efficacy. This proposed project aims to develop an
intranasal spray that contains biocompatible and
biodegradable polypeptides that can effectively kill
SARS-CoV-2 coronavirus in the respiratory tract for
Development of intranasal prevention of the viral infection. Students will be
spray against Covid-19 trained to synthesize polypeptides with varying
pandemic structures and compositions, perform in vitro
characterization for antiviral activity, cytotoxicity, and
functional mechanisms using state-of-the-art
equipment. The students will also be trained to
conduct
With theanimal
increasedstudies for evaluation
prevalence of drugof in vivo in
resistance
antiviral efficacy, toxicity and biodistribution
infection, there is an urgent need for development etc. The
of
students will be supported and trained by
innovative antimicrobial and antiviral strategies. This a world
Antimicrobial and antiviral leading
researchmultidisciplinary
is focused on design and productive team with
and development of
To develop
expertise in disruptive technologies
bioengineering, chemistry,
biodegradable polycarbonates or polypeptides and biology and
engineering
medicine.
their deliveryThesystems
studentsfor will also have
targeting opportunities
bacteria to
and virus.
work with local and international collaborators,
Artificial intelligence (AI)/machine learning will be and
many
applied ofto
them are internationally
accelerate the development renownedof thescientists
in their respective fields.
macromolecules and their nanoparticulate delivery
systems. Students will be trained to synthesize
polycarbonates or polypeptides with varying
Biodegradable
structures and compositions, perform in vitro
polymers/polypeptide-based
characterization for antimicrobial and antiviral
antimicrobial and antiviral
activity, cytotoxicity, and functional mechanisms
strategies that overcome drug
using state-of-the-art equipment. The students will
resistance
also be trained to conduct animal studies for
evaluation of in vivo antimicrobial and antiviral
efficacy, toxicity and biodistribution etc. The students
will be supported and trained by a world leading
multidisciplinary and productive team with expertise
in bioengineering, chemistry, biology and medicine.
Redox active materials and The students will also have
Redox active materials and opportunities to work
their bio-applications
their bio-applications with local and international collaborators, and many
of them are internationally renowned scientists in
their respective fields. Two to three new students can
be trained in this research area.
We have developed novel drug carriers derived from
DNA nanogels and green tea-based micellar
complexes as effective, safe delivery systems for drug
Biomaterials for Therapeutic and RNA therapies targeting cancer and various
Delivery and Cell Culture My lab studies
diseases. We haveneural
alsomechanisms
generated novel underlying natural
nanoparticles
Systems behavior
as syntheticmotivated by rewards
cell culture substratesandandrisks. Our
research focuses on applying
antimicrobial/antifouling the insights
systems. Our work gained
also from
such studies
involves to model
hydrogels for phenotypes
organoid culture associated with
for in vitro
human
toxicologybrain
anddisorders which include substance
drug screening.
dependence, depression, anxiety disorders,
neurodegeneration, and dementia. Towards this end,
a substantial portion of the work in our lab in the past
Modeling human brain few years has revolved around developing the
disorders in animals using a appropriate methodology to perform quantitative
neurogenetics approach. behavioral
Zebrafish are studies and analyses
freshwater fish thatusing thesmall
live in zebrafish
shoalsin
the laboratory. See a recent example
in the wild. We have found that social partners arehere (FM
Nathan, C Kibat,inT alleviating
highly effective Goel, J Stewart,
fear inAfish.
Claridge-Chang,
We are now
AS Mathuru* Contingent stimulus delivery
interested in understanding the neural mechanisms assay for
zebrafish reveals a role for CCSER1 in alcohol
underlying this social buffering in fish. More broadly
preference Addiction Biology
we are also interesting DOI:
in understanding social
https://doi.org/10.1111/adb.13126).
cognitive abilities of zebrafish, the brain More examples
regions
can be found at
Oxytocin signaling in social and involved, and the molecular players participating in
non-social behaviors. https://mathurulab.com/publications/
these behaviors, specifically using the oxytocin
receptor mutant lines that we have generated
recently. (Ref A Gemmer, K Mirkes, L Anneser, T
Eilers, C Kibat, AS Mathuru, S Ryu, E Schuman
Oxytocin receptors influence the development and
maintenance of social behavior in zebrafish (Danio
rerio). Sci Rep 12, 4322.
https://doi.org/10.1038/s41598-022-07990-y)
Accumulating evidence supports the hypothesis that
commensal microbiota can influence our dietary
responses and decisions; however causal insights are
still lacking. In this project, we will leverage the
simple yet conserved gut-brain circuits of the larval
Microbiome control of dietary zebrafish model to elucidate specific mechanisms via
choice and intake which the gut microbiome modulates food decision-
making. The goal is to identify novel gut-brain
signaling pathways linking diet and microbiome
Hundreds
function tooffeeding geneticdecisions,
variants have which beencould associated
then be
with
targetedhuman for obesity,
the treatment food intake, and dietary
of eating-related
preference,
disorders. yet causal mechanistic insights have been
difficult to achieve solely using mammalian models.
The zebrafish model shares conserved genes,
Neurogenetics of appetite and physiology and anatomy with mammals. Here we will
food choice ALS is a fatal adult-onset
systematically dissect theneuromuscular
effects of the most disease
characterized
promising candidate by the genes,
progressive includingdegeneration
those identified of
upper and lower motor
from Singaporean cohorts, neurons. It has significant
on zebrafish physiology
medical
and needbehaviour.
feeding due to theThe enormous
goal isby emotional,
to efficiently link
Our food and
physical, decisions
financial areburdens
modulated on themany patient factors,
and
gene
such function to human phenotypes, and lay the
familyasand
groundwork
dietthe andlackstress. In this project,
of medications
for precision nutrition that
and
wehaltwill
or dissect
reverse
therapeutics.
the neural circuits that govern
disease progression. The variability of clinical food choice using the
larval zebrafish as a model. We
presentation has contributed to difficulties with will use cutting-edge
imaging
diagnosis, and circuitdelays
causing manipulationin diagnosis toolsbytoan identify
average
Neural circuits for food
neuronal
of 12-18 months from symptom onset, and cues and
pathways that respond to dietary
decision-making
modulate
challengesfeedingwith precise decisions, clinical as profiling
well as the foreffect
clinical of
stress on these circuits. The goal
trials and translation of results from preclinical is to uncover new
principles
studies to of feeding
clinical proof regulation,
of concept. andThe to develop
absence of an
interventions and therapeutics
established biomarker, in addition to clinical for eating-related
disorders.
complexity,
The sGSK labmakes diagnosis
in Singapore even more
originally challenging.
discovered and
Genotype-phenotype
Obesity
characterizedand itsthe associated correlations
group1 PAKs metabolic exist
(PAK1-3), but
diseases andpatients
such as
has
with
morethe
diabetes same genotypes
increasingly
recently investigated inthe
thegroup
are responsible samefor IIfamilies can
significant
kinases PAK4
Disease pathways and
have
economicvariable
and PAK5 which clinical
and social are more phenotypes,
burdens in many
selective suggesting
countries.
in terms of RhoAs
biomarkers in motor neuron
contributions
such,
GTPase there is an
binding. from Weenvironmental
urgent showed need that factors,
for efficacious
the PAK4 isobesitynot
diseases
microenvironmental
therapies
regulated to bycombat
"activation cuesloop"
this and cell-cell
epidemic. Obesity
phosphorylation interactions
develops
(being
which
when could affect
energy intake
constitutively cell-cell variation
exceeds energy
phosphorylated) and functional
expenditure,
and therefore PAK4and
heterogeneity.
the
kinasecurrent
activity treatment
needs toofbeobesity assessed hasby been other primarily
means.
focused
Indeed there on reducing
is currently energy no intake.
'biomarker' Unfortunately,
for PAK4 or
We
these
PAK5 purpose
measures
activity two aims:
were
in vivo. Inlargely
most inefficient
cell lines, PAK5 in maintaining
protein
long-term
levels are much weightlower loss. thanThe recent
PAK4; this discoveryobservationof brown
1)
canNewly
adipocytes established
be explainedcapable byof multi-omics
the burning
fact that fatPAK4databases
in adult from
humans
is largely
Investigatingthe role of group II patient
has derived
provided iPSCs have
an excitingcells) recently
new while
therapeutic become available.
approach
inactive (in mammalian PAK5 has high
PAKs in the brain Using
for bioinformatics
theactivity.
prevention and
and treatmentpathway analysis,
of obesity we can
through
basal Our current model suggests PAK5 self-
uncover
enhancing disease
associationenergy mechanisms
interferes expenditure which correlate
via thermogenesis.
with its auto-inhibition, with
thus
different
Unlike theclinical
maintaining phenotypes
conventional
its high whiteand
activity. fat,affect
Converselybrown prognosis.
fathave
we could
burn
shown the fatsproteins
that to produce heat and
call Inka1 andin the process,
Inka2 act as
2) Based
allow
cellular the on proposed
individual
inhibitors of togroupdisease causing
lose IIweight.
kinases. ToWork pathways
promote is from
(1),
brown we
currently can investigate
fatunder
activity, way cellular
it’stoessential
understand and
to gainsubcellular
the abasis for PAK4
phenotypes
comprehensive
localization to using electron
understanding
cell-cell microscopy
junctions, ofand the which on iPSC-
molecular of the
Targeting Obesity through Fat derived
mechanism neurons.
proximal proteins Such
that governs phenotypes
(in cell-cellbrown may
fat development
junctions) be novel and
are
Burning- a Brown Fat biomarkers
function.
substrates of disease.
During
downstreamthe process of fatsignaling.
of metabolic
Cdc42 development, This
Obesity and its associated diseases such as
Connection PPARγ
project is considered
will therefore as the
extend master
these
diabetes increasingly are responsible for significant regulator
ongoing playingina
studies
central
of PAK4role
economic andandinPAK5,
controlling
socialinburdens a large
the context number
in manyof their of
regulation
countries. As
downstream
such, there is an urgent need for efficaciouswe
of development adipogenic
in the CNS.genes. In addition, had
obesity
demonstrated
therapies to combat that epigenomic
this epidemic. reprogramming
To develop novel is
fundamentally involved in
obesity therapies, it’s essential to gain a regulating brown fat
function.
comprehensive Recently, we identified
understanding ofathe novel brown fat
molecular
Multi-omics analysis of Non- activating factor which physically interacts with
mechanism that governs fat development and
Human Primates to identify PPARγ and promotes PPARγ activation. Given that it is
function. In this project, we adopted a Multi-omics
factors critically involved in the also an epigenomic writer, we hypothesize that it acts
analysis approach to systematically identify primate-
regulation of metabolic as a key integrator connecting PPARγ signalling with
specific factors critically involved in the regulation of
homeostasis epigenomic reprogramming to control brown fat are
metabolic homeostasis. Methodologies involved
development and function. This
Transcriptomics, Epigenomics, Single-Cell analyses, project aims at
deciphering
Translatomics, its Lipidomics,
molecular mechanism Metabolomics integrating
and
PPARγ
Quantitative Proteomics. Through the analysis, wein
signalling with epigenomic reprogramming
brown fat development.
aim at unveiling new mechanisms The knowledge regulating obtained
from this project will provide
metabolic homeostasis and identifying novel us with novel drug
drug
targets and open new avenues
targets for the development of metabolic medicine. for anti-obesity
therapy. Methodologies involved are epigenomic
profiling and animal phenotypic characterization.
how different neural circuits change their function
and configuration is still poorly understood. Tuberal
somatostatin neurons were recently found to play a
critical role in feeding regulation and they are the
only hypothalamic neurons respond preferentially to
palatable food. A better understanding of tuberal
Age-related macular somatostatin neurons will provide important insights
degeneration
investigate the(AMD) is a and in understanding how our brain respond to palatable
functional
medical condition in eye. food and how we develop over consumption of food
circuit maladaptation of AMD
is the leading
tuberal severe, and obesity. The current project aims to understand
cause ofneurons
somatostatin
permanent how tuberal somatostatin neurons gain their
in obesity vision loss in people
over age 60 worldwide. response to palatable food and how such response
My team and our collaborators change in obesity induced by high fat diet. We’ll also
are currently working on investigate how the
while the central tuberal
nervous somatostatin
system neurons
plays a critical role
elucidating the role of Age- input
in regulating feeding behavior, how the gut to
and output pattern change in obesity gain a
transmit
related maculopathy better understanding
Age-related
the information macular
about about
degeneration
nutrientshowto the change
(AMD)
the is ainmedical
central
neuronal
susceptibility 2 (ARMS2) gene condition function
in eye.and
nervous system result
AMD how from
is the
such and
leading contribute
gut-brain to
cause of severe,
investigate the gut brain
in the pathogenesis of Age- circuit maladaptation.
permanent vision Together,
loss in people this
over project will
communication changes in obesity areagestill60poorly
communication
related macular in feeding
degeneration provide
worldwide. a better understanding about how a key
understood. Through genetic profiling and in vivo
regulation and obesity
(AMD). Also, we recently found My hypothalamic
teamthe feeding
andcurrent regulation
our collaborators circuit
arefor is
currently changed in
imaging, project aims a betterworking
that ARMS2 protein is obesity
Somatic
on and
elucidating
understanding explore
activatingthe
of how potential
mutations
role strategies
gutinsenses
of Age-related
the epidermal for treating
growth
maculopathy
nutrient
stabilized in one of the age obesity
factor by targeting
receptor
susceptibility
information (EGFR)
2 (ARMS2)
and specific
influences gene feeding
contribute
the incentral
the regulation
to pathogenesis
more than 50%
nervous of
related cellular stress circuits.
of patients
Age-related
system inmacular
Singapore
to regulate andbehavior.
degeneration
feeding Asia with lungAlso, we
(AMD).
conditions. Our current work adenocarcinoma.
recently found that Targeting
ARMS2 proteinEGFR with EGFR-tyrosine
is stabilized in one
focuses on finding the kinase inhibitors
of the age related(TKI) represent
cellular stress aconditions.
major advance Our in
functional role of ARMS2 in the therapy.
current workHowever,
focuses TKI-responsive
on finding thepatients functional usually
role of
retinal pigment epithelial (RPE) relapse
ARMS2 in with
theaggressive
retinal pigmentcarcinoma within(RPE)
epithelial one cells
year.
cells and investigating the Therefore new approaches
and investigating the pathologicalin tacklingroleEGFR
of themutant
ARMS2-
pathological role of the patients are critical. We
variant (rs10490924) and others
in AMD. Currentlyhavethereshown arethat
not
ARMS2-variant (rs10490924) in non-small cell lung cancer
much biochemical, (NSCLC)and
cell biological cells with activated
functional
AMD. Currently there are not EGFR studieshave a defective
on ARMS2. Givenendosomal/lysosomal
this scenario, our current pathway
much biochemical, cell causing
work ondefective
ARMS2 isdegradation
of significantofinterest
EGFR mutantto the
biological and functional proteins. Our hypothesis
ophthalmologists is that mutant
and researchers working receptor-
on eye-
studies on ARMS2. Given this tyrosine kinases (RTKs)
related diseases. We areare stabilized
currently by a settoofstudy
planning
scenario, our current proteins due to their aberrant activity or inactivity,
Identification of geneswork on the mitochondrial and metabolomic part of the
ARMS2 leading to dysfunctional endosomal/lysosomal
stabilizing EGFR mutants and ARMS2-WT and –A69S in ARPE-19, ES-derived RPE
is of significant interest
to pathways, contributing to the cancer recurrence. In
targeting them in lung cancer cells and validate these findings in patient derived-iPS
the ophthalmologists and
researchers working on eye- order to test
based-RPE this hypothesis, we will perform an
cells.
related diseases. We are unbiased high-throughput RNAi screen of the whole
currently planning to study the genome in the EGFR-mutant cells to identify the
mitochondrial and genes responsible for defective degradation of EGFR
metabolomic part of the mutant. The major goal is to reveal the molecular
ARMS2-WT and –A69S in ARPE- This project responsible
mechanism aims to characterize and validate
for stabilization of EGFR novel
19, ES-derived RPE cells and proteome-based
mutants. This will subclasses
lead to the identified
identificationby JGofgroup for
critical
Proteomic dissection of triple
validate these findings in prioritizing
components potential
responsible prognostic/surrogate
for the action of markers
mutated
negative breast cancer
patient derived-iPS based-RPE for
heterogeneity
targeted
oncogenic treatment
EGFR which may and response
be potential monitoring
therapeutic (Ref:
cells. Kosok
targetsandfor Alli-Shaik et al 2020,
NSCLC. Together, iScience)the
elucidating using clinical
specimens.
molecular detail of proteins that’s stabilize EGFR-
mutant will lead to identification of new therapeutic
targets that will target downstream events shared by
This project aims
TKI-sensitive and/or to develop
resistantadvanced tools to RTKs
cancers harboring
identify
mutations next generation functional biomarkers
1. Development of novel
(diagnostic protein markers and potential drug
proteomic-centric
targets) from already accumulated advanced mass
computational biology
spectrometry-based cancer proteomics data through
pipelines for functional cancer
meta-analysis in combination with AI/Deep learning
biomarker discovery
and functional network analysis and validate them in
available clinical cohorts.
This project aims to transform JG group’s proof of

Mass spectrometry (MS)-based concept assay (Wee et al 2019, PNAS) to a one-shot
pathogen diagnostic tool clinical MS platform for a wide range of pathogen
development detection (e.g. respiratory viruses) and disease
severity monitoring.
dependent proteasome degradation, and several
ubiquitinating enzymes were identified to target
Hippo components. However, not much work on
ubiquitinating and deubiquitinating enzymes has
been shown to regulate Hippo components. Several
recent studies have revealed a few ubiquitinating and
deubiquitinating enzymes regulating Hippo pathway
Ubiquitinating/
components, including USP9X deubiquitinating
Deubiquitinating enzymes of
enzyme identified in our lab. The research on
the Hippo Pathway and their
ubiquitination/deubiquitination of Hippo pathway
potentials as cancer diagnostic
components is still nascent but represents an exciting
markers and therapeutic
new area of the Hippo pathway. To identify
targets
ubiquitinating and deubiquitinating enzymes for the
Hippo pathway, we searched our protein interacting
We inviteofPhD
network thestudents
Hippo pathway to investigate constructed the biological
in the lab
basis
through of “gut-feelings”,
proteomic analysis. how bacteria in the gut signals
Several ubiquitinating
to
andthe host to influence
deubiquitinating behaviour.
enzymes wereUsing identifiedrodents as a
as high
powerful
confidentpre-clinical
interacting mammalian proteins of the model,Hippo wepathway
will
Microbiome, Brain & Behaviour investigate
and we havehow diet modulates
published deubiquitinating the gut microbiome
enzymes
Cell
and
USP9X metabolic
hostasphenotypes.
a tumor status isThe
suppressorthecandidate
consequence
stabilizing willLATSof cross-
have the
kinases
talks between
opportunity
and other tointernal
upstream shapeHippo andproject
the external
components with factors. In the
ustotosuppress
synergize
meantime,
with
tumor our it is Our
larger
growth. also lab
theme involved
of in the
use-inspired
currently process
is working basic on of gene
several
expression
neuroscience
ubiquitinating regulation,
atandA*STAR. cell function, enzymes
deubiquitinating even cell which
Our previous
differentiation
regulate Hippo studies
and fate
pathway. identified
determination. immuneWe
Since ubiquitinating subsets
willandas
the predictive
determine
deubiquitinating the biomarkers
metabolic which
enzymesrequirements
play importantare superior toroles toand
maintain other
known
proper biomarkers
neuronal
are potential to predict
drugfunctions,
targets and
for the toresponsiveness
various uncover
diseases the of
Metabolic profiles changes and anti-PD-1/PD-L1
adaptive cancers,immunotherapy
including response of neurons
our work aims in lung
studyand
in reprogramming
to thelivertheir
effects on neurotransmission cancers.
metabolic
hypothesis Anti-PD-L1
networks
that these therapy
inenzymes
response wasregulate
just
to approved
altered themetabolic
Hippoby
and cognitive functions FDA in 2019
environments.
pathway to to Wetreatwill
control PD-L1-positive
cell further
proliferation unresectable
investigate and how
tumor the
Much
locally remains unknown about Triple the interaction of
loss of advanced
growth,
SARS-CoV-2compensatory
offeringwith
or metastatic
novel
the adaptation
opportunities
immune system;
Negative
of metabolic
for alterative
studies
Breast
to date
Cancersfor
targets (TNBC).
reprogramming cancer We
impacts therefore
treatment on peripheralaimnew to accurately
neurotransmission
and diagnostic and
have been limited
quantitatefunctions.
and perform by using deep phenotyping blood, of theacid
cognitive
methods.
pulmonary Finally, we will studytechniques.
amino
cytotoxic
metabolism T samples
cells andand
regulation M1bylow throughput
macrophages
critical metabolic from enzymes
both
In this and
blood proposal,
tumour wesamples
aim to perform ofbrain
TNBCand comprehensive
patients, to in
and selected
high-dimensional transporters
profiling of in thesurvival
immune their roles
Understanding the spatial ascertain
basic their association
neurotransmission, aswith
well as and
age-related
microenvironment
responsiveness proximal
to both standard to SARS-CoV-2
therapy and viral
immune microenvironment neurological diseases.
antigen on gastrointestinal and hepatic tissues of
proximal to SARS-COV-2 viral immunotherapy.
COVID-19 decedents and patients. We will build ofa the
antigen in gastrointestinal and We
The hypothesize
Cell Fate Engineering that the precise andpipeline quantification
Therapeutic Laboratory
novel in
cytotoxic house bioinformatic to analyse the
hepatic tissues focuses
spatial onT 1) cells
information
and M1 macrophages
identifyingthat the transcriptional
gain from the
populations
and in
TNBC couldswitches
epigenetic yield prognostic
during The and cell
stem predictive
renewal models
and cell-
abovementioned
for both standard profiling.
therapy and knowledge
immunotherapy. gleaned
fate
from determination,
these studies and 2)advance
would developing our novel tools,
understanding
In order to deeply
technologies profile and in-situ
and therapeutics map the of
for restoration
Deep profiling and in situ on diseaseT pathogenesis,
cytotoxic cells and M1 ultimately
macrophages, leading to
prospectively
diseased
improved tissues.
clinical Using
management embryonic and stem
national cellsstrategic
as a
mapping of cytotoxic T cells 50 TNBCwe
model, patients in Singapore
have previously Generalnovel
uncovered Hospital genomic
planning.
and M1 macrophages of Asian (SGH), willknown
be recruited
domains as DiSCand (Domainstheir fresh-frozen
involving Setdb1 tumour
Triple Negative Breast Cancers: samples and blood will be analysed
and Cohesin). SETDB1is traditionally associated with using 24-markers
Building a prognostic model for Flowcytometry
histone lysine 9and reciprocally(H3K9me3).
trimethylation validated with Our study
precision medicine in the era of Multiplex-Immunofluorescence
identified region of SETDB1and Cohesin in the matchedbinding FFPE
cancer immunotherapy samples.
without any TheH3K9me3.
selected immune-subsets
Further works confirmed will be further that
validated on tissue microarrays
SETDB1-Cohesin co-regulate target gene expression constructed from 400
TNBC diagnosed
and genome between
topology, thus2003 and 2015
controlling cellinfate
SGH.and The
prognostic value of each of the
lineage determinations (Warrier et al, Nucleic Acids cytotoxic T cells and
M1
Res.macrophages
“Mitotherapy”,
2022 in press; orwill
the be
Warrier evaluated
transplantation
et al, bioRxiv by of the
Cell fate Engineering of improvement
mitochondria,
2022.01.27.478011). of the proprietary
is an approach
Further studies prognostic
where we model
envision
confirmed that
the
which
Cytotoxic cells for Cell Therapy the was
functional
existence previously
of DiSC organelle published
in multiple itselfcell and
is thetypes, built
therapeuticby
including our
group.
humanLastly,
modality. the
lineprognostic
It involves
cancer the introduction
K562. and predictive
Of importance, of healthy powerDiSC
in K562,
will be tested
mitochondria
regulated genes on
into an
are independent
cells
enrichandfor tissues cohort
to replaced
cancer-linked of initial
biopsies
diseased
processes. from
orThe 200
defective andmitochondria
discovery 50of TNBCDiSCpatients that can
represent received
abe a
novel
standard
result
method of tochemotherapy
genetic mutations,
characterize, and
perturb anti-PD-L1
oxidative damage or
and molecularly
immunotherapy
advanced
target normal age.and respectively.
While autologous
diseased cells. mitotherapy
The current project has
Inclusion
been of
will bereported
1) probingdata generated
a Phase
the unique from
I clinical DiSC cytotoxic
trial has T of
signature cells
cord-and
M1 macrophages
demonstrated
and iPSCsafety as novel
and panel
NKefficacy to the
in pediatric to patients
Mitochondrial Transplantation blood
prognostic/predictive
derived
model
cells comparing
can equip pathologists
treated
peripheral forbloodischemia, this
terminally approach
matured would
NK not2)be
cells
Therapy for Metabolic Diseases and oncologists with a better tool to evaluate TNBC
applicable
Manipulating for using
patients suffering from
CRISPR-Cas9 sgRNA, mitochondrial
to toggle
(Mitotherapy) patients, ultimately improving clinical management
DNA (mtDNA)
effector and mutations,
repressor where
switches the
to disease-causing
derive
and patients’
mutations
therapeutically quality
in mtDNA functionalof
would lifeandin
bethe era ofincytotoxic
present
enhanced all bodily NK
immunotherapy.
cell
cellstypes. Here, we
3) To further propose that
understand of how our allogenic
solid tumour
mitotherapy
could be targeted platform would serve
by cytotoxic cells,asthrough
a universal the use
source of human
of single-cell mitochondria
CRISPR-Cas9 knockout for treatment of
libraries targeting
metabolic
genome-wide disorders.
genes and Apart highfrom treating spatial
resolution mtDNAmulti-
disorders,
omics. we envision that this platform would also
benefit metabolic diseases as well as degenerative
conditions where acute metabolic rescue would be
beneficial.
There is no cure for spinal cord injury and advanced
spinal cord degeneration. Current treatment practices
aim to prevent further deterioration by spinal
stabilization surgery and rehabilitation therapy. These
approaches do not repair the spinal cord and patients
Downregulation
typically experience of the histone
varying methyltransferase
degrees of paralysis
Development of an injectable Setdb1
depending in the on intestine
the site and is associated
severity ofwith injury.chronic
Our
cell therapy product for Spinal inflammation,
proposed cell therapy loss of stem cells, involves
approach disruptedthe
Cord Injury differentiation
transplantationand associated
of purified spinalimpairment
cord neural of stem
epithelial
cells derived barrier
fromfunctions, contributing
human induced to
pluripotent stem
inflammatory bowel disease.
cells that are suspended in anPreliminary
alginate hydrogel.evidence We
indicates
hypothesize thatthat
Setdb1 is also selectively
the alginate hydrogel will expressed
reduce
within epithelial
shear stress duringgland bases and
injection harboring
promote Lgr5/Aqp5-
expressing
engraftment stem
andcells in the distal
long-term stomach,
survivability of thebut its
Using
graftedmouse
functions models and
in regulating
cells. ex vivo homeostasis
epithelial cancer organoids, and
Evaluating Setdb1 functions we haveinrecently
disease this tissueidentified AQP5 as
are currently a functional
unknown. This
during epithelial homeostasis marker of tumour-resident
project will employ a varietystem-likeof mousecells modelsin gastric
and disease in the stomach cancers
(including (Nature,
a novel2020). In vivo ablation
stomach-specific CreERT2of these line) and
cancer
ex vivo stem
organoidscells effectively
to evaluateameliorates
setdb1 functions tumour in
growth
epithelial and metastasis,and
homeostasis highlighting
disease via thelineage
therapeutictracing,
potential
conditional of loss
targeting AQP5+ tumour
of function/gain cells in in
of function the
clinic. However,
combination withgastric tumours
multi-omics can survive
profiling transient
strategies.
loss of theloss
Potential AQP5+ cells by
of setdb1 replenishing
expression duringthishuman
population
through an as yet
gastric disease willundefined
be evaluated mechanism
in patients of cellular
with
We haveand
plasticity,
gastritis recently
leading
cancer. developed
to re-emergence
Mechanistic accurate mouse
of aggressive
insight into any models
role
Characterizing the niche for of
AQP5+ CSC’s in Gastric Cancer foradvanced
cancers. Thishuman
dysregulated project gastric
setdb1 cancer
willexpression
seek that
to elucidate facilitate
in driving the
investigation
mechanism
stomach disorders ofofgastric
theisunderlying
tumour cell
expected mechanisms
to plasticity
reveal novel driving
following
gastric
AQP5+ carcinogenesis
cell ablation,
opportunities from initiation
focusing
for therapeutic on through
the role
intervention of the tolocal
invasion
tumour niche and dissemination
environment.to secondary organs
A multimodal approach
(Nature Cell Biol.
incorporating In press).
single This project
cell RNAseq, spatialwill employ
these next generation
transcriptomics, in vivomouse
ablation models, together
and lineage with
tracing
ex vivoanorganoid
using array of models and multi-omics
mouse models and ex vivo gastric
technologies
cancer organoids to decipher the expression
will be employed. changes goal
The ultimate
Deciphering the mechanism of accompanying
is to reveal novel tumour invasion
therapeutic of the submucosa
opportunities for and
cancer invasion and metastasis subsequent metastasis
effectively targeting thetoresident
the liver, lungcells
stem and
in the stomach abdomen.
responsibleThis for approach is expected
driving gastric cancer to revealand
growth novel
biomarkers
metastasis and critical effectors of cancer
progression for improved disease diagnosis and
Cancer
treatment willinaffect 1 in 3 Candidate
the clinic. of us, yet human
effectors cells
willarebe
highly
evaluatedresistant to neoplastic
via genetic transformation
KO/overexpression for
in mouse
reasons that are
gastric cancer poorlyand
models understood.
using mouse Thisgastric
inter- cancer
disciplinary
organoids via project will deploy
orthotopic recently developed
transplantation. The efficacy
Targeting Tumour suppressive technologies
and selectivity(eg., Emery ettargets
of selected al., CellinChem Biol (2021);
ameliorating
networks for early intervention De et al.,progression
disease Cell Rep (2020)) will betovalidated
parse networks
using matched of
in cancer cellular signals and molecular
human normal/gastric cancer interactions
organoids that
suppress carcinogenesis in epithelial tissues (eg.,
Venkitaraman, Science (2014)) in order to develop
Maintaining
novel therapeutic energyapproaches
homeostasis forrequires accurate
early intervention
sensing
(eg., Scottof etincoming
al., Cellnutritional
Chem Biol substrates
(2021)) and
internal metabolic demands, coupled with
mechanisms to direct and utilize available resources.
As an integrator of long term energy balance, our
Peripheral neural circuits in
brains receive signals from peripheral energy stores
metabolic regulation.
to direct food intake and energy expenditure. This
projects aims to uncover the neural mechanisms
involved in peripheral sensing of metabolic state and
downstream effector functions controlled by the
brain.
Agrin mechanobiology in
Agrin mechanobiology in cancer and tissue repair
cancer and tissue repair
MicroRNAs are ubiquitous short RNAs that regulate
gene expression. Since their discovery, the
mechanisms that underlie their biology, and how they
regulate their target genes, have been intensely
studied. We are interested in functional roles for
microRNA in disease, and have identified several
MicroRNA regulatory pathways
microRNA mutants that exhibit age-associated
in intercellular communication
neurodegeneration. We aim to characterise these
and disease RNA therapeutics,
mutants to identifylike antisense
conserved oligonucleotides
neuroprotective
(ASOs),
mechanisms siRNA/shRNA
that can for RNA interference,
be used for translatingand guide
novel
RNA used in We
treatments. CRISPR are alsogeneinterested
editing, show great
in roles for
promise.
microRNAHowever,in intercellularan important current obstacle
communication, and aimisto
cell-type-specific
identify moleculartargeting factors that of therapies
underpininthese a scalable
manner.
processes. Our lab develops RNA technologies based on
genetically
Adipose-derived encodable stem functional
cells (ASCs)RNA exhibitsensors,
various
An RNA-based platform for cell- including Pandan, a fluorescent
biological functions and hold great therapeutic microRNA sensor (Aw
targeting of RNA therapeutics et. al., Nucleic Acids Research
potentials. We have performed comprehensive 2016). We also recently
developed an RNA-based platform
characterization of human ASCs with whole genome for RNA signal
transduction,
gene expression, which could be cell
secretome, usedsurface
as a scalable
markers
method for cell-specific targeting
screening and metabolomics, and identified of RNA novel
therapeutics.
factors that regulateWe have available
stem cell and projects in the lab to
differentiation
refine
capabilities of ASCs. We discovered potentgene
this platform, and to develop it for
therapy applications
antimicrobial effects in of cancer biology and
ASCs, especially during
neurological
Novel differentiating stem cell- Cellular
differentiation diseases.
agriculture is an emerging
into mature adipocytes. field Weof novel
havefood
based therapeutic approaches development
identified novel to anti-microbial
make alternative meat that is
peptides also
to chronic wound infection environment
exhibit anti-biofilm and animal friendly.
activities and workFat isagainst
an important
but oftenstrains
bacterial neglected component
resistant to standardof meat. With The
antibiotics.
support
peptides,ofinfunding
addition from Singapore Food
to ASC-derived Story R&D
extracellular
Programme, our lab established
vesicles (exosomes), are currently new fat-derived
investigated incell
lines
wound from edible fish
associated species,
infection stem cell
models culture
(in vitro, exand
vivo,
differentiation
and in vivo), which conditions
will pave into themature
way for fatacells.
new The
best cell lines
therapeutic exhibit doubling
approach. The student time willas fast as ~12
investigate
hours
the and near 100%
anti-bacterial differentiation
mechanism of these efficiencies. The
Cell-based healthy fat from fish
student will
is take
proteins/peptides
The heart one of parttheinmost
using our projects
these modelstoand
metabolically study
other
active
species for alternative meat
molecular
experimental basis of these
approaches. cell
tissues in the human body, relying heavily on lines using
transcriptomics
mitochondrial ATP andproduction
metabolomics, developthe
to maintain improved
high
cell culture
energy
We found demand media
that when and differentiation
of contracting conditions
cardiomyocytes.
primed adipose-derived stemthat
are serum-free,
Cardiac aging,
cells (ASCs) food
which
exhibit grade, nutritional
is associated
potent and
with structural
anti-microbial cost
effects, and
effective.
especially 3D
functional and differentiation.
changes
during scale-up cultureisTheir
in the heart, system
a major will
riskalso
bactericidal be
factor
investigated.
in developing
potency This
is through project
cardiovascular involves
secretion disease. team work and
The process of
of anti-microbial
multi-industrial/academic
cardiac
peptides. aging
We is characterized
identified novelcollaborations
by the presence
peptides across
that of
exhibit
Stem cell-derived antimicrobial Singapore
hypertrophy, and overseas.
fibrosis effects The goal
and arrhythmias. is to develop
Biochemically,
robust anti-bacterial that also work against
peptides for wound-associated healthy
biofilms cultivated
accumulation fish fat that
of misfolded
and antibiotic-resistant can
proteins, complement
strains. In this taste,
dysfunctional
infection texture and
mitochondria nutrition
with increasedof alternative
production meat. of reactive
project, the student will investigate molecular basis of
oxygen species (ROS)
these peptides. Both in and suppressed
vitro and in vivo mitophagy
wound- are
also associated
associated with models
infection cardiac will aging.beWhiledevelopedseveral FDA
that
approved drugs such bactericidal
will aid in evaluating as mTOR inhibitorseffects and (rapamycin
restoring
and everolimus)
physiological have been demonstrated to improve
functions.
both lifespan and healthspan in animal models,
A metabolomic approach to Hippo
patients signaling pathway is an
taking rapamycins evolutionarily
to prevent organ
unravel mechanisms regulating conserved pathway that
transplant rejection havecontrols
presented organ size by
adverse side
human cardiac aging using 3D regulating cell proliferation,
effects including apoptosis, and stemhigh
stomatitis, thrombocytopenia, cell
organoids self
serumrenewal. The pathway
triglycerides has threeand
and cholesterol, components:
impaired the
upstream
wound healing regulatoryprocesses.factors, the kinasetreatment
In contrast, cascade (Mst- with
Sav-Lats-Mob),
-ketoglutarate,and the downstream
a biological compound transcriptional
found
machinery,
naturally in whichthe human consistsbody of has
YAP,shown
TAZ (transcription
to improve
co-activators)
healthspan of and animal TEAD (transcription
models factor).
without significant
Formation
increase in of YAP/TAZ-TEAD
their lifespans. The complexes
impact ofleads - to the
transcription
ketoglutarate of in growth-promoting
improving human genes. isThe
health currently
Structural studies on Hippo
abnormal
being studiedactivation
in an of YAP/TAZ
ongoing trial.has been associated
pathway and drug
with
In thismultiple
study, we types of cancers.
propose to model The cardiac
main focus aging of this
development
project
using 3Discardiac
to investigateorganoids howthat thewere
Hippoderivedpathway from
regulates
SIRT3 andcell SIRT6 proliferation
knockout human and to translate
iPS cell lines. this Of the
fundamental
Sirtuins, SIRT3knowledgeand SIRT6 into havepotential
shown promise drug as
candidates.
cellular targets Thetospecific aims of this
delay processes ofproject
aging and are: (1)
To elucidate
promote the molecular
healthspan. As such, mechanism
we hypothesize governing thatthe
regulation of the kinase
cellular knockout modelscascadeof SIRT3(2)and To SIRT6
develop kinase
would be
cascade
relevant inhibitor
aging models for tissue
that can regeneration
lead to the (3) To
develop Lats inhibitor
identification of novel for agingcancer immunotherapy; (5)
modifiers.
To develop potent lead compounds that can disrupt
YAP/TAZ-TEAD interactions for cancer therapeutics.
the body axis, sensory perceptions like vision and
olfaction as well as respiratory, brain and kidney
physiology. A wide spectrum of genetic and metabolic
diseases arise from dysfunction of cilia, collectively
called ciliopathies. The project aims to utilize genetic
analysis in zebrafish, mice and cultured human stem
cell based tissues an organoids to identify the
mechanisms involved in ciliary disorders. This will
Chromatin
involve theregulatorsgenerationhelp andto cellestablish
biological cell-type
Genetics and therapeutics of specific gene expression
characterization of zebrafish, programs.
mouseWhereas and human the cell
ciliary diseases stability
mutants of forchromatin
a varied set structure
of ciliary is proteins
central for utilizing
maintaining
state-of-the-art cellular identity,such
techniques its inherent
as CRISPR/Cas9 plasticity gene
also
editing,provides
confocal, a means for cell stateand
super-resolution (re)programming,
electron
which
microscopy may also as wellbe exploited
as proteininbiochemistry
pathologicallike
circumstances1.
immunoprecipitation My lab and has a long-standing
BioID. Informationinterest gleaned
in
from understanding
these mechanistic the epigenetic
studies will mechanisms
then be utilized of to
lineage
explore plasticity
human diseases in earlyarising
development
from ciliary (Nat disorders.
Cell Biol.
Drug
Theseresistance,
2020 Feb;22(2):175-186).
include polycysticeither intrinsicMore or
kidney acquired,
recently,
disease, we have
airway
Investigating a role of represents aourmajor bugbearmalformations
into precision medicine.
broadened
disease, infertility,investigations
cardiac study how andcancer It
embryonic factor reactivation is increasing clear that epigenetic reprogramming
cells
scoliosisundergoof the epigenetic
spine. reprogramming
Therapeutic strategies to induce
will be
in cancer cell plasticity mechanisms contribute topostulate
transcriptional plasticity in
phenotypic
invented to plasticity.
ameliorate Wethe that reactivation
disease symptoms
cancer
of cells
embryonic
through enabling
factors lineage
a combination may drive
of the transformation of towards
cellular plasticity
discovery
aprograms
‘drug-tolerant
pharmacological in cancer persister’ (DTP)
cells through
modulators state. These rareor
epigenetic
of ciliary pathways
population
mechanisms,
gene therapy of leading
DTP cancer
techniques cells
to tumour
to acquire
evolution
complement transcriptomic
andactivity
the
and
of the epigenetic
adaption mutant features
to therapy.
protein resembling
Bywith
combining
the wild-type that of
single-cell earlyRNA
counterpart.
embryonic
sequencingcells that are developmentally
(scRNA-seq), spatial profiling and plastic.genetic
Diabetes
Accordingly,
manipulations, is a they
debilitating
aim tochronic
wesurvive and adapt disease
systematically readily that tohas
investigate
Identifying epigenetic drivers of spiraled
the rolesout
Totipotent
therapeutic of control,
ofcells
pressures,
early-embryonic affecting
have unrestricted
and over more
time
factors than
developmental
incan 400
re-populate
tumorigenesis
cancer therapeutic resistance million
potential
the
and tumour.
how people
andUsing
their in the
represent world.
the Often,
established
heterogenous pinnacle people
commercial
expressions of the with
may cellular
cell line
diabetes
hierarchy
and develop
of distinct
patient-derived
correlate to severe
developmental complications
xenograft
cancer potency.
cell and such models
Therefore,
organoid
states. as
cardiovascular
understanding
of resistance, we diseases
how and tokidney
the epigenome
propose isolatefailures,
of
and totipotent leading
characterize cellto
an
theastronomical
supports
DTP cancermaximal healthcare
cellscellular burden.
plasticity
to identify Because
holds
the epigenetic great ofdrivers
this,
Singapore
potential
of therapeutic indeclared fieldWar
theresistance. onToDiabetes,
of regenerative and
this end,medicine.
we havethe nation
We
is currently
recently
developed very focused
established
epigenetic inon addressing
antechnologies
vitro thatits
embryonic aredisease
stem cell
amenable
mechanisms.
(ESC)-based
for low inputmodel material. of totipotency
We intend to that enables
also use us to
study the factors
pharmacologic and mechanisms
approaches to identify underlying
epigenetic
Investigating the molecular In Asia,thatit isimpede
increasingly recognized that the failure
mechanisms of cell fate
totipotency
drugs (Nat Cell the Biol. 2020 Feb;22(2):175-186),
formation or progression of in
humanand
DTPs, pancreatic
circumventing assess thefor beta cells isofthe
challenges
improved primary
working
clinical with
outcomes culprit infor
early
plasticity the development of diabetes. Despite so,
mouse/human
combination embryos.
with This work
standard-of-care has opened up
treatments.
mechanisms
new opportunities underlying human pancreatic
for regenerative medicine beta andcell
to
failure
interrogate during thehuman
early development of diabetes remain
tissue development. In this
unclear.
project, we Therefore, we at the
wish to utilize our Stem
ESC modelCells and of Diabetes
Laboratory
totipotencyseek to use human
to uncover pluripotent
novel principles stem cells
of cellular
(hPSCs),
plasticityhuman islets and
and translate thishuman
knowledge beta cellintolinenewto
investigate
experimental diabetes
strategies disease
to mechanisms
engineer human occurring
cells with in
Using human in vitro models This project involves the use of human pluripotent
humans.
maximum developmental plasticity for therapeutic
for studying diabetes disease stem cells (hPSCs), human islets and human beta cell
mechanisms purposes.
line to investigate diabetes disease mechanisms. The
Ph.D.
student students
can expect can expect to be very
to be exposed well-trained in
to methods/skills
our young and vibrant laboratory
such as hPSC/human islet/human beta cell cultures,
(http://www.adrianteolab.com/),
gene knock down/out and overexpression, be very well-versed
in
manipulation of signalling pathwaysvery
Stem Cells and Diabetes, and be andwell-numerous
connected
other molecular techniques. The studentSurgeons
with Diabetes Clinicians and is expected
whom
to be highlywe interact
motivated, with readextensively in the landscape.
the literature
Human in vitro models for We seek to place
extensively, our staff knowledge
gain in-depth and students oninthe anresearch
exciting
studying diabetes disease position
topic, master basic molecular biology techniques is
of working on translational research that
mechanisms highly
quicklyrelevant
and carry tooutboth our clinicianwith
experiments collaborators and
our patients.
guidance/mentorship. It will be ideal if the student
has had some prior research experience. This project
The studentto
is expected is give
expected to be highly
the student an early motivated,
stage read
the
appreciation for research as a career. knowledge
literature extensively, gain in-depth
on the research topic, and master the art of
performing
The studentresearch with close to
is also encouraged guidance
read upand on the
mentorship.
Stem Cells and Overtime,
Diabetes the student
Laboratory is expected to
Human in vitro models to study gainHuman in vitro models
confidence and mature to study intodiabetes
an disease
independent
diabetes disease mechanisms (http://www.adrianteolab.com/)
mechanisms
scientist with excellent knowledge
to find
and
out more
skills in the
about our research.
areas of Stem Cells and Diabetes.
We have developed an ex vivo drug testing platform
as well as patient-derived models of soft tissue
sarcomas. Systemic therapies have been applied to
patients based on this platform as off-label
indications. A clinical trial is also planned for the near
Ex vivo drug testing in patient- future. The candidate will investigate the link
derived models of soft tissue between disease response or resistance to specific
sarcomas drugs and potential mechanisms which may form
predictive biomarkers in soft tissue sarcoma. The
Colorectal
candidate will cancer also(CRC) is the third
be intricately most prevalent
involved in all
cancer
aspectsand theproject,
of this second leadingwhich sees cause of cancer
collaborations
1.
betweenResearch
mortality. Although
IMCB, Summary patients have
the National Cancer more treatment
Centre
options
Singapore, for NUS,
CRC patients, the prognosis is poor for
CSI and industry.
Study an interesting gene in Our lab hasCRC
metastatic 3 majorpatients.streams: UIBR, Translational
Ferroptosis, a newly
the development and research
discovered and formSpinofoff companies.
regulated cell death driven by
progression of colorectal iron-dependent excessive lipid peroxidation, has been
cancer via regulating 1) UIBR: 2inthemes
implicated in UIBR and therapeutic
the development
ferroptosis responses of various types of tumors. In our project,
a) RNAs and
we mainly focus proteins that regulate
on elucidating Inflammation
the mechanism of
and Cancer:in the development and progression of
ferroptosis
Inflammation
CRC to exploreinvolving potentialthe innate andtargets
therapeutic adaptivefor CRC
immune
patients. systems is a normal response to infection.
However, it is now known that when allowed to
In this project,
continue unchecked,we willchronicutilise clinical
inflammationsamples is to
a key
Charatactering hepatocellular The mitogen-activated
perform cutting edge
underlying cause for the development of protein
single cell kinase
and (MAPK)
spatial
carcinoma at spatial resolution signalling
transcriptomic
autoimmune pathway playsneurodegenerative
to reconstruct
disorders, a fundamental
the ecosystem rolediseases,
in the
that
carcinogenesis
make up of
hepatocellular colorectal and
carcinoma.
metabolic syndromes such as diabetes and cancer. numerous other
neoplasms.
Our lab studies Theadevelopment
transcriptionof targeted
factor called agents
NFkB that
inhibit MEK 1/2 has created the
which is a master regulator of inflammation. Indeed potential for
downstream
deregulated activity blockade of ofNFkBtheprecedes
MAPK pathway. Though
and is causally
MEK inhibition has demonstrated
linked to chronic inflammation and the development clinically significant
efficacy
of several in human
several ailmentstumor types, therapeutic
including metabolic success
has
syndromes and cancers. However, given thatThus,
been limited in colorectal cancer (CRC). NFkB
Identification of SATB2 as
potential
signaling isrational
also essentialcombination for many strategies and the
housekeeping
biomarker for drug response in
investigation into potential predictive
cellular and developmental events in normal biomarkers human of
CRC
response will be in urgent need.
beings, simply blocking NFkB to curb inflammation is In this project, we
have
not anidentified
option. Hence, SATB2,deciphering
a nuclear matrix-associated
the regulation of
transcription factor
NFkB signaling is crucial to and epigenetic
understanding regulator,the which
could serve as a promising
mechanism and role of uncontrolled/unwanted NFkBdiagnostic biomarker to
predict
Inflammationdrug response
activity seen ininvolving especially
human ailments the innate for
andand MEK1/2
in adaptive
developing
inhibitors.
immune
better and Next,
safer we
systems is awill
normala) understand
anti-inflammatory response drug. the
to infection.
We are
b) Understanding TERT mechanism
However, by which
it isefforts
now known SATB2 regulates
that RNA whenand drug
allowed response
to
focusing our to identify protein
promoter reactivation: Key for in vitro that
continue and in vivo
unchecked, b) develop
explore inflammation
chronic the role of SATB2 in
is ablock
key
targets will help drugs which will
making cancer cell specific vivo using
underlying genetic
cause for more engineered
the development CRC mouse model
of hence may
NFkB /inflammation selectively and
telomerase inhibitors autoimmune
have less sidedisorders, effects. neurodegenerative diseases,
metabolic syndromes such as diabetes and cancer.
Our
b) lab studies a transcription
Understanding TERT promoter factorreactivation:
called NFkBKey
which
for makingis a master
cancerregulatorcell specific of inflammation.
telomerase inhibitors Indeed
deregulated
(NRF-CRP funded): activity of NFkB precedes and is causally
linked
Cancers toarechronic
a leading inflammation
cause of death and the in development
Singapore,
RNAs and proteins that of
butseveral human ailments
the treatment of various including
kinds ofmetabolic
cancers is often
regulate Inflammation and syndromes
unsuccessfuland duecancers.
to the majorHowever, given that
differences NFkB
in the way
Cancer signaling
the cancers is also
ariseessential
and grow. forCancers
many housekeeping
are often treated
cellular
by two main and developmental events in normal human
approaches - chemo/radiotherapy, and
beings,
Targeted therapies, which specifically stop cancer is
targeted simply
therapy blocking
– each NFkB
with to
hugecurb inflammation
limitations. The
not an option.
sledgehammer
growth drivers Hence, approach
(oncogenes), deciphering the regulation
of chemo/radiotherapy
are costly and requireof
NFkB
causes signaling
massive is
sidecrucial
effectsto
tedious patient stratification. It is unsuitableunderstanding
on normal the
cells. Targeted
for some
mechanism
therapies, and
which role of uncontrolled/unwanted
specifically
patients and extends survival by only a few months.stop cancer growth NFkB
Understanding TERT promoter activity
drivers seen
called in human
oncogenes, ailments
are and
costly
Our first of its kind globally research, aims to create in
and developing
require
reactivation: Key for making better
tedious
drugs thatand safer
patient
will anti-inflammatory
stratification
work effectively alldrug.
forindriver We
oncogene
kinds are
of cancers,
cancer cell specific telomerase focusing
identification.our efforts
Targeted to identify
therapies
without the need for stratification. To achieve this, RNA areandalsoprotein
not
inhibitors targets
suitable that
we identified for allwill help develop
apatients,
potential and drugs which
generally
pharmacogenetic extendwill blockto
patient
method
NFkB
specifically block an enzyme called telomerase, amay
survival /inflammation
by only a few more
months.selectively
Our and
lab’s hence
research, the
have
first less
of its side
kind effects.
globally, aims
growth engine in 90% of cancers. Success will mean to create drugs that will
work
cheaper effectively
drugs, minimal in all kinds sideofeffects
cancers, andwithout
possiblythe a
need for stratification.
universal therapy Towards this goal, we have
identified a potential pharmacogenetic method to
specifically block an enzyme called telomerase, a
growth engine in 90% of cancers. If successful, this
method will result in cheaper drugs, which cause
minimal side effects and likely work as a universal
therapy in most human cancer types.
requires a limited amount of agent for a therapeutic
effect. Second, it is easily accessible for targeted
treatment and the presence of the blood-retinal-
barrier limits systemic exposure, reducing the
chances of off-target effects. As such, gene therapy
has seen its successes in ophthalmology, such as
LUXTURNA (voretigene neparvovec), a viral-vector
based treatment for leber congenital amaurosis, an
Developing non-viral vectors inherited retinal disease associated with extremely
for gene therapy of inherited poor vision[1]. However, at a cost of USD 425, 000
retinal diseases per eye, the treatment is still out of reach of many
patients.
A contributing factor to the price of viral-vector based

gene therapy is the complexity and low yield of the
manufacturing process. In contrast, non-viral vectors
Generating immunodeficient
are usually cheaper and easierzebrafish models that
to manufacture.
Humanised immunodeficient
expresses human
Furthermore, theycytokine, thus allowing
are also generally engraftment
less cytotoxic
zebrafish for
of
andhuman primary cells
immunogenic. and immune
However, cells. Designing
such platforms usually
xenotransplantation
methodologys for transplantation
have lower delivery of humanto
efficiency as compared cells into
viral-
approaches
these
based zebrafish mutants.
delivery. As such, there is a need to develop
non-viral vectors, which demonstrate significant
transfection efficiency.
Despite
Dissectingadoptive
first linecell therapies
therapy and immune
resistance in
checkpoint inhibitors
First line therapy resistance in hepatocellular haveusing
carcinoma shown particular
single cell sequencing
hepatocellular carcinoma at encouraging results to treat
approaches. Identifying and tumors, many cancer
gaining mechanistic
single cell resolution patients still doof
understanding not respond
therapy to treatment.
resistance tumorThese
failures may be related to an inefficient persistence of
subpopulation.
the immune response. Therefore, many studies have
focused on chemical mediators to enhance T cell
functions. Few recent studies have shown the
possibility to modulate T cell functions by providing
Immune checkpoint
physical signals. blockade
Therefore, wetherapies
propose to such as
stimulate T
Investigating the effect of programmed death-1electric
(PD-1) blockade are having
cells with alternating fields similar to the
alternating electric fields on promising results in clinical trials
tumor-treating-field (TTF) that aretoFDA
improve
approvedanti- for
human T cell proliferation, tumour T cell functions for different cancers,
the treatment of glioblastoma and mesothelioma.
activation and metabolism including
Changes inmelanoma. However,
T cell activation, there are and
proliferation still major
limitations,
metabolismsuch as assessed
will be low response rate and adverse
and characterized by
immune-mediated
flow cytometry, 3D side effects,assays
functional because andthe
genomic
molecular
analysis. The mechanisms
possibility ofto Tcontrol
cell inhibitory signalling
T cell functions by
remain
electric very
fieldspoorly
could understood.
pave the wayThe forproject
enhancingaimsthe to T
combine a melanoma
cell antitumor response murine model and
and improve the Tclinical
cell
Investigating inhibitory
receptor
outcome (TCR)
of transgenic
current and mice
new together with a 3D
immunotherapeutic
signalling during anti-tumor T
microfluidic-based multicellular culture platform to
cell responses using a 3D tumor strategies. This project will allow the PhD student to
study ex vivo
carry out the molecular mechanisms
an interdisciplinary work involving of PD-1
model
receptor
immunology, signalling during
oncology andCD8+ T cell anti-melanoma
bioengineering.
responses. The useadenocarcinoma
Pancreatic ductal of a 3D culture system(PDAC) willis oneallow
of
us to create a more physiologically
the leading causes of cancer-related death relevant system
compared
worldwide.toTherapeutic
other 2D orapproaches
3D culture assays
for PDAC that fail to
benefit
reproduce the complex extracellular
only a few patients due to the asymptomatic nature matrix-cancer
Investigating interactions and/or
of the disease and toutilize a gravity-mediated
the challenges posed by the
microenvironment-associated interaction between cells. These proposed
tumor microenvironment (TME). In particular,
mechanisms of pancreatic experiments will potentially identify
stromal and immune cells have beenentirely
reported novel
to
ductal adenocarcinoma molecular mechanisms regulating PD-1 inhibitory
influence tumor progression. The
The immunosuppressive tumor microenvironment proposed project
progression signalling.
aims
(TME)toisuse a 3Drecognized
widely microfluidic-based PDAC for
as responsible modelthe to
elucidate the role of monocytes, resident
failure of many clinical trials for solid tumors.
macrophages
Nevertheless, and stromalthe
disrupting cells during tumor
pro-tumor activity of the
progression.
TME remains a challenge. Therefore, we propose to
design tumor-targeting polymer nanoparticles (NPs)
Novel tumor-targeting polymer
able to efficiently deliver immunomodulatory
nanoparticles to delivery
molecules to the TME-associated immune cells, to
immunomodulatory molecules
promote their tumor suppressive functions.
and chemotherapeutic drugs
Chemotherapeutic drugs will be also loaded on the
NPs and delivered to TME for achieving a synergistic
cytotoxic effect on the tumor cells. The engineered
NPs will be validated within a microfluidic-based 3D
micro-physiological in vitro model mimicking the
multicellular TME, and in in vivo murine models
vaccination and tumor elimination, especially in the
cases of high mutational burden cancers of the skin
and lung, have been demonstrated, but an anti-
cancer vaccine that is broadly applicable between
Protein
patientsTyrosine
and across Phosphatases
cancers remains (PTPs)elusive are a class to date. of
enzymes
One of the that biggestfunction hurdles to remove phosphorylations
in the discovery path of
from tyrosinecandidates
such vaccine residues inissignaling the lack proteins.of sharedThese cancer
Inositol
antigensisthat
enzymes a highly
act incanthebe bioactive
opposite
detected carbohydrate
way by as kinases,
profiling involved
to return
methods. in
signalling,
the
Thissignaling
project and will glucose
proteins
combine toand lipid metabolism.
ground
intelligent state, thereby
antigen The
Intelligent neoantigen placenta
enabling is andrich sophisticated
in inositols and acts as the gateway
predictiontemporal control to phospho-tyrosine
prioritisation algorithms,
discovery towards broad- regulating
signaling bysupply
providing of nutrients
an alternative toand theknowledge
fetus.
route to Henceregulate
with targeted antigen profiling of
spectrum cancer vaccination placental
the intensity function and is a major
duration of determinant
growth of fetal
signaling.
intrinsic tumor vulnerabilities that should be shared
growth.
betweenaFetal
Indeed, number
tumors growth and disorders
of PTPs
patients, haveto are
been associated
arrive implicated
at rational within
increased
metabolic risks
diseases,
design of anti-cancer of later for cardiometabolic
instance PTPN2 in
vaccines. disorders
obesity in and
offspring such as obesity
insulin resistance, but also andthediabetes.
loss of function of
Urinary
several
This SINGA inositol
other willPTPs is increased
support haveinvestigations
been inlinked
both large tointo and(i) small
potentiation
for gestational-age
towards
understanding cancerthe human
development.
rules newborns
governing In addition,
cancerand in there is an
antigen
Role of Protein Tyrosine intrauterine
emerging
presentation, role growth (ii)restricted
predicting(IUGR)
for receptor-type
and piglets.
PTPsvalidating
and in immune Highcell
Phosphatases (PTPs) in the placental
sub-populations,
clinically inositol
effective appears
where to protect
infiltration
cancer-specific
Maternal mental health stresses during pregnancy, of the
antigens fetus
these from
receptor
that can be
progression of liver steatosis to the
PTP
used pro-adipogenic
positive
to immunize immune effects
cells
individuals
presenting as anxiety and depression, are associated of
may maternal
have
against glycaemia.
deterministic
developing
hepatocellular carcinoma (HCC) Before
roles
colon in inositol
cancer
cancer
with later and
offspring supplementation
progression
the metastatic
psychopathology,or benign can be
spread exploited
after initialasofa
resolution.
independent
potential
diagnosis intervention in
postnatal maternal mental health status. cancer.
and resection offetal
primarygrowth colon disorders,
Studiesthere of
is
Singaporean children demonstrate strong linksmay
a
This need
project to understand
aims to how
elucidate placental
the inositol
involvement of
regulate
PTPs
between in the fetal growth.
progression
maternal Different
antenatal from depressive
healthyinositol to isomers
steatotic
symptoms and
their
liver, highly
but also diverse
the array
irreversible of
and differential brain microstructure around birth and derivatives
transition are
from known to
have quite
steatosis to different
liver bioactivities
cirrhosis
childhood, which is associated with behavioural and and
finally some may
hepatocellular also
Using magnetic resonance
inhibit the bioactive effects beof toothers.
imaging and spectroscopy to carcinoma.
Preterm
issues during The
premature focusrupture
infancy will increased
and of investigate
the fetal the impact
membranes
vulnerability to
This
of project
PTP activity will in use
both magnetic
precancer resonance
states of imaging
the liver as
investigate the role of placental (PPROM)
conditionsissuch a pregnancy
as majorcomplicationdepressive disorder accounting in for
later
techniques
well as in
approximately
life. Intrauterine to
infiltratingquantify
one thirdof
signals and
immune spatially
ofmaternalcell localise
compartments.
preterm births, inositol
which
stress received The
inositol in fetal growth
isomers
overall
results
by the fetusinand
aim higher other
isviato therisk metabolites
understand
of infantthe
placenta are within the
pathophysiology
mortality
thought and whole
to program in
regulation
placental
liver diseases
morbidity.
the fetal brain organ,
PPROM and
pertaining
during within
is preceded to smaller
PTPs
pregnancybyand and biopsies
identify
programmed
influence of
placenta
druggable
events
subsequent and
that targets umbilical
remodels in the
neurodevelopment. cord
fetalPTP tissue.
pathway
amnio-chorionic Results will be
to prevent
Mood
compared disturbances,
irreversible between
liver damage such leading
placenta as anxious
obtained up and
to fromdepressive
hepatocellular
membranes,
This projectas
symptoms, aiding
aims well toas in the weakening
identify
stress, the
are key highly and
placental ultimate
prevalent,
pregnancies
carcinoma.
rupture.
pathways This of
involved babies
includes in born small,
collagen
maternal-fetal normal,
modifications, or largeof
transmission for
including
gestational-age.in the Singapore Associations population.
will also While
be made
apoptosis,
mental
diagnosed health inflammation,
risk. An patients
psychiatric oxidative
integrative stress and
bioinformatics
receive
Investigating the mechanistic between
senescence. placentalClinical inositol
trials measures
of myo-inositol and in-utero
approach
pharmaceutical will be applied
orwith behavioural to available
treatments, data (eg.thoseclinical,
role of the placenta in fetal growth
supplementation and in newborn
pregnancy birthweight.
had reported This will
neurodevelopmental outcomes, placental omics)
maternal-fetal transmission of individuals
allow
reductions
with moreof
the unravelling
in preterm
modest,
the and
birth
subclinical
metabolic PPROM.
complaints
networks
from
are notongoing
typically mother-offspring
eligible for such cohorts
medical toHowever,
determine
care. Yet,
mental health risk involved
the mechanism in how inositols
involved may
is impact
unknown. placental
We
significant
subclinical transmission
mental pathways,
health issues can which
resultwillcan
in abe severe
function
hypothesized
validated and fetal
that
in areduction
separate growth.
myo-inositol
cohort These findings
ofsuppresses
samples then
a be
premature
using
and chronic
corroborated using data of the quality
from separate of life
ongoingand may
fetal
range
lead membrane
to plethoraremodeling
ofa laboratory oftechniques
otherwhere andincluding
health weakening,
issues,term thereby
molecular
such as poor
mother-offspring
reducing
biology to the risk
investigate cohorts,
of PPROM
gene and
expression longer
preterm birth.
changes, Toin
sleep, cognitive
offspring growth deficits,
and immunedata
metabolic disturbances,
is available.
investigate
vitro cultures
obesity, this
cardiovascularforhypothesis,
functional we
analysiswill
or gastrointestinal culture
and fetal
magnetic
problems.
In conclusion,
membranes
resonance – this
imaging obtained project
and from willuncomplicated
spectroscopy clarify the role
to analyse of
singleton
Consequently,
placental inositol poor in mental
fetal health
growth is not
regulation only and
Myo-Inositol and Fetal pregnancies
placental
associated a at
structure termand
diminished elective
measure
quality caesarean
ofmetabolites
life but section
can also –will
with
Membrane Remodeling and pave the
different
respectively. way for
concentrations development of of
myo-inositol. inositol We will
lead to significant
interventions for economic
fetal growth cost due to reduced
disorders, which may
Weakening subsequently
Understanding
productivity andassess
the the
precise
health markers
care mechanisms
costs. of fetalby membrane
which the
ultimately
remodeling
effects of mitigate
in
maternal the the
tissue
mood risk
and of
are future
culture
transmitted cardiovascular
medium via using
the
Individuals
disorders.
Increasingly with
powerful subclinical machine affectivelearning complaints
tools often
areELISA,
various
placenta
rely on techniques
to the
self-help fetus such
strategieswill as QPCR,
generate
to cope western
novel
with blot,
knowledge
their
being
gel applied
zymography across senescence
domains as assay. diverse Inengineering,
critical
symptoms.
business, Theseand
for designing
marketing,
interventions
include behavioural
andstrength
clinical
thatstrategies
medicine.
can parallel,
minimise
However,
we
(e.g.
will
the measure
risk
sports, of
relaxation in the
vertical tensile
transmission
techniques, of
yoga) of the
mental
as wellmembranes
health
as the use
their
and applications
associate
vulnerability, thealcohol
and medicine
biochemical
improve and
changes
long-term public health
induced
neurocognitive have
by
of
beensupplements,
suboptimal because or cigarettes.
ofofan insufficient Given the
Investigation of mood- myo-inositol
and
impactbehavioural treatment
outcomes with the weakening
offspring, andattention
ofinthe
to bothand
membranes.
ultimately technicalprevalence and human
Additionally,
optimising
of
domain mood
to study
disturbances
specific
potential the issues.
rescuing
and
the
A salient
reducing effect
enhancing effects of nutritional general
example population,
is theofalmost there is
uniformly a clear need
poorfetal for
body of
bioactives through digital of myo-inositol,
societal
efficacious, costs we
poor will precondition
mental health.
literature forsafe
membranes with
and
ML/AI-driven well-substantiated
myo-inositol models followed
solutions,
for predicting
by treatment
biomarkers including
COVID-19 credible
incidence nutritional or nutraceutical
with known
approaches. inducers&ofprognosis. PPROM (i.e. In health
tumor and necrosis
human
factor-α, potential
thrombin applications,
and challenges are
lipopolysaccharide) andfurther
In order to effectively
compounded byassessment
biased study
sampling and substantiate
and informative mood
perform
enhancement similar in a general yetof remodeling
vulnerable markers
population,
missingness;
and tensile strength. highly heterogenous,
Understanding multi-modal
theoutcome
role of myo- data;
the development
small, unbalanced ofsamples;
valid and sensitive
weakly labeled outcomes;
inositol
measures in regulating
as well asclinical the biochemical
diagnostic tools and
to identify the
and multi-factorial
biomechanical properties utility
of fetal considerations.
membrane is The
Advanced clinical prediction target population
project will develop are essential.
and apply methodsmay
These include
to design
better
essential
optimized to substantiate
subjective ratingsand facilitate
as well the
as novel, moreof
modelling for health and utilize rich,
future clinical clinical-
trials and research-
investigating derived
the efficacy measures
of myo-
human potential objective
(brain and measures,
body imaging, including digital biomarkers
multi-omics, wearable from
inositol
(bio)sensors prophylaxis against
and lifestyle parameters preterm birth.
derived from
sensors, anthropometrics, psychometrics,
digital sources.
environmental measures, etc.) in developing and
The projectclinical
validating will involve prediction integratedmodelsresearch for maternal streams and
that aim to substantiate
child health and wellness. The student will have mood-enhancing nutritional
bioactives
access to GUSTO, in clinical one trials
most and simultaneously
deeply characterized identify
and
birth cohorts in the world, as well as several states
validate novel digital biomarkers of mood
as sensitive, objective
collaborating cohorts around mood state the world.outcomes. For the The
research involves extensive
project, the student will gain transdisciplinary use of decentralized
study
mastery methodology.
in state-of-the-art The interplay methods of from
behavioral
science, nutrition, clinical
bioinformatics, data science / machine learning, science, sensor technology, and
and data sciences allows
biostatistics and have the opportunity to lead for a truly multidisciplinary
environmentally- driven effects. Genetically- driven
causes may be studied by experiment or newer
techniques (e.g. Mendelian Randomization), but such
effects may not generally apply to relevant conditions
or interventions. On the other hand, environmentally
driven effects may be more broadly applicable but
subject to many non-experimental biases.
Innovations in molecular profiling and machine
Machine learning for multi- learning-supported efficient effect estimators may
omic treatment effect provide a way forward. Applying more flexible and
estimation in clinical sciences powerful control of nuisance parameters (e.g.
and molecular epidemiology confounding & selection bias) using theory and multi-
omic data, can help refine signals, drive trials, and
optimize outcomes amongst intervention policies
Many
acrossfactors
many clinicalaffect the trajectory
domains. The of child will
student
development.
participate in on-going This PhDwork programme to identify seeks to
understand
developmental the effects
causal relationship
on child andbetween adolescent health
environmental
by triangulatingeffects genomics, and child development
epigenomics,
Multi-modal data analysis and
outcomes.
transcriptomics, The key andtechnical
metabolomics competencies to be
across numerous
causal inference for child
developed
matched tissues in this(e.g. programme
maternalisblood, machine cord learning
tissue, and
development Recent
the use advances
placenta, ofchild
causality in our
blood) understanding
theories
using in machine
deeply oflearning
phenotypedboth normalto
and
learn
cohortsabnormal
causal
in Singapore (e.g. cancerous)
relationships of child
and abroad. tissues have
development.
For the informed
project, This
the
our
work
studentstrategies
willwill
be gain fortransdisciplinary
based the
onin vitro rich
a very screening
multi-modal
mastery of naturaldata
in state-of-
extracts
had
the-artbeen orcollected
methodschemical fromincompounds
abioinformatics,
large Singapore for biological
datacohort.
science /
activity.
machineInlearning,
many cases, the difference
and biostatistics andinhavedimensional
the
context
opportunity of these to lead models,
impactfuli.e. 2D vs 3D may
scientific lead to
publications
different
and contributeoutcomes, to both with thetranslation
local 3D tissue models and often
Biomaterials for in vitro 3D
being more representative
international collaborative research of the in vivo efforts.phenotype
tissue models based on plant-
and thus making the better model. In our laboratory,
derived cell-adhesive factors
we have developed hydrogels based on natural
polymers and plant-derived cell-adhesive factors for
Food
the wasteof
The culture
developing management
cells,
fetus towards
is highlyis aconstruction
national
sensitivechallenge
toofthe theseof3D
Singapore.
tissue models. At the
Being same time,
non-animal
exposure of substances present in maternal blood increasing
derived, consumer
these
awareness
hydrogels
during gestation. of health,
offer a new nutrition
class of
It remains and wellness
sustainable
extremely has ledtoto
challenging
abiomaterials
rising demand for for
both enrichment
food
determine the fetal exposure to both essential and of foods
healthcare with
Enzymatic valorization of food functional
applications.
nutrients and ingredients
harmful like isomalto-oligosaccharides
chemicals, which in turn
waste to high value Increasing
(IMOs), its domestic, independent
determines the optimal doseshealth-associated
which prevent many food supply to
for supplementation
isomaltooligosacharides as support
and safe exposure limits. Although maternalurbanized
problems. a growing
Our overallpopulation
objective under
is highly
enzymatic blood
functional food ingredient. constraints
production
concentrations is ahigh
of goal whichIMOs
are value
commonly Singapore
from starch
used, aimsare
they to tackle
rich food
a poor
through
waste the “30 by 30” initiative.
proxy for fetal blood concentrations, as maternal-a
(e.g. bread waste). Our focus Thisis project
developing enables
independent,
novel enzyme domestic,
fetal transport for overcoming
is restricted resilient,theand
by the urban barrier.
industrial
placental challenge
food/protein
of producing supply. It establishes
non-/partially-digestible
Trans-placental movement is controlled by a state-of-the-art
IMOs with
urban
degree single-cell
of polymerization
metabolizing enzymesprotein asproduction
(DP) as
well ≥4.uptake platform to
and efflux
produce consumer relevant bright
transporters. In addition, both the maternal and fetal yellow biomass
Urban Single-Cell Protein from heterotrophic
physiologies microalgae.
are dynamically The project
changing through the
Production Harnessing innovates supply-chain eco-efficiency
first, second and third trimesters, adding andfurther
Emerging Microalgae-based productivity
complexity totothe mitigate costs through
determination of fetal (i) exposures.
food
Up- and Downstream Concepts industry side-stream utilization
Finally, the placental capacity for nutrient transport and (ii) pulsed electric
field (PEF)-based process innovations.
has been shown to vary greatly in healthy versus It investigates
food concept
gestational development
diabetes mellitusto(GDM) provide viable driven
mothers,
solutions for different customer
by up or downregulation of placental transporters segments (e.g., agefor
groups, ethnicity, and income
macro and micronutrients. Here, we aim to extend levels) across
Modelling the kinetics of Singapore’s
our established entire society.
virtual human Establishing
model platform climate-for
maternal-fetal transfer of resilient
healthy adults to the maternal-fetal unit, by and
agri-food systems to produce meat
nutrients and chemicals using a seafood
considering alternatives
3 aspects:also aids sustaining the
physiologically-realistic virtual population with healthy, nutritious food
human model 1. Changes in maternal physiology across the
trimesters, such as cardiac output, tissue blood flow
rates, blood and plasma volumes, plasma protein
concentrations, body fat percentages, liver and
kidney enzyme and transporter abundances.
2. Quantifying the expression of enzymes and
This project will
transporters involve screening
in placental tissue from NPLhealthy
fungal and
Fungal biofactory for food
collection
GDM mothers, to identify
whichstrainscontrols suitable for food of
the movement
ingredient production
ingredient
nutrients and production
chemicals across the placenta and is
the key determinant of fetal exposure.
3. Changes in fetal physiology across the trimesters,
such as tissue volumes, perfusion rates, blood and
plasma volumes, placenta, umbilical cord, amniotic
fluid and plasma protein concentrations.
Once constructed, we aim to Aapply the model to

guide the development of novel food ingredients,
formulations and dietary recommendations in healthy
and GDM pregnant women to support optimal
maternal nutrition and reduce fetal exposure to
chemical) and 3) patient serum specific screens to
determine IgE antibody binding and potential
antibody cross-reactivity. Though widely adopted, all
of these approaches lack harmonization and their use
in risk assessment requires further validation.
In this project, we aim firstly to investigate the

applicability of human granulocyte
Development of fungal mycelia activation/degranulation
This
This project
project will
will involve in
be run inscreening the assessment withof
NPL fungal
collaboration Agilent
as sustainable sources of food allergenic
collection potential
to identify of ingredients
strains
life sciences and is focused on the applicationsuitableor formulation
for single-cell in
of LDIR
proteins these
protein novel protein
production food sources.
imaging as a potential tool to rapidly acquire and These in vitro
assays
enhance will be conductedof
measurements bytoxicity
assaying whole
and geneticblood
from
damage in tissues and cells exposed to Xenobioticsto
donors with and without known food allergy
various reference
(with a specific food allergens
interest and selected
in food related materials testand
substances. The allergenic
exposure to the gastrointestinal tract). potential of test
substances and purified allergenic proteins will be
In vitro assessment of food determined
Work will focus by their
on the ability to trigger and
development activation and of
validation
allergenicity and gut degranulation of exposed granulocytes
optical staining techniques and compare these to which include
inflammation with human upregulation of CD63+ and release
classical immunohistochemical of histamine,
approaches following
reconstructed 3D gut model proteases (chymase, tryptase), cytokines,
exposure to known food chemicals and toxicants. The
and granulocytes prostaglandins
exact range andand type leukotrienes.
of materialsSecondly, the
for investigation is
potential of the test substances
open dependent on the interests and expertise of theto induce intestinal
inflammation
candidate. However, and dysregulation in the gut
FRESH has specific will bein
interest
modelled
the effect of 1) genotoxicants and 2) allergens on 3D
with commercial human reconstructed the
intestinal
gut and has microtissues-macrophage
active research programmes co-cultures.
lookingRNAat
Investigation of gut-food sequencing will be used
markers of toxicity for both.to detect the changes
We propose initialinwork
the
chemical interactions using expression of inflammation
to centre around our in-house 3D reconstitutedrelated genes and
Laser Directed Infra-Red (LDIR) multiplex ELISA will
human intestinal be performed
epithelia micronucleito quantify
cytomethe assay
imaging release of inflammatory
protocol (Lim et al 2022: cytokine panels. Intestinal
barrier dysfunction will be assessed with a trans-
https://doi.org/10.1007/s00204-022-03228-y) and
epithelial
assess if we electrical
can clearly resistance (TEER)
distinguish meter and
toxicant-induced
fluorescein
micronucleiisothiocyanate
formation from(FITC)–dextrancontaminatingtrans- fragments
epithelial permeability
such as DNA particles, microvesicles assay. Lastly, weandwill explore
the possibility using
apoptosomes to develop broadco-culture
field infraredmodel of human
spectroscopy.
reconstructed 3D intestinal microtissues
We are also keen to see if we can enhance endpoint and
Dietary chronobiotics for leukocytes. Thebetter
co-culture systemmodes
is hypothesized to
Dietary
detection chronobiotics
and for reducing
understand cardiometabolic
of action of
reducing cardiometabolic better recapitulate the crosstalk between native
disease
through risk
the identification
Bacteriophages possess of specific spectralenzymes
disease risk intestinal
markers epithelium
of genetic anddiverse
damage. immune and unusual
cells,
Spectroscopic hence a more
for the synthesis
predictive model of
for nucleotides
food and nucleictechniques
allergenicity. acids,
are
many powerful
of which tools
haveforfound detecting
uses inand studyingbiology.
molecular DNA
lesions and IR spectral changes
The increasing availability of bacteriophage have been observed
in live cells in
sequences and isolated
public nuclei associated
databases presents anwith
physical
opportunity for the discovery of new(e.g.
and chemical DNA damage Sofinska
enzymes andet
al: https://doi.org/10.3390/molecules25030561).
DNA modifications with potential applications in
Advantages
existing and and emerginglimitations of the Agilent This
DNA technologies. 8700project
LDIR
Enzyme discovery in for such analysis will be investigated.
will involve learning about nucleotide and nucleic acid
bacteriophages
biosynthetic pathways in diverse bacteriophages,
theorizing about potential new DNA modifications,
genome mining for bacteriophage biosynthetic
enzymes with potentially new activities, and wet lab
biochemistry to investigate the biochemical
hypotheses. Enzyme candidates with potential
academic or commercial interest will be engineered
Phytochemical and nutritional to alter or improve
Phytochemical and catalytic
nutritional activity.
properties of
properties of mushrooms and
mushrooms and its Impact on human health
its Impact on human health
1) Nutrimetabolomics, 1) This project will identify and characterize new and

Metabolomics, Purification and known bioactive nutritional compounds fom edible
structure elucidation of food (plants, edible fungi and other) through a
bioactive nutritional and novel metabolomics-based workflow. 2) To develop
compounds 2) Determination analytical capabilities and standards to support the
of chemical contaminant measurement needs of the fresh produces
profiles in fresh produces measurement
Acute diseases such as Sepsis involves microbial
infection with potentially deadly consequences1
having high incidence
This project aims to use in CO2-derived
Singapore2 (and acetate around as thethe
world), where early
main feedstock detection
to produce utilizing point-of-care
value-added chemicals
testing
and (POCT) can improve
bioingredients. aim overall efficiency of care
A biosensor
delivery3,4. typicallyWe
Gold-standard consists toofimprove
bacterial 3 components: the utilization
culture an
Microbial utilization of CO2- efficiency
analyte-sensitiveof acetate in:
constituent 1) enhancing
which the
ideally uptake
reacts of
derived acetate to produce confirmation
acetate and 2)can take days
improving theorconversion
longer (for of resource-
acetate
specifically
strapped to a target,
hospitals). a transducer
Similarly, development to convert of athe 3)
high-value bioingredients into acetyl-CoA
corresponding by reducing
reaction to a the
readable ATP consumption;
signal, and a
microfluidic
diversifying bacterial sensing
acetyl-CoA to differentplatform can reduce
value-added
display component
diagnosis such duration to relate
for more effective the signal to the
antibiotics
products
concentration as terpenoids,
of the analyte. polyketides and fatty
treatment to improve
acids. patient As it is bothIn
outcomes. challenging
this
and time-consuming
project, antimicrobialtoresistance, design sensors and immune for specific
target analytes, a customizable
responses such as cytokine storms, implicated molecular imprintingto
with colorimetric transduction
acute conditions such as Sepsis (and even to sensing methodology
will be explored
infectious diseases in this
like project
COVID-19), to develop
will be smartstudied to
Development of smart biosensors suitable for
elucidate our understanding of Sepsis field testing. Miniaturization
pathogenesis.of
molecular imprinted biosensors such a developed
Bacterial biosensors sensor
can be canminiaturized
also find applications into a in
microfluidics, where multiple
microfluidic (lab-on-a-chip) device as an indicative lab processes can be
conceivably
Although
biomarkersafe forperformed
food handling
Sepsis. on a fluidic
Micro- practices chipand
and nanofabrication (lab-on-a-
procedures
chip)
are within
implemented
technologies the size
will also of
at every one’s palm.
stage of the food
be correspondingly Critical research
life cycle
explored to
challenges
and supplyreduce
drastically include
chain, there enabling
reagent could robust
volume measurements,
be instances
requirement where and
reusability
food products
help reduce andcost real-time
are per test or
mishandled long-term
while or monitoring
inadvertently
enabling simultaneous
capabilities.
contaminated.
tests to be performedSuch biosensors
There iswith growing have
a small applications
demand
device for footprint,in
Development of a rapid, in- foodborne
technologies
making it suitable pathogen
that ensure detection,
the safetyand
for field-testing infectious
of food disease
rapidproducts,
point-of-
vitro Sepsis diagnostics detection
in lieuSepsis
need of the and environmental
numerous
diagnosis. monitoring, while
food contamination they
incidents
platform can also be utilized for biomolecules
across the world. Notwithstanding the development and organ-on-
chip
of studies.
several
References commercial freshness indicators in recent
years,
(1) Rudd, mostK.ofE.; them are forS.one-time
Johnson, C.; Agesa,usage, K. M.;or are
Cardiovascular
non-reversible
Shackelford, K. indicators.diseases
A.; Tsoi, D.; (CVD)
Such isindicators
Kievlan, a major
D. R.;disease
are also not
Colombara,
burden
suitable infordeveloped
D. V.; Ikuta, end-point
K. S.; Kissoon, countries.
consumerN.; Finfer,Current
usage S.;duediagnosis
et al.toGlobal, for
CVD requires
packaging
Regional, aNational
multitude
requirements
and of clinical
and
Sepsis significant
Incidence examinations
and costs.toIn
unit
evaluate
this project,
Mortality, the extent ofofheart
markers
1990–2017: microbial
Analysis abnormalities,
forloadthe such
Global such
asBurden as of
that
coronary
Salmonella
of Disease angiography
spp. from
Study. Lancet and
seafood cardiac
2020, catheterization,
(particularly
395, 200–211. shellfish
Real-time microbial monitoring both of which are highly invasive. Lipoprotein levels
and
(2) oysters) will be explored.I.;Other
Cai, Y.; Venkatachalam, Tee, N. food W.;matrices
Yen Tan,
for food safety and quality in
T.;the
such asblood
Kurup, A.;serum
fruits and dairy
Wong, account
S. Y.; products
Low,for C. 30% Y.; of
may all heart
also
Wang, beY.; Lee,
attacks,
W.; Liew,while
incorporated 50%
Y. X.;whereet al.ofthere
thoseiswith
Prevalence heart
applicability
of disease
Healthcare-in theoccurs
among
developed
Associated those with normal
sensing
Infections approach. lipidCritical
and Antimicrobial levels1. Detection
research
Use among of
We identified
small,
challenges
Adult dense
Inpatients a novel
low-density
include premature
in fabricating
Singapore lipoprotein ageing
a food-safe
Acute-Care (sdLDL)syndrome
indicator,
Hospitals:
characterized
subfractions
design
Resultsand fromchoicecanby help
the progressive
identify
of sensor
First National and
architecture
Point degenerative
individuals with normal
and
Prevalence
neuropathy
lipid levels
substrate,
Survey. Clin.as together
but high
well
Infect. CVD
asDis. with
maintaining
2017,skinThis
risk. atrophy
64, approach
operational
S61–S67. and dramatic
can be
hair
(3) whitening.
miniaturized
robustness
Kip, M.under into
M. Through
A.;adifferent
Hummel, mapping
microfluidic real-life
J. M.; and
chip, whole-exome
with
scenarios.
Eppink, lipoprotein
E. B.; Smart
Development of a miniaturized sequencing,
separation
packaging
Koffijberg, may H.; we
conductedidentified
also
Hopstaken,bevia a biallelic
high-voltage
explored
R. M.; to germline
device.
potentially
Ijzerman, M. J.; and
bring
sensing platform for studying mutation
investigated
the sensor
Kusters, R.inunit
the
along NS1BP
cost
Understanding with
down gene.
a study NS1BP
drastically
the of immune
Adoption encodesandcells
through an to
Use of
CVD pathogenesis evolutionary
elucidate
integration
Point-of-Care the conserved
withrole mass
Tests protein
ofininflammation
production
Dutch General believed CVDto serve
onPractices
techniques, such asas
Using
an E3 ubiquitin
pathogenesis.
roll-to-roll
Multi-Criteria ligase
The
fabrication.
Decision adaptor.
physics With behind
Analysis. such Previous
nanoscale
technology,
2019, studies
1–10.
showed
lipoprotein
mishandled
(4) Wang, thatsubtype
the
food
S.; ubiquitin-mediated
separation
products
Lifson, M. A.;that Inci, will
mayF.;alsoproteasome
result
Liang, be L.;explored
in health
Sheng,
pathway
in
Y.;this
hazards
Demirci, is an
project,
can beessential
U. while
identified
Advances thecellular
developed
inpromptly. machinery
Addressing lipoprotein
There often
will
Technical also be
linked
subtype toseparation
significantly
Challenges ageing.
ofreduced Wemethodology
therefore
Point-of-Careinstances hypothesize
of
Diagnostics can thatfood
beinvalidated
unnecessary Resource-
NS1BP
Limitedcontrols
through
wastage due to proteostasis
potential
Settings. collaborations
uncertainty
2016, and
of
16, 449–459. food protects
with medical
freshness. cells from
the degenerative
institutes. With effectsminiaturization
further of ageing. We aim of to
this
Deciphering the role of NS1PB
investigate
process, it isthe molecularthat
conceivable mechanisms
multiple by which
tests with
as a novel target for skin/hair
NS1BP
minimal maintains
use of cellularwill
reagents homeostasis
make it and for more
suitable
pigmentation and ageing in
understand
accurate andhow its losspoint-of-care
low-cost drives premature skin and
CVD diagnostics.
humans 3D human skin constructs in vitro have skin beencells widely
hair depigmentation. Patient's primary as
used
well asforiPSC
Reference many willapplications
be used to generate – including 2Dcosmetics,
and 3D in
dermal
vitro therapeutics
models
(1) Quantimetrix to study and
thedisease
Corporation. disease modelling.
in a dish. AOur
LIPOPRINT However,
currently
second
Breakthroughaim available
willInbe skin
to constructs
identify
Cholesterol are severely
the substrates
Management. of NS1BP
limited in terms
in skin cells of complexity,
to delineate both in structure
novel intervention pointsand for
biological
the treatment constituents
of more (such common as cell skintypes
disordersand and
Development of biomimetic extracellular
ageing. This research matrix components),
will bring novel owing to difficulties
fundamental
3D-printed skin model using in assembling
insights into how well-organized
NS1BP regulates tissues and re-creating
ubiquitin-mediated
decellularized human skin the optimal microenvironment.
proteasome and how its loss specifically Herein, we aim to
affects skin
overcome
lineages inthese humans. issues Wethrough
anticipate thethat controlled
it will bring
deposition
translational ofinsights
“bioinks” into(bioprinting)
more common derived ageing- from
decellularized
related disorders human skin. This enables
and potentially allow the precise
positioning
identification of ofvarious
new targetscell types for in theirdiseases.
these native
microenvironments, to reconstruct a physiological
skin model.
The metazoan nucleus is equipped with a meshwork
of intermediate filament proteins called the A- and B-
type lamins. Lamins lie beneath the inner nuclear
membrane and serve as nexus to maintain the
architectural integrity of the nucleus, chromatin
Epigenetic alterations on organization, DNA repair
Epigenetic alterations on and replication.
wound healing of aged skin
wound healing of aged skin Perturbations or mutations in components of the
nuclear lamina result in a large spectrum of diseases
called laminopathies. One of the most well-
characterized laminopathy is Hutchinson-Gilford
progeria (HGPS), a premature aging disorder that
resembles normal human aging. HGPS patients
exhibit alopecia, skin abnormalities, osteoporosis and
Role of histone succumb to cardiovascular complications in their
methyltransferases in Role
teens.ofOur
histone
goal methyltransferases in epidermal and
is to elucidate the molecular
epidermal and hair follicle hair follicle development and regeneration
mechanism that triggers progeria and to understand
development and regeneration its relevance to normal aging.
HGPS is caused by a mutated form of lamin A, called

progerin. Progerin expression causes rapid loss of
heterochromatin, persistent activation of DNA
damage checkpoint, impaired proliferation and
The role of heterochromatin in
premature senescence, an irreversible growth arrest.
the accelerated aging
We previously demonstrated that progerin-induced
syndrome Hutchinson-Gilford
senescence can be prevented by ectopic expression
Progeria
of telomerase, a ribonucleoprotein that elongates
telomeres, or by modulating the DNA damage
response specifically at telomeres (Chojnowski, eLIFE
2015; Aguado, Nature Comm 2019). In addition,
expression of the lamina-associated polypeptide α
Role of specific microRNAs in (LAP2α) delays premature senescence in progerin-
pro-inflammatory skin expressing cellsmicroRNAs
Role of specific (Chojnowski,in Aging Cell 2020). skin
pro-inflammatory
disorders and therapeutic However,
disorders and therapeutic implications.understanding
we currently lack a detailed
implications. as to how both telomerase and LAP2α can prevent
progerin-induced premature aging. In addition,
progerin causes a variety of disease-associated
phenotypes and it remains unclear how they are
causally and temporally linked. To address these
questions, we use doxycycline-inducible expression
system to delineate the temporal chain of events that
Targeting a defective molecular occurs upon progerin-expression and ultimately
Targeting a defective molecular switch to prevent
switch to prevent metastasis of causes senescence. Ultimately, our goal is to
metastasis of squamous cell carcinoma
squamous cell carcinoma investigate how these mechanism(s) relate to
chronological human aging and identify novel
pathways and factors that can delay aging of human
skin cell types.
Atopic dermatitis (AD) is a highly prevalent chronic
inflammatory skin condition which seriously affects
Targeting a pro-survival patients’ quality of life. Generally referred to as
Targeting a pro-survival oncomiR to prevent relapse
oncomiR to prevent relapse of “eczema”, AD is characterized by intense pruritus, a
of malignant
recurrent andgliomas.
relapsing skin disease, afflicting up to
malignant gliomas.
20% of children and 2-10% of adults. Usually starting
in early childhood, AD can continue into adulthood,
and ranks most severe among common skin diseases
by disability-adjusted life-years (DALY) and years lived
with a disease. Clinical management of AD is
currently limited to controlling inflammation in order
Design and development of to mitigate pain and itching associated with skin
novel therapeutics to treat lesions. Defective skin barrier and exposure to
atopic dermatitis allergens are known to initiate the development of
AD. Therefore, there is a crucial need for a more
rational approach focused on restoring barrier
function as an alternative, or potentially
complementary, strategy for the treatment of AD. We
recently identified a microRNA, miR-335, as a key
driver of the keratinocyte differentiation and
cornification, which is required for the establishment
of a healthy skin barrier. Analysis of AD lesions
reveals a significant loss of miR-335. Our objective is
to modulate miR-335 expression as a viable and novel
therapeutic strategy for the treatment of AD.
Diabetic foot ulcers (DFUs) are a devastating
complication of diabetes; one in four diabetics will
develop at least one non-healing chronic foot ulcer,
which potentially leads to lower limb amputations. A
5-year mortality rates range internationally from 39-
Design and development of 80%, worse than most cancers. This globally
Design and development of targeted therapeutics to
targeted therapeutics to treat escalating medical issue lacks approved
treat chronic wounds
pharmacologic options. Accelerating wound healing
chronic wounds
in DFUs is essential to prevent complications such as
infection and gangrene, which lead to amputations.
Wound healing requires an orchestrated integration
of complexgliomas,
Malignant biological in events
particular including cell migration,
glioblastoma
proliferation and extracellular
multiforme (GBM), is the most common and remodeling withthematrix
deposition, globally stimulated
deadliest cancer with very poor prognosis. Its by growth factors.
Design and development of Small
resistance non-coding RNAs, microRNAs
to conventional therapies,(miRNAs)rapid growth
nucleic acid therapeutics for for regulate gene expression
and infiltrative nature necessitate in this regenerative
the use of highly process.
chronic diabetic foot ulcers We identified a defective molecular
aggressive therapies including surgical resection, switch in chronic
DFUs; a consequence of dysregulated
radiation, and chemotherapy. GBM is uniquely TGF-b
signalling.
resistant toThe defective
standard switch allows
anti-cancer therapy sustained
due to the
Squamous-cell
expression of carcinoma
miRNA-198, (SCC)
which isinhibits
the most common
keratinocyte
existence
lethal of
malignancy therapy-resistant,
worldwide, tumor-initiating
with a high glioma
migration,
stem cells wound which
(GSCs), re-epithelialization
re-initiate andpropensity
wound
tumorigenesis.
for metastasis
healing. Targeting andmiR-198
consequent death.DFUs,
in chronic SCCs arise our from
Therefore,
aobjective
range ofissitesa therapeutic
including strategy anddesigned
head strategy neck,tolung, to ablate
GSCs to develop
is criticalbladder
to prevent a novel
GBM recurrence. accelerate
Design and development of oesophagus,
wound closure. Towards andthis,cervix. usingSquamous cell
Intriguingly, we have identified thatan integrated
oncogenic
novel therapeutic strategies to carcinoma
miRNA results from
therapeutics the uncontrolled
approach, we have growth of
designed
microRNA
squamous –cells,
miR-138 is a molecular
a subtype of epithelial determinant
cell. of
Epithelial
treat malignant gliomas sequence-specific, chemically modified antagomiR
GSCs,
carcinomasvital for their
are well growth
known and
to survival.
activate atarget Furthermore,
prolonged
oligonucleotides,
miR-138 directlyprogram which
mediates canacquired
effectively temozolomide miR-
wound-healing
198. Our objective is to that promotes
develop a novel malignant
therapeutic
(TMZ) chemo-resistance
transformation. Wound via targeting
closure requires thethe apoptosis
to accelerate
regulator BIM healing
and of DFUs,
depleting mitigate
miR-138 the
stimulates
activation of keratinocyte
complications associated migration
with chronic viawounds,
a dual-state and
apoptosis,
molecular inhibits
switch. proliferation
This switch involves and tumorigenesis
production ofin
prevent
orthotopic amputations.
xenograft models. More importantly, in
either the anti-migratory
Inflammatory diseases microRNA
inexpression
skin have is miR-198
been shown or the
to
Design and development of GBM patients, miR-138 higher in
pro-migratory
develop from Follistatin-like 1 (FSTL1) proteinskin from a
novel therapeutics to target recurrent
single GBMaberrant
transcript relative
in a
interactions
to first diagnosis
context-specific
between
manner.and In
metastasis in squamous cell immune
correlates cells
with and resident
poor prognosis cellsand of the tissue.
overall The
patient
normal skin,
innate immune expression of exonic
arm, specifically miR-198
macrophages from have
carcinoma survival. Our objective is to successfully target miR-
Follistatin-like-1
beeneradicate (FSTL1) mRNA
shown totherapeutically-resistant,
play critical roleswitches
in drivingto theFSTL1
disease
138,
protein expression upon wounding, tumor-
thus enhancing
conditions
initiating GSCssinceand depletion
abrogate oftumor
macrophages
recurrence.
temporal cell migration and wound
significantly reduces inflammatory burden in skin. re-
epithelialization
While the crosstalk Investigation
between macrophagesof wound-healing and skin
switch in head and
compartments has been studied neck SCC & cutaneous
largely atSCC the level of
revealed
cytokinesaand defect in the switch,
chemokines, much which
less hasrestrains
been miR-
Epithelial Immune Cross Talk in The198 expression
skin is anatimportant
understood perpetually,
the level of barrierallowing
metabolic sustained
that protects
crosstalkour
Homeostasis and Inflammation expression
body
between of FSTL1. Maintaining
frommacrophages
exogenous and other askin
environmental prolonged
and wound-
pathogenic
compartments.
healing
insults.
In our work,phase,
The barrier the
we have defective
function switch contributes
of skin is supported
used embryonic skin specific to
by
uncontrolled
resident
integrin b1 innate migration
immune
KO model and metastasis.
cells includingto
of inflammation Our
epidermalobjective
investigate
is
the tometabolic
target the
Langerhans cellshijacked
and, dermal
crosstalk molecular
between dendriticswitch
skin and
cells
compartmentsand develop
amacrophages.
novel strategy
with macrophages to
These prevent
toimmune
understandmetastasis
cellstheplay of SCC with
an important
initial event
improved
role
that not
drive patient
onlyinflammatory outcome.
in their surveillance
responsesfunctions in skin. This but allows
also
help in re-establishing
us a rather simplified system homeostasis. since the Tissue resident
embryonic skin
macrophages
lacks the adaptive get recruited
immune arm. to theWe skinareduring
now early
Epithelial Immune Crosstalk in embryonic
translating development
these findingsduring primitive and
to understanding the role of
Development and Disease definitive
innate immune haematopoiesis. Interestingly,
cells in inflammatory skinthisdisorders
recruitment
like psoriasisisand concomitant
AD. with the development of
skin epithelia and appendages which raises
speculation that these macrophages have a
developmental role which remains to be understood.
In the Raghavan lab, we are working to understand
the crosstalk between different skin compartments
and the resident macrophages both in skin
development and in inflammatory skin conditions
such as atopic dermatitis and psoriasis.
A*STAR Supervisor Designation Email Address
amit_singhal@idlabs.a-
Amit Singhal Principal Investigator
star.edu.sg
Amit Singhal Principal Investigator
star.edu.sg
guillaume_carissimo@idlabs.as
Guillaume Robert Carissimo Investigator
tar.edu.sg
Pablo_Bifani@IDlabs.a-
Juan Pablo BIFANI Associate Professor
star.edu.sg
Pablo_Bifani@IDlabs.a-
Juan Pablo BIFANI Associate Professor
star.edu.sg
matthew_tay@idlabs.a-
Tay Zirui Matthew Young Investigator
star.edu.sg
senior PI, Deputy Director
Chandra Shekhar verma chandra@bii.a-star.edu.sg
Research

Research

Research
FAN Hao Senior Principal Investigator fanh@bii.a-star.edu.sg
Hao Fan Senior Principal Investigator fanh@bii.a-star.edu.sg
Hao Fan Senior Principal Investigator fanh@bii.a-star.edu.sg
kumar_selvarajoo@bii.a-
Kumar Selvarajoo Senior Principal Investigator
star.edu.sg
kumar_selvarajoo@bii.a-
Kumar Selvarajoo Senior Principal Investigator
star.edu.sg
Lee Hwee Kuan Senior Principal Investigator leehk@bii.a-star.edu.sg
Lee Hwee Kuan Senior Principal Investigator leehk@bii.a-star.edu.sg
Peter John Bond Senior Principal Investigator peterjb@bii.a-star.edu.sg
Peter John Bond Senior Principal Investigator peterjb@bii.a-star.edu.sg
Sebastian Maurer-Stroh Executive Director sebastianms@bii.a-star.edu.sg
Sebastian Maurer-Stroh Executive Director sebastianms@bii.a-star.edu.sg

Principal Scientist, Group
Bi Xuezhi Leader of AS&T (Protein bi_xuezhi@bti.a-star.edu.sg
Analytics) Group
Deputy Executive Director,

Institute Scientist, Group
Choo Boon Hwa Andre andre_choo@bti.a-star.edu.sg
Leader of Biotherapeutics
Development Group
Senior Scientist, Group Leader

Zhang Wei of Downstream Processing zhang_wei@bti.a-star.edu.sg
Group
Principal Investigator and liang_kaicheng@ibb.a-

Liang Kaicheng
Senior Scientist II star.edu.sg
Chen Kok Hao Senior Research Scientist chenkh@gis.a-star.edu.sg
Chew Wei Leong Senior Research Scientist chewwl@gis.a-star.edu.sg
Jay W Shin Group Leader jay_shin@gis.a-star.edu.sg

Jianjun Liu DED/Senior Group Leader liuj3@gis.a-star.edu.sg
GIS Fellow (Junior Principal

Jinyue Liu liu_jinyue@gis.a-star.edu.sg
Investigator)
Li Jingmei Group Leader lijm1@gis.a-star.edu.sg
Li Jingmei Group Leader lijm1@gis.a-star.edu.sg
Associate Director and Senior

Niranjan Nagarajan nagarajann@gis.a-star.edu.sg
Group Leader
Rajkumar Dorajoo Senior Research Scientist dorajoor@gis.a-star.edu.sg
Rajkumar Dorajoo Research Scientist dorajoor@gis.a-star.edu.sg

Rajkumar Dorajoo Research Scientist dorajoor@gis.a-star.edu.sg
Ramanuj DasGupta Senior Group Leader dasguptar@gis.a-star.edu.sg
Roger Foo Adjunct Research Director Roger_Foo@imcb.a-star.edu.sg
Roger Foo Adjunct Research Director Roger_Foo@imcb.a-star.edu.sg
Senior Group Leader and

Shyam Prabhakar prabhakars@gis.a-star.edu.sg
Associate Director
Group Leader & Deputy
Tam Wai Leong tamwl@gis.a-star.edu.sg
Executive Director

Executive Director

Executive Director

Executive Director
teh.bin.tean@singhealth.com.s
Teh Bin Tean Senior Group Leader
g
Torsten Wuestefeld Group Leader wustefeldt@gis.a-star.edu.sg

Yue Wan Group leader wany@gis.a-star.edu.sg
Yue Wan Group leader wany@gis.a-star.edu.sg
Amit Singhal Senior Principal Investigator
star.edu.sg
Amit Singhal Senior Principal Investigator
star.edu.sg
guillaume_carissimo@IDLabs.a
-star.edu.sg
-star.edu.sg
-star.edu.sg
matthew_tay@idlabs.a-
Matthew Zirui Tay Young Investigator
star.edu.sg
stefan_oehlers@idlabs.a-
Stefan Oehlers Principal Investigator
star.edu.sg
stefan_oehlers@idlabs.a-
Stefan Oehlers Principal Investigator
star.edu.sg
Senior Principal Investigator &

S. Sendhil Velan Head, Metabolic Imaging sendhil_velan@sics.a-star.edu.sg
Group
Senior Principal Investigator &

S. Sendhil Velan Head, Metabolic Imaging sendhil_velan@sics.a-star.edu.sg
Group
Cyrus Beh Principal Investigator beh_cyrus@bti.a-star.edu.sg

Cyrus Beh Team Leader beh_cyrus@bti.a-star.edu.sg
Cyrus Beh Senior Scientist beh_cyrus@bti.a-star.edu.sg
Seow Yiqi Senior Research Scientist seowy@gis.a-star.edu.sg
Seow Yiqi Senior Research Scientist seowy@gis.a-star.edu.sg
Yi Yan YANG Covering Executive Director yyyang@bti.a-star.edu.sg
Covering Executive Director,

Yi Yan Yang yyyang@bti.a-star.edu.sg
Senior Principle Investigator

Yi Yan Yang CED, Senior PI yyyang@bti.a-star.edu.sg

Zhang_Yugen@isce2.a-
Yugen Zhang Senior PI
star.edu.sg
A*STAR Senior Fellow and

Jackie Y. Ying jyying@imre.a-star.edu.sg
Director, NanoBio Lab
Ajay Mathuru Joint Principal Investigator ajaym@imcb.a-star.edu.sg
Ajay Mathuru Joint Principal Investigator ajaym@imcb.a-star.edu.sg

Caroline Lei Wee Principal Investigator weel@imcb.a-star.edu.sg
Crystal Yeo Clinician Scientist crystaljjyeo@cantab.net
Edward Manser Senior Principal Investigator ed.manser@imcb.a-star.edu.sg
Feng Xu Principal Investigator fxu@imcb.a-star.edu.sg
Feng Xu Principal Investigator fxu@imcb.a-star.edu.sg

Fu Yu Senior Principal Investigator fu_yu@imcb.a-star.edu.sg
Fu Yu Senior Principal Investigator fu_yu@imcb.a-star.edu.sg
Gandhi T. K. Boopathy Research Scientist gandhibtk@imcb.a-star.edu.sg
Gandhi T. K. Boopathy Research Scientist gandhibtk@imcb.a-star.edu.sg
Herath Jayantha Gunaratne Senior Principal Investigator jayanthag@imcb.a-star.edu.sg

Hong Wanjin Executive Director mcbhwj@imcb.a-star.edu.sg
Tan_Hwei_Ee@imcb.a-
Hwei-Ee Tan Junior Investigator
star.edu.sg
Jiong TANG Group Leader tang_jiong@imcb.a-star.edu.sg
Joe Yeong poh sheng Group Leader yeongps@imcb.a-star.edu.sg
Joe Yeong poh sheng Group Leader yeongps@imcb.a-star.edu.sg
Loh Yuin Han Research Director yhloh@imcb.a-star.edu.sg
Ng Shi Yan Principal Investigator syng@imcb.a-star.edu.sg

Ng Shi Yan Principal Investigator syng@imcb.a-star.edu.sg
Nick Barker Research Director Nicholas_barker@imcb.a-star.edu.sg
Director, Disease Intervention

Prof Ashok Venkitaraman csidir@nus.edu.sg
Technology Lab, IMCB
Sarah Luo Xinwei Principal Investigator sarah_luo@imcb.a-star.edu.sg
Sayan Chakraborty Research Scientist sayanc@imcb.a-star.edu.sg

Sherry Shiying Aw Principal Investigator syaw@imcb.a-star.edu.sg
Sherry Shiying Aw Principal Investigator syaw@imcb.a-star.edu.sg
Shigeki Sugii Principal Investigator shigekis@imcb.a-star.edu.sg
Soh Boon Seng Principal Investigator bssoh@imcb.a-star.edu.sg
SONG HAIWEI Research Director haiwei@imcb.a-star.edu.sg

Sudipto Roy Senior Principal Investigator sudiptor@imcb.a-star.edu.sg
Tee Wee Wei Principal Investigator wwtee@imcb.a-star.edu.sg
Teo Kee Keong Adrian PI ateo@imcb.a-star.edu.sg
Teo Kee Keong Adrian PI ateo@imcb.a-star.edu.sg
Teo Kee Keong Adrian PI Ateo@imcb.a-star.edu.Sg

Research Clinician and Group
Valerie Shiwen Yang yangswv@imcb.a-star.edu.sg
Leader
Vinay Tergaonkar Research Director vinayt@imcb.a-star.edu.sg
Vinay Tergoankar Research Director vinayt@imcb.a-star.edu.sg

Xinyi Su Principal Investigator xysu@imcb.a-star.edu.sg
Yan Chuan Junior Investigator yan_chuan@imcb.a-star.edu.sg
Yan Chuan Junior Investigator yan_chuan@imcb.a-star.edu.sg
giulia_adriani@immunol.a-
Giulia ADRIANI Principal Investigator
star.edu.sg
star.edu.sg
star.edu.sg
star.edu.sg
wu_wei@immunol.a-
Wu Wei Principal Investigator
star.edu.sg
wu_wei@immunol.a-
Wu Wei Principal Investigator
star.edu.sg
Chan Shiao yng Associate Professor obgchan@nus.edu.sg
jeroen_schmitt@sifbi.a-
Jeroen Schmitt Senior Principal Investigator
star.edu.sg
jonathan_huang@sics.a-
Jonathan Huang Principal Investigator
star.edu.sg
jonathan_huang@sics.a-
Jonathan Huang Principal Investigator
star.edu.sg
Senior Principal Investigator

Lee Hwee Kuan (using SICS
(using SICS joint appointment leehk@bii.a-star.edu.sg
joint appt position)
position)
Andrew_Wan@SIFBI.a-
Andrew Wan Principal Investigator
star.edu.sg
Dr. Md Mahabubr Rahman Team Leader (Principal rahman-talukder@sifbi.a-

Talukder Investigator) star.edu.sg
Melanie_Weingarten@sifbi.a-
Dr. Melanie Weingarten Deputy Director
star.edu.sg
james_chan@sifbi.a-
James Chan Chun Yip Platform Lead
star.edu.sg
Ng Siew Bee Senior PI ngsb@sifbi.a-star.edu.sg

Ng Siew Bee Senior PI ngsb@sifbi.a-star.edu.sg
SMITH, Benjamin Paul Director, Future Ready Food

ben.smith@ntu.edu.sg
Chapman Safety Hub (FRESH)
SMITH, Benjamin Paul Director, Future Ready Food

ben.smith@ntu.edu.sg
Chapman Safety Hub (FRESH)
sumanto_haldar@sifbi.a-
Sumanto Haldar Principal Investigator
star.edu.sg
Wei Yifeng Scientist weiyf@sifbi.a-star.edu.sg
Xinyan Bi Senior Research Fellow Bi_xinyan@sifbi.a-star.edu.sg
yoganathank@sifbi.a-
Yoganathan Kanagasundaram Senior Principal Investigator
star.edu.sg
congqiang_zhang@sifbi.a-
Zhang Congqiang Junior PI
star.edu.sg
Leon Chan Cong Zhi Scientist II czchan@SIMTech.a-star.edu.sg
carine.bonnard@sris.a-
Carine Bonnard Principal Investigator
star.edu.sg
Liang Kun Research Scientist kun_liang@sris.a-star.edu.sg

Lim Chin Yan Principal Investigator chinyan.lim@sris.a-star.edu.sg
Lim Chin Yan Principal Investigator chinyan.lim@sris.a-star.edu.sg
oliver.dreesen@sris.a-
Oliver Dreesen Principal Investigator
star.edu.sg
Prabha.sampath@sris.a-
Prabha Sampath Senior Principal Investigator
star.edu.sg
star.edu.sg
star.edu.sg
Prabha Sampath Senior Principal Investigator sampathp@asrl.a-star.edu.sg

star.edu.sg
srikala_raghavan@asrl.a-
Srikala Raghavan Principal Investigator
star.edu.sg
srikala_raghavan@sris.a-
Srikala Raghavan Principle Investigator
star.edu.sg
Website University Collaborator University
https://www.a-star.edu.sg/
idlabs/about-us/people/our- Kevin Pethe NTU
investigators/amit-singhal
idlabs/about-us/people/our- Tsin Wen Yeo NTU
idlabs/about-us/people/our-
Benoit Malleret NUS
investigators/guillaume-
carissimo
Pablo Bifani NUS
Pablo BIFANI NUS

https://www.a-star.edu.sg/bii/
Yuguang Mu NTU
research/bsmd/asdb
Yuguang Mu NTU
research/bsmd/asdb
Ali Miserez NTU
research/bsmd/asdb
www.a-star.edu.sg/bii/
YEW Wen Shan NUS
research/bsmd/sldd
Yao Shao Qin NUS
research/bsmd/sldd
Wen Shan Yew NUS
research/bsmd/sldd
Chit Fang CHEOK NUS
research/bsfd/cbol
Alan Prem Kumar NUS
research/bsfd/cbol
https://web.bii.a-star.edu.sg/
Lee Hwee Kuan NUS
~leehk
https://web.bii.a-star.edu.sg/
Lee Hwee Kuan NUS
~leehk
Thorsten Wohland NUS
research/bsmd/msmd
EE Pui Lai Rachel NUS
research/bsmd/msmd
NUS
research/bsfd/psa
NUS
research/bsfd/psa
https://www.linkedin.com/in/
xuezhi-bi-41000130/;
https://www.duke- NUS
nus.edu.sg/directory/detail/bi-
xuezhi
www.liangresearch.com
https://khchenlab.github.io/
chewlab.github.io - NUS or NTU

Jianjun Liu NUS
gis/our-people/faculty-staff
https://jinyueliu0.github.io/
Foo Jia Nee NTU
Lab/
https://sites.google.com/
Li Jingmei NUS
view/drjingmei/home
https://mtms-lab.github.io
gis/our-people/faculty-staff/ Vitaly Sorokin NUS
members/rajkumar-dorajoo
National Cancer Center
Elaine Lim
Singapore
Dan Yock Young NUS
http://foo-lab.sg/ Roger Foo NUS
http://foo-lab.sg/ Roger Foo NUS
https://prabhakarlab.github.io/
https://www.tamlab.org/ Tam Wai Leong NUS
http://tbtlab.org/index.html
NA Yu Chun Kong, Victor NUS
NA Dan Yock Young NUS

Torsten Wuestefeld NTU
idlabs/about-us/people/our- Tsin Wen Yeo NTU
Benoit Malleret NUS
carissimo
Benoit Malleret NUS
carissimo
Benoit Malleret NUS
carissimo
idlabs/about-us/people/our- Laurent Renia NTU
investigators/matthew-tay
idlabs/about-us/people/our- Philip Ingham NTU
investigators/stefan-oehlers
investigators/stefan-oehlers
https://orcid.org/0000-0002-4096-0722
Dr. Mark Muthiah NUS
https://orcid.org/0000-0002-4096-0722
Prof. Johan Eriksson NUS
ibb/our-scientists/cyrus-beh's-
laboratory
Hanry Yu NUS
https://www.a-star.edu.sg/ NUS, CDE, Biomedical

ibb/our-scientists/cyrus-beh's- Engineering (Adjunct Assistant NUS
laboratory Prof.)
ibb/our-scientists/yi-yan-
yang's-laboratory
yang's-laboratory
yang's-laboratory
yang's-laboratory
https://orcid.org/0000-0001-
6938-2113
https://mathurulab.com
https://mathurulab.com
www.carolineweelab.com Suresh Jesuthasan NTU-LKC
Ong Wei Yi NUS
crystal-yeo-b690b5131/
imcb/imcb-research/scientific-
programmes/
neurometabolism-in-health-
diseases
programmes/
diseases
programmes/
diseases
www.yufulab.com
www.yufulab.com
programmes/innovative-
technologies
technologies
technologies
Hong Wanjin NUS
programmes/cancer-signaling-
therapies
NA
NA
https://www.rsc.a-star.edu.sg/
technologyplatforms/scientific-
side-menu/scientific- XIA yingcun NUS
information/histopathology/
multiplex-ihc-immuno-mapping
https://www.rsc.a-star.edu.sg/
technologyplatforms/scientific-
side-menu/scientific- Joanne Ngeow NTU
information/histopathology/
multiplex-ihc-immuno-mapping
http://stemcellslab.sg/ Chan Woon Khiong NUS
NA
NA
https://en.wikipedia.org/wiki/
Prof Ashok Venkitaraman NUS
Ashok_Venkitaraman
NUS
https://www.sherryawlab.org/ Soong Tuck Wah NUS
https://www.sherryawlab.org/ Soong Tuck Wah NUS
Shigeki Sugii Duke-NUS
programmes/cell-biology-and-
therapies/shigeki-sugii
Shigeki Sugii Duke-NUS
Soh Boon Seng NUS
therapies
SONG HAIWEI NUS
therapies
Cynthia He NUS
therapies
Tee Wee Wei NUS
therapies/wee-wei-tee
Tee Wee Wei NUS
therapies/wee-wei-tee
https://wwteelab.com NUS
http://www.adrianteolab.com/ Adrian Teo NUS

therapies/valerie-yang
https://tergaonkar-lab.com/ Tan Soo Yong NUS
NUS
retinalab.sg
Xiao Tianshu NTU SBS
therapies/chuan-yan
Xiao Tianshu NTU SBS
therapies/chuan-yan
sign/people/principal- Andy Tay NUS
investigators/giulia-adriani
Nicholas Robert John
sign/people/principal- NUS
Gascoigne
sign/people/principal- Veronique Angeli NUS
sign/people/principal- Li Jun NUS
sign/people/principal-
investigators/wei-wu; Wu Wei NUS
https://pharmacy.nus.edu.sg/t
eam/a-prof-wu-wei/
sign/people/principal-
investigators/wei-wu; Wu Wei NUS
https://pharmacy.nus.edu.sg/t
eam/a-prof-wu-wei/
Chan Shiao yng NUS
Chan Shiao yng NUS
Chan Shiao yng NUS
jeroen-schmitt-bba7876/
jonhuang.org
jonhuang.org
Lee Hwee Kuan NUS, NTU
nil Prof. Seeram Ramakrishna NUS
nil Prof. Seeram Ramakrishna NUS
To be determined NUS
jameschancy/
TBD NUS/NTU
TBD NUS/NTU
www.ntu.edu.sg/fresh Dr. Hui Kheng Lim NTU
www.ntu.edu.sg/fresh Dr Hui Kheng Lim NTU
cnrc/about-us/principal-
investigator
NUS/NTU/SUTD
research/trd/npc
https://scholar.google.com/
National University of
citations? Zhou Kang
Singapore
user=SDgjKwIAAAAJ&hl=en
https://www.linkedin.com/in/ National University of

Lim Chwee Teck
leonchan7 Singapore
https://www.linkedin.com/in/ Nanyang Technological

Hou Han Wei
leonchan7 University
https://www.linkedin.com/in/ Future Ready Food Safety Hub

Benjamin Paul Chapman Smith
leonchan7 (FRESH)
https://www.linkedin.com/in/ Nanyang Technological

Hou Han Wei
leonchan7 University
Ng Kee Woei NTU

sris/people/principal- Peter Droge NTU
investigators/oliver-dreesen
NA
NA
NA
NA
asrl/principal-investigators/
srikala-raghavan

Scholarships SINGA 2023-06-21-BMS

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Research Institute Course Category Focus Area

A*STAR Infectious Diseases

A*STAR Infectious Diseases

A*STAR Infectious Diseases

A*STAR Infectious Diseases

A*STAR Infectious Diseases

A*STAR Infectious Diseases Bioengineering &

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Molecular Biosciences

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Molecular Biosciences

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Gene Therapy/ Therapeutics

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Molecular Biosciences

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Molecular Biosciences

All of the above. Computing,

All of the above: Computing,

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Chemical Biology

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Infectious Diseases

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Health & Nutrition

Bioinformatics Institute (BII) Biomedical Sciences (BMS) Genetics/ Genomics

Centre For Frontier AI Research Bioengineering &

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore Biostatistics, Diseases,

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Institute of Molecular & Cell

Institute of Molecular & Cell

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Genome Institute of Singapore

Infectious Disease Labs (ID

Infectious Disease Labs (ID

Infectious Disease Labs (ID

Infectious Disease Labs (ID

Infectious Disease Labs (ID

Infectious Disease Labs (ID

Infectious Disease Labs (ID

Singapore Institute for Clinical Interdisciplinary (Biomedical

Singapore Institute for Clinical Interdisciplinary (Biomedical

Bioprocessing Technology Bioengineering &

Genome Institute of Singapore

Genome Institute of Singapore

Bioprocessing Technology Bioengineering &

Bioprocessing Technology Bioengineering &

Bioprocessing Technology Bioengineering &

Bioprocessing Technology Bioengineering &

Institure of Sustainability for

Institute of Materials Research Bioengineering &

Institute of Molecular & Cell

Institute of Molecular & Cell

Institute of Molecular & Cell

Institute of Molecular & Cell