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Table Of Contents

Cancer and somatic evolution
1.1 What is cancer?
1.2 Basic cancer genetics
1.3 Multi-stage carcinogenesis and colon cancer
1.4 Genetic instability
1.6 Evolutionary theory and Darwinian selection
Mathematical modeling of tumorigenesis
2.1 Ordinary differential equations
2.2 Partial differential equations
2.3 Discrete, cellular automaton models
2.4 Stochastic modeling
2.5 Statistics and parameter fitting
2.6 Concluding remarks
Cancer initiation: one-hit and two-hit stochastic models
3.1 A one-hit model
3.1.2 Analysis of a one-hit process
3.2 A two-hit model
3.2.1 Process description
3.2.2 Two ways to acquire the second hit
3.2.3 The regime of tunneling
3.3.1 Description of the model
3.3.2 A one-hit process
3.3.3 Three types of dynamics
3.3.4 Probability to create a mutant of type "C"
3.3.5 A two-hit process
3.4 Overview
4.1 Some biological facts about genetic instability in colon cancer
4.2 A model for the initiation of sporadic colorectal cancers
4.3 Sporadic colorectal cancers, CIN and MSI
4.4 FAP
4.5 HNPCC
4.6 Insights following from this analysis
Cellular origins of cancer
5.1 Stem cells, tissue renewal and cancer
5.2 The basic renewal model
5.3 Three scenarios
5.4 Mathematical analysis
5.5 Implications and data
Costs and benefits of chromosomal instability
6.1 The effect of chromosome loss on the generation of can- cer
6.2 Calculating the optimal rate of chromosome loss
6.3 Why does CIN emerge?
6.4 The bigger picture
DNA damage and genetic instability
7.1 Competition dynamics
7.2 Competition dynamics and cancer evolution
7.2.1 A quasispecies model
7.2.2 Strong apoptosis
7.2.3 Weak apoptosis
7.3 Summary of mathematical results
7.4 Selection for genetic instability
7.5 Genetic instability and apoptosis
7.6 Can competition be reversed by chemotherapy?
Tissue aging and the development of cancer
8.1 What is aging?
8.2 Basic modeling assumptions
8.3 Modeling healthy tissue
8.4 Modeling tumor cell growth
8.5 Checkpoints and basic tumor growth
8.6 Tumor growth and the microenvironment
8.7 Theory and data
Basic models of tumor inhibition and promotion
9.1 Model 1: Angiogenesis inhibition induces cell death
9.2 Model 2: Angiogenesis inhibition prevents tumor cell division
9.2.1 Linear stability analysis of the ODEs
9.2.2 Conclusions from the linear analysis
9.3 Spread of tumors across space
9.3.1 Turing stability analysis
9.3.2 Stationary periodic solutions
9.3.3 Biological implications and numerical simulations
9.4 Somatic cancer evolution and progression
9.5 Clinical implications
Mechanisms of tumor neovascularization
10.1 Emergence of the concept of postnatal vasculogenesis
10.2 Relative importance of angiogenesis versus vasculoge- nesis
10.4 Mathematical analysis
10.5 Applications
10.5.1 Dynamics of BM-derived EPCs
10.5.3 Tumor growth kinetics
Cancer and immune responses
11.1 Some facts about immune responses
11.2 The model
11.3 Method of model analysis
11.4 Properties of the model
11.5 Immunity versus tolerance
11.6 Cancer initiation
11.7 Tumor dormancy, evolution, and progression
11.8 Immunotherapy against cancers
Therapeutic approaches: viruses as anti-tumor weapons
12.1 Virus-induced killing of tumor cells
12.2 Effect of virus-specific CTL
12.3 Virus infection and the induction of tumor-specific CTL
12.4 Interactions between virus- and tumor-specific CTL
12.5 Treatment strategies
12.6 Evaluating viruses in culture
Exact formula for total probability of double mutations
Bibliography
Index
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Ebooksclub.org Computational Biology of Cancer Lecture Notes and Mathematical Modeling

Ebooksclub.org Computational Biology of Cancer Lecture Notes and Mathematical Modeling

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Published by Nasser Khakpash

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Published by: Nasser Khakpash on Nov 26, 2011
Copyright:Attribution Non-commercial

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10/23/2012

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