Linking epidemiology to epigenomics--where are we today?

Cornelia M Ulrich, William M Grady
Author Information
  1. Cornelia M Ulrich: National Center for Tumor Diseases Heidelberg (NCT), Division of Preventive Oncology, Im Neuenheimer Feld 460, D-69120 Heidelberg, Germany. neli.ulrich@nct-heidelberg.de

Abstract

cancer is the consequence of genetic and epigenetic alterations. Genetic mutations likely result in part from exposure to environmental carcinogens, giving rise to a large field of cancer-prevention study of these carcinogens and ways to develop strategies to avoid them. Our understanding of regulatory epigenetic mechanisms associated with DNA methylation, histone modifications, and microRNA production is increasing rapidly. The involvement of these processes in carcinogenesis raises the possibility that environmental exposures may promote or prevent cancer through affecting the epigenome. Modifying the epigenome to prevent cancer is particularly intriguing because epigenetic alterations are potentially reversible, unlike gene mutations, and because certain dietary factors, such as the B-vitamin folate, may affect genes' DNA methylation status (as reported by Wallace et al., beginning on page 1552 in this issue of the journal). Rapidly improving techniques for assessing epigenetic alterations promise to yield important insights for cancer prevention.

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Grants

  1. R01 CA 114467/NCI NIH HHS
  2. R01 CA 120523/NCI NIH HHS
  3. R01 CA105437/NCI NIH HHS
  4. R01 CA105437-04/NCI NIH HHS
  5. R01 CA112516-05S1/NCI NIH HHS
  6. R01 CA120523-04/NCI NIH HHS
  7. R01 CA 112516/NCI NIH HHS
  8. R01 CA112516/NCI NIH HHS
  9. R01 CA114467/NCI NIH HHS
  10. R01 CA114467-05/NCI NIH HHS
  11. R01 CA120523/NCI NIH HHS

MeSH Term

DNA Methylation
Epigenesis, Genetic
Epigenomics
Humans
Neoplasms

Word Cloud

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