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Function of oncogenes in cancer development: a changing paradigm
Author(s) -
VicenteDueñas Carolina,
RomeroCamarero Isabel,
Cobaleda Cesar,
SánchezGarcía Isidro
Publication year - 2013
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2013.97
Subject(s) - biology , reprogramming , carcinogenesis , oncogene , cancer , epigenome , genome instability , cancer research , cancer cell , cell growth , phenotype , epigenesis , function (biology) , genetics , cell , dna methylation , cell cycle , dna damage , gene , dna , gene expression
Tumour‐associated oncogenes induce unscheduled proliferation as well as genomic and chromosomal instability. According to current models, therapeutic strategies that block oncogene activity are likely to selectively target tumour cells. However, recent evidences have revealed that oncogenes are only essential for the proliferation of some specific tumour cell types, but not all. Indeed, the latest studies of the interactions between the oncogene and its target cell have shown that oncogenes contribute to cancer development not only by inducing proliferation but also by developmental reprogramming of the epigenome. This provides the first evidence that tumorigenesis can be initiated by stem cell reprogramming, and uncovers a new role for oncogenes in the origin of cancer. Here we analyse these evidences and propose an updated model of oncogene function that can explain the full range of genotype–phenotype associations found in human cancer. Finally, we discuss how this vision opens new avenues for developing novel anti‐cancer interventions.