Authors: Tissot, T; Ujvari, B; Solary, E; Lassus, P; Roche, B; Thomas, F
Source: BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 1865 (2):147-154, APR 2016
Brief summary of the paper: By definition, a driver mutation confers a growth advantage to the cancer cell in which it occurs, while a passenger mutation does not: the former is usually considered as the engine of cancer progression, while the latter is not.
Actually, the effects of a given mutation depend on the genetic background of the cell in which it appears, thus can differ in the subclones that form a tumor. In addition to cell-autonomous effects generated by the mutations, non-cell-autonomous effects shape the phenotype of a cancer cell.
Here, we review the evidence that a network of biological interactions between subclones drives cancer cell adaptation and amplifies intra-tumor heterogeneity. Integrating the role of mutations in tumor ecosystems generates innovative strategies targeting the tumor ecosystem’s weaknesses to improve cancer treatment.