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Evolution and cancer: A mathematical biology approach

Edited by Professor Marek Kimmel

Collection published: 20 April 2010

Mathbiol

Cancer is, in some sense, a condensed-time laboratory of evolution. Dedifferentiated cells form colonies that survive in a hostile environment, and they evolve new metabolic circuits and aggression and resistance mechanisms. They also can muster cooperation of fibroblasts and lymphocytes, and attract blood vessels. Modeling of these phenomena, well underway, will also help understand basic mechanisms of life. Taken together, the articles in this thematic series illustrate the substantial progress that occurred over the past decade. Qualitative and quantitative understanding of cancer is a necessary condition for engineering approaches to fight it. The latter are still scarce.


Editorial   Open Access Highly Accessed

Evolution and cancer: a mathematical biology approach

Marek Kimmel Biology Direct 2010, 5:29 (20 April 2010)

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Research   Open Access

A mathematical model of bone remodeling dynamics for normal bone cell populations and myeloma bone disease

Bruce P Ayati, Claire M Edwards, Glenn F Webb, John P Wikswo Biology Direct 2010, 5:28 (20 April 2010)

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Oscillatory dynamics in a model of vascular tumour growth - implications for chemotherapy

IJ Stamper, MR Owen, PK Maini, HM Byrne Biology Direct 2010, 5:27 (20 April 2010)

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A new stochastic and state space model of human colon cancer incorporating multiple pathways

Wai Y Tan, Xiao W Yan Biology Direct 2010, 5:26 (20 April 2010)

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A theoretical quantitative model for evolution of cancer chemotherapy resistance

Ariosto S Silva, Robert A Gatenby Biology Direct 2010, 5:25 (20 April 2010)

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The evolutionary impact of androgen levels on prostate cancer in a multi-scale mathematical model

Steffen E Eikenberry, John D Nagy, Yang Kuang Biology Direct 2010, 5:24 (20 April 2010)

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Tumor morphological evolution: directed migration and gain and loss of the self-metastatic phenotype

Heiko Enderling, Lynn Hlatky, Philip Hahnfeldt Biology Direct 2010, 5:23 (20 April 2010)

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Episodic, transient systemic acidosis delays evolution of the malignant phenotype: Possible mechanism for cancer prevention by increased physical activity

Kieran Smallbone, Philip K Maini, Robert A Gatenby Biology Direct 2010, 5:22 (20 April 2010)

Abstract | Full text | PDF | PubMed | Cited on BioMed Central |  Editor’s summary

A mathematical model predicts that repeated episodes of systemic acidosis - through exercise, for example - may interrupt the evolution of cancer.

Research   Open Access

Selection in spatial stochastic models of cancer: Migration as a key modulator of fitness

Craig J Thalhauser, John S Lowengrub, Dwayne Stupack, Natalia L Komarova Biology Direct 2010, 5:21 (20 April 2010)

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Disruption of a Quorum Sensing mechanism triggers tumorigenesis: a simple discrete model corroborated by experiments in mammary cancer stem cells

Zvia Agur, Yuri Kogan, Liora Levi, Hannah Harrison, Rebecca Lamb, Oleg U Kirnasovsky, Robert B Clarke Biology Direct 2010, 5:20 (20 April 2010)

Abstract | Full text | PDF | PubMed | Cited on BioMed Central |  Editor’s summary

A simple cellular automata model prediction, that incessant stem cell proliferation results primarily from inefficient quorum sensing, that is, from poor inter-cell communication, was validated in vitro using MCF7 cells.

Review   Open Access

Cancer models, genomic instability and somatic cellular Darwinian evolution

Mark P Little Biology Direct 2010, 5:19 (20 April 2010)

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