News from CEXS-UPF
Cancer results from the accumulation of genetic alterations in a cell's genome. According to recent studies, the number of mutations varies according to age and tissue: tumors caused by environmental exposures (such as melanoma, caused by the exposure to UV rays, or lung cancer, due to tobacco smoke) harbor the highest mutation rate among cancers of the adult. By contrast, pediatric tumors are associated with the lowest mutational rates.
The formation of a tumor implies the presence of two or more cell populations genetically distinct within a tissue: the ill population, from which the tumor arises, and the health population. When an organism arisen from a single fertilized egg carries more than one genetically diverse cell population we are talking about genetic mosaicism. Thus, tumors constitute an example of mosaicism.
Until recently, scientists assumed that mutations leading to tumors of the adult occur during adult life. Although this is likely to be true for many mutations, there is growing evidence that the genetic profile of a cancer is established over many years before diagnosis. Unfortunately, our understanding of the genetic make‑up of the earliest preneoplastic lesions is limited, among other reasons, by the fact that studies have largely dismissed histologically normal cells that can carry genetic changes visually imperceptible.
Francisco X. Real, professor of the Department of Experimental and Health Sciences (DCEXS) of UPF and leader of the research group on Epithelial Carcinogenesis of the Spanish National Cancer Research Centre (CNIO), Luis C. Fernández, researcher at the CNIO, and Miguel Torres, researcher at the Spanish National Center for Cardiovascular Research (CNIC), think about the role played by genetic mosaicism in the development of cancer in a review article published in Nature Reviews Cancer.
Luis C. Fernández, Miguel Torres, Francisco X. Real. Somatic mosaicism: on the road to cancer. Nature Reviews Cancer, Desembre 2015. doi:10.1038/nrc.2015.1