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Branching Process Models of Cancer

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TLDR
This chapter uses multitype branching processes with mutation to model cancer, with cancer progression, resistance to therapy, and metastasis in mind, and investigates the time of the first type k mutation and the growth of the number of type k cells.
Abstract
In this chapter, we will use multitype branching processes with mutation to model cancer. With cancer progression, resistance to therapy, and metastasis in mind, we will investigate τ k , the time of the first type k mutation, and σ k , the time of the first type k mutation that founds a family line that does not die out, as well as the growth of the number of type k cells. The last three sections apply these results to metastasis, ovarian cancer, and tumor heterogeneity. Even though martingales and stable laws are mentioned, these notes should be accessible to a student who is familiar with Poisson processes and continuous time Markov chains.

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The mathematics of cancer: integrating quantitative models

TL;DR: The recent expansion of quantitative models addresses many questions regarding tumour initiation, progression and metastases as well as intra-tumour heterogeneity, treatment responses and resistance.
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Extremely high genetic diversity in a single tumor points to prevalence of non-Darwinian cell evolution

TL;DR: A single tumor is evaluated by sequencing or genotyping nearly 300 regions from the tumor and the number of coding region mutations was estimated to be greater than 100 million in this unexceptional tumor, suggesting non-Darwinian evolution should be heeded in cancer treatments even for microscopic tumors.
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Quantification of subclonal selection in cancer from bulk sequencing data.

TL;DR: Application of the method to high-depth sequencing data from breast, gastric, blood, colon and lung cancer samples, as well as metastatic deposits, showed that detectable subclones under selection consistently emerged early during tumor growth and had a large fitness advantage.
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Mutation and Cancer: Statistical Study of Retinoblastoma

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Comprehensive genomic characterization defines human glioblastoma genes and core pathways

Roger E. McLendon, +233 more
- 23 Oct 2008 - 
TL;DR: The interim integrative analysis of DNA copy number, gene expression and DNA methylation aberrations in 206 glioblastomas reveals a link between MGMT promoter methylation and a hypermutator phenotype consequent to mismatch repair deficiency in treated gliobeasts, demonstrating that it can rapidly expand knowledge of the molecular basis of cancer.
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