Crosslinks and crosstalk: human cancer syndromes and DNA repair defects.

Cancer cell ·Vol. 6 ·No. 6 ·2004-12-00 ·Pages 539-45

Risinger MA, Groden J

Abstract

A subset of human cancer syndromes result from inherited defects in genes responsible for DNA repair. During the past few years, discoveries concerning the intersection of certain DNA repair processes have increased our understanding of how the disruption of specific DNA repair mechanisms leads to genomic instability and tumorigenesis. This review focuses on the human genes MUTYH, BRCA2/FANCD1, and BLM.

MeSH Terms

Adenosine Triphosphatases/genetics,metabolism BRCA2 Protein/genetics,metabolism Bloom Syndrome/genetics,metabolism Colorectal Neoplasms/genetics DNA Glycosylases/genetics,metabolism DNA Helicases/genetics,metabolism DNA Repair/genetics Fanconi Anemia/genetics,metabolism Humans Models, Genetic Mutation Neoplastic Syndromes, Hereditary/genetics,metabolism RecQ Helicases

Chemicals

BRCA2 Protein DNA Glycosylases mutY adenine glycosylase Adenosine Triphosphatases Bloom syndrome protein DNA Helicases RecQ Helicases

Authors & Affiliations

2 authors, click to expand affiliations / ORCID

Risinger Mary A

Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267, USA.

Groden Joanna

Article Info

Journal

Cancer cell

Abbr.

Cancer Cell

ISSN

1535-6108

DOI

10.1016/j.ccr.2004.12.001

Published

2004-12-00

Pages

539-45

Language

English

Region

United States

NLM ID

101130617

Subset

External Links

PubMed source DOI: 10.1016/j.ccr.2004.12.001 View journal details

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Crosslinks and crosstalk: human cancer syndromes and DNA repair defects.

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