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Nat Rev Cancer. 2012 Jun 14;12(7):479-86. doi: 10.1038/nrc3220.

Developmental reprogramming of cancer susceptibility.

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  • 1Institute of Biosciences and Technology, Texas A&M Health Science Center, 2121 W. Holcombe Boulevard, Houston, TX 77030, USA.

Erratum in

  • Nat Rev Cancer. 2012 Aug;12(8):578.


Gene-environment interactions have been traditionally understood to promote the acquisition of mutations that drive multistage carcinogenesis, and, in the case of inherited defects in tumour suppressor genes, additional mutations are required for cancer development. However, the developmental origins of health and disease (DOHAD) hypothesis provides an alternative model whereby environmental exposures during development increase susceptibility to cancer in adulthood, not by inducing genetic mutations, but by reprogramming the epigenome. We hypothesize that this epigenetic reprogramming functions as a new type of gene-environment interaction by which environmental exposures target the epigenome to increase cancer susceptibility.

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