Journal
NATURE REVIEWS GENETICS
Volume 7, Issue 1, Pages 21-33Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrg1748
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Funding
- NATIONAL CANCER INSTITUTE [R37CA054358, R01CA054358] Funding Source: NIH RePORTER
- NCI NIH HHS [R37 CA054358, R37 CA054358-16, R01 CA054358] Funding Source: Medline
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Cancer is widely perceived as a heterogeneous group of disorders with markedly different biological properties, which are caused by a series of clonally selected genetic changes in key tumour-suppressor genes and oncogenes. However, recent data suggest that cancer has a fundamentally common basis that is grounded in a polyclonal epigenetic disruption of stem/progenitor cells, mediated by 'tumour-progenitor genes'. Furthermore, tumour cell heterogeneity is due in part to epigenetic variation in progenitor cells, and epigenetic plasticity together with genetic lesions drives tumour progression. This crucial early role for epigenetic alterations in cancer is in addition to epigenetic alterations that can substitute for genetic variation later in tumour progression. Therefore, non-neoplastic but epigenetically disrupted stem/progenitor cells might be a crucial target for cancer risk assessment and chemoprevention.
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