Increased signaling entropy in cancer requires the scale-free property of protein interaction networks.

ABSTRACT: One of the key characteristics of cancer cells is an increased phenotypic plasticity, driven by underlying genetic and epigenetic perturbations. However, at a systems-level it is unclear how these perturbations give rise to the observed increased plasticity. Elucidating such systems-level principles is key for an improved understanding of cancer. Recently, it has been shown that signaling entropy, an overall measure of signaling pathway promiscuity, and computable from integrating a sample's gene expression profile with a protein interaction network, correlates with phenotypic plasticity and is increased in cancer compared to normal tissue. Here we develop a computational framework for studying the effects of network perturbations on signaling entropy. We demonstrate that the increased sig

SUBMITTER: Teschendorff AE 

PROVIDER: S-EPMC4412078 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature