Too much or too little
نویسندگان
چکیده
The global effort to understand the molecular drivers of cancer onset and progression is now coming to fruition with the identification of specific genomic and epigenomic events that influence signaling through key oncogenic pathways. Genetic studies using inducible expression of the critical growth controlling oncogenes MYC, RAS, PI3K and AKT have shown unequivocally that, in conjunction with secondary genetic mutations, they can drive transformation and induce oncogene addiction. Since the majority of human tumors exhibit dysregulated signaling via one or more of these pathways, this provides an unprecedented opportunity to improve patient outcome by therapeutically targeting this addiction. These key drivers of malignant transformation do so by controlling many of the processes regarded as hallmarks of cancer, including proliferative cell growth and resistance to apoptosis, reprogramming of energy metabolism, angiogenesis and metastasis. Paradoxically, however, the MYC, RAS and PI3K/AKT oncogenic pathways can also induce cellular senescence in non-transformed cells. Pandolfi and colleagues proposed that RAS oncogene-induced senescence (OIS) differs from loss of the tumor suppressor PTENinduced cellular senescence (PICS) by the absence of a DNA damage response, and our publication demonstrated oncogenic AKT-induced senescence similar to PICS. In all three cases, senescence relies on modulating p53 levels and activity and/or INK4A mediated inhibition of cyclin-dependent kinases (CDKs) and, thus, inactivation of the retinoblastoma Too much or too little Harnessing senescence to control oncogene-driven cancer
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عنوان ژورنال:
دوره 11 شماره
صفحات -
تاریخ انتشار 2012