Journal
CURRENT OPINION IN ONCOLOGY
Volume 12, Issue 1, Pages 68-73Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001622-200001000-00012
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- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD037687] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM059377] Funding Source: NIH RePORTER
- NICHD NIH HHS [HD37687] Funding Source: Medline
- NIGMS NIH HHS [GM59377] Funding Source: Medline
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Abnormalities of genomic methylation patterns have been attributed a role in carcinogenesis since the early 1980s, when large-scale demethylation of the genome was thought be an early event in multistep colorectal carcinogenesis. In the 1990s, local de novo methylation (with or without global demethylation) at tumor suppressor loci was held to be involved in silencing of tumor suppressor genes. The mechanisms that might mediate methylation and demethylation in carcinogenesis remain obscure, and there are questions as to whether the methylation changes are a cause or consequence of cellular transformation and clonal expansion. It is also important to derive a set of defined criteria by which a tumor suppressor gene can be concluded to have been inactivated by DNA methylation in a manner that contributes to carcinogenesis. (C) 2000 Lippincott Williams & Wilkins, Inc.
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