BIOEN 472

 Welcome to the 5th edition of the course!

 Design-centered course
 Learn design principles  cancer-related
 Dissect designs
biosensors
 Practice making designs (in lab)

 Please take notes in class – it helps memorize.

 Flexibility to decide: No midterm / no final? (Explain – I need
to grade!  )
 BIOEN 472
 Lectures in Foege
 LABs in Foege N140 [Advanced Computing Lab] (for
design), in CoMotion (for fabrication) and in Folch lab (for
testing)

 Labs will be run by Arman Naderi (also grader)

 Digital manufacturing by laser cutting
 Design in AutoCAD  you have to design a microfluidic
device of your choice from a set of given designs (provided
by Arman in Google Drive). One design per student, so first
come first serve!
 Device building in CoMotion
 Device testing in Folch lab
 25% of the grade of the course
Section 1: It’s a small world BIOEN 455 (BioMEMS, Folch)
 Great Expectations
 Student Learning Goals
 Know the state of the art of biosensors for cancer
(lectures)
 Learn to design/operate from scratch a microfluidic

device (lectures + labs)

 “Inverted Classroom” approach to teaching

I will first introduce a topic

 You will obtain the information (you are already good at

that, but you will learn the relevant material doing so)
 You will deliver it to me (you are the “teacher”) IN TEAMS

 You learn to deliver information

 I will provide a template before delivery,

guidance/interaction during delivery, and feedback after

delivery
 Great Grade Expectations
 Final grade: 0-4
 There will be presentations every day
 Each person will get to present every other week in
teams of 2
 Graded 0-4, 75% of the total grade of the course
 Teams 1&2 present on Wed, Teams 3&4 present on
Fri
 8 teams of 2 people ea.; Lowest-number teams only
PhD students
 Grading:
 Graded only on content
 Class gives feedback on presentation clarity

 5 presentations
 Great Expectations
 No midterm, no final
 I’ll give you personalized feedback (you may opt out)
around midterm to let you know how you are doing
with your presentations
 + 1 Lab report (25% of grade). Needs to be neat and
a precise account of what you did in the lab  take
notes!
 + 0.1 participation
Great Expectations
I need everyone’s participation!
Wed Sep 30 – 30 min Intro to Cancer & Biosensors
Fri Oct 2 – [TOPIC1] (How to Build a Presentation)
– Digital Manufacturing Tutorial
Tue Oct 6 – Lab in Foege N140 (AutoCAD intro)
Wed Oct 7 – In-class directed team research on [TOPIC1] (40 min)
– Digital Manufacturing Tutorial (20 min)
Fri Oct 9 – Intro to [TOPIC2] (20 min)
– Digital Manufacturing Tutorial (40 min)
Tue Oct 13 – Lab in Foege N140 (AutoCAD design) 1st cycle
Wed Oct 14 – Intro to [TOPIC3] (20 min)
– Presentation #1 by TEAMS 1&2 (20 min each)
Fri Oct 16 – Intro to [TOPIC4] (20 min)
– Presentation #1 by TEAMS 3&4 (20 min ea.)
Tue Oct 20 – Lab in CoMotion MakerSpace (safety & intro to laser cutting)
Wed Oct 21 – Intro to [TOPIC5] (20 min)
– Presentation #1 by TEAMS 5&6 (20 min ea.)
Fri Oct 23 – Intro to [TOPIC6] (20 min)
– Presentation #1 by TEAMS 7&8 (20 min ea.)
Tue Oct 27– Lab in CoMotion MakerSpace (design work day)
Wed Oct 28 – Intro to [TOPIC7] (20 min)
2nd cycle
– Presentation #2 by TEAMS 1&2 (20 min ea.)
Fri Oct 30 – Intro to [TOPIC8] (20 min)
– Presentation #2 by TEAMS 3&4 (20 min ea.)
CANCER RESULTS FROM ONE RENEGADE (STEM) CELL
Many cancer phenotypes in all tissues
Resistance to chemotherapy
Tumor heterogeneity
The 7 Hallmarks of Cancer
No two cancers are alike

NEED FOR PERSONALIZED

CANCER THERAPY
Cancer Stem Cells (CSCs) have been pinpointed as
the cellular “culprits” of cancer therapy
• Their discovery in 1994 generated great excitement
because people expected complete cure from CSC ALDH1+ breast CSCs
eradication
• However, conventional chemotherapy (which
targets fast-growing cells and/or induce apoptosis)
is inefficient against CSCs because:
• CSCs are quiescent and/or slow-cycling
• overexpress antiapoptotic proteins
• contain multidrug resistance proteins
• Not fundamentally very different
from normal stem cells!

Any systemic application

is likely to be potentially
toxic
Adoptive immunotherapy

select for CD4+ and CD8+ T cells

GMP
LIMITATIONS
• Expensive GMP facilities and
personnel

• Cost of equipment

• Cost of lentivirus
infect/electroporate with genes:
• Tumor heterogeneity and
• CAR (chimaeric antigen receptor)
• control genes resistance
• Limited (~1) number of
genes for targets and
safety controls
 Metastasis

Primary Tumor
Epithelial-to-Mesenchymal Transition (EMT)

Circulating Tumor Cells

Secondary Mesenchymal-to-Epithelial Transition (MET)

Tumor
 Myeloid cell origin of metastasis
Myeloid cells have great differentiation
potential similar to EMT  MET

Myeloid cells are motile and can be

activated/their phenotype changed with
cytokines

Macrophages have phagocytic activity

Tumor Associated Macrophages (TAMs)!

Species without leukocytes do not metastasize their tumors

Macrophage-tumor cell fusion == “EMT”

Example of very exciting paper (relevant to Section 1):
Scott Manalis Nature 2007 paper