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.
Do cell-autonomous and non-cell-autonomous effects drive the structure of tumor ecosystems?
Tissot, T.; Ujvari, B.; Solary, E.; Lassus, P.; Roche, B.; Thomas, F.
Biochim Biophys Acta
2016-04 / vol 1865 / pages 147-54
10.1016/j.bbcan.2016.01.005 S0304-419X(16)30014-2 [pii]
0006-3002 (Print) 0006-3002 (Linking)