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Unanswered questions about the role of promoter methylation in carcinogenesis

Timothy H Bestor1

  • 1Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA. THB12@columbia.edu

Annals of the New York Academy of Sciences
|May 2, 2003
PubMed

Insights

Epigenetic silencing via DNA methylation may not cause cancer progression but rather follow gene inactivation. Genetic evidence does not support a causal role for methylation in cancer development.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Tumor suppressor gene inactivation is crucial in cancer development.
  • Epigenetic silencing through DNA methylation is proposed as an alternative mechanism to mutation.
  • The precise role of DNA methylation in cancer progression remains debated.

Purpose of the Study:

  • To critically evaluate the proposed role of ectopic de novo methylation in tumor suppressor gene silencing during cancer progression.
  • To investigate whether DNA methylation is a cause or consequence of gene inactivation in cancer.

Main Methods:

  • Review of existing genetic and molecular data on DNA methylation and tumor suppressor genes in cancer.
  • Analysis of the temporal relationship between gene inactivation and promoter methylation.
  • Examination of mutations in DNA methyltransferase genes in cancer patients.

Main Results:

  • No genetic data currently implicate ectopic de novo methylation as a direct cause of cancer.
  • No mutations in DNA methyltransferase genes have been identified in any cancer.
  • Promoter methylation may be a consequence of transcriptional inactivity resulting from mutations elsewhere in cellular pathways.

Conclusions:

  • The role of DNA methylation in initiating cancer may be overestimated.
  • Consequences of genetic alterations, such as methylation, might be mistaken for causes.
  • Further research is needed to clarify the causal relationship between epigenetic changes and cancer etiology.

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