Open AccessImplications of a simple mathematical model to cancer cell population dynamics
Author(s) -
Garner A. L.,
Lau Y. Y.,
Jordan D. W.,
Uhler M. D.,
Gilgenbach R. M.
Publication year - 2006
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.2006.00368.x
Subject(s) - cell cycle , population , cell , biology , cancer cell , cancer , cell growth , cancer stem cell , microbiology and biotechnology , stem cell , cancer research , biochemistry , genetics , medicine , environmental health
. Recent research in cancer progression and treatment indicates that many forms of cancer arise from the development of a small subpopulation of abnormal cancer stem cells (CSCs) that promote cancer growth and spread. Many potential treatments preferentially interact with cells at certain stages of the cell cycle by either selective killing or halting the cell cycle, such as intense, nanosecond‐duration pulsed electric fields (nsPEFs). Simple mathematical models of unfed cancer cell populations at the plateau of their growth characteristics may estimate the long‐term consequences of these treatments on proliferating and quiescent cell populations. Applying such a model with no transition from the quiescent to proliferating state shows that it is possible for the proliferating cell population to fall below 1 if the quiescent cell population obtains a sufficient competitive advantage with respect to nutrient consumption and/or survival rate. Introducing small, realistic transition rates did not appreciably alter short‐term or long‐term population behaviour, indicating that the predicted small cell population behaviour (< 1 cell) is not an artefact of the simpler model. Experimental observations of nsPEF‐induced effects on the cell cycle suggest that such a model may serve as a first step in assessing the viability of a given cancer treatment in vitro prior to clinical application.