Journal
NATURE GENETICS
Volume 38, Issue 4, Pages 468-473Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ng1768
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Funding
- NCI NIH HHS [K01 CA89267-02, P01 CA91955, K07 CA89147-03] Funding Source: Medline
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Neoplasms are thought to progress to cancer through genetic instability generating cellular diversity(1,2) and clonal expansions driven by selection for mutations in cancer genes(3,4). Despite advances in the study of molecular biology of cancer genes(5), relatively little is known about evolutionary mechanisms that drive neoplastic progression. It is unknown, for example, which may be more predictive of future progression of a neoplasm: genetic homogenization of the neoplasm, possibly caused by a clonal expansion, or the accumulation of clonal diversity. Here, in a prospective study, we show that clonal diversity measures adapted from ecology and evolution can predict progression to adenocarcinoma in the premalignant condition known as Barrett's esophagus, even when controlling for established genetic risk factors, including lesions in TP53 (p53; ref. 6) and ploidy abnormalities(7). Progression to cancer through accumulation of clonal diversity, on which natural selection acts, may be a fundamental principle of neoplasia with important clinical implications.
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