Developmental reprogramming of cancer susceptibility.
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.
Institute of Biosciences and Technology, Texas A&M Health Science Center, 2121 W. Holcombe Boulevard, Houston, TX 77030, USA. cwalker@ibt.tamhsc.edu
Cheryl Lyn
CL
Walker
Shuk-mei
SM
Ho
D004198:Disease Susceptibility / Q000209:etiology*; D044127:Epigenesis, Genetic / Q000502:physiology*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology*; D059647:Gene-Environment Interaction; D006801:Humans; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000235:genetics* / Q000473:pathology*