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Cited by 1,628

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

DNA hypermethylation in tumorigenesis: epigenetics joins genetics

Open access
Baylin, Stephen B, Herman, James G·2000·Trends in Genetics

Abstract

Recently, the concept that epigenetic, as well as genetic, events might be central to the evolution of human cancer is re-emerging. Cancers often exhibit an aberrant methylation of gene promoter regions that is associated with loss of gene function. This DNA change constitutes a heritable state, not mediated by altered nucleotide sequence, that appears to be tightly linked to the formation of transcriptionally repressive chromatin. This epigenetic process acts as an alternative to mutations to disrupt tumor-suppressor gene function and can predispose to genetic alterations through inactivating DNA-repair genes. Dissecting the molecular processes that mediate these methylation changes will enhance our understanding of chromatin modeling and gene regulation and might present novel possibilities for cancer therapy. Methylation changes constitute potentially sensitive molecular markers to define risk states, monitor prevention strategies, achieve early diagnosis, and track the prognosis of cancer.

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Metadata

Authors
Baylin, S. B., & Herman, J. G.
Venue
Trends in Genetics
Publisher
Elsevier BV
Published
2000-04
Volume
16
Issue
4
Pages
168-174
ISSN
0168-9525 (ISSN-L)
OpenAlex
W2054823635
Cited by
1,628
References
9
FWCI
7.05
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: DNA hypermethylation in tumorigenesis: epigenetics joins genetics. https://app.cochat.ai/papers/10.1016/s0168-9525(99)01971-x
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Baylin, S. B., & Herman, J. G. (2000). DNA hypermethylation in tumorigenesis: epigenetics joins genetics. Trends in Genetics. https://doi.org/10.1016/s0168-9525(99)01971-x

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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