Somatic mosaicism: on the road to cancer

被引:88
作者
Fernandez, Luis C. [1 ]
Torres, Miguel [2 ]
Real, Francisco X. [1 ,3 ]
机构
[1] Spanish Natl Canc Res Ctr CNIO, Canc Cell Biol Programme, Epithelial Carcinogenesis Grp, Melchor Fernandez Almagro 3, Madrid 28029, Spain
[2] CNIC, Melchor Fernandez Almagro 3, Madrid 28029, Spain
[3] Univ Pompeu Fabra, Dept Ciencies Expt & Salut, Barcelona, Spain
关键词
ACUTE LYMPHOBLASTIC-LEUKEMIA; DETECTABLE CLONAL MOSAICISM; FAMILIAL ADENOMATOUS POLYPOSIS; TRANSFORMED EPITHELIAL-CELLS; COPY-NUMBER-VARIATION; STEM-CELLS; FIELD CANCERIZATION; TUMOR-SUPPRESSOR; PRENATAL ORIGIN; EPIDERMAL NEVI;
D O I
10.1038/nrc.2015.1
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Diversity is the basis of fitness selection. Although the genome of an individual is considered to be largely stable, there is theoretical and experimental evidence-both in model organisms and in humans-that genetic mosaicism is the rule rather than the exception. The continuous generation of cell variants, their interactions and selective pressures lead to life-long tissue dynamics. Individuals may thus enjoy 'clonal health', defined as a clonal composition that supports healthy morphology and physiology, or suffer from clonal configurations that promote disease, such as cancer. The contribution of mosaicism to these processes starts during embryonic development. In this Opinion article, we argue that the road to cancer might begin during these early stages.
引用
收藏
页码:43 / 55
页数:13
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