Friday, November 29, 2013
Tuesday, November 26, 2013
A multi-phenotypic cancer model with cell plasticity
(Submitted on 25 Nov 2013)
The conventional cancer stem cell (CSC) theory indicates a hierarchy of CSCs and non-stem cancer cells (NSCCs), that is, CSCs can differentiate into NSCCs but not vice versa. However, an alternative paradigm of CSC theory with reversible cell plasticity among cancer cells has received much attention very recently. Here we present a generalized multi-phenotypic cancer model by integrating cell plasticity with the conventional hierarchical structure of cancer cells. Based on our model, we theoretically explain the universality of the phenotypic equilibrium phenomena reported in various cancer cell lines. By applying our model to concrete biological examples with real experimental data, we show that cancer cell plasticity plays an essential role in transient regulation of cancer heterogeneity. Our work may pave the way for modeling and analyzing the cell population dynamics with cell plasticity.
Friday, November 1, 2013
(Submitted on 31 Oct 2013)
Cancers are caused by the accumulation of genetic alterations. Since this accumulation takes time, the incidence of most cancers is thought to increase exponentially with age. However, careful measurements of the age-specific incidence shows that the specific incidence for many forms of cancer rises with age to a maximum, then decreases. This decrease in the age-specific incidence with age is an anomaly. Understanding this anomaly should lead to a better understanding of how tumors develop and grow. Here I derive the shape of the age-specific incidence, showing that it should follow the shape of a Weibull distribution. Measurements indicate that the age-specific incidence for colon cancer does indeed follow a Weibull distribution. This analysis leads to the interpretation that for colon cancer two sub-populations exist in the general population: a susceptible population and an immune population. Colon tumors will only occur in the susceptible population. This analysis is consistent with the developmental origins of disease hypothesis and generalizable to many other common forms of cancer.link: http://arxiv.org/abs/1310.8619