Crosslinks and crosstalk: human cancer syndromes and DNA repair defects.
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.
Risinger
Mary A
MA
Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267, USA.
Groden
Joanna
J
D000251:Adenosine Triphosphatases / Q000235:genetics / Q000378:metabolism; D024682:BRCA2 Protein / Q000235:genetics / Q000378:metabolism; D001816:Bloom Syndrome / Q000235:genetics / Q000378:metabolism; D015179:Colorectal Neoplasms / Q000235:genetics; D045647:DNA Glycosylases / Q000235:genetics / Q000378:metabolism; D004265:DNA Helicases / Q000235:genetics / Q000378:metabolism; D004260:DNA Repair / Q000235:genetics*; D005199:Fanconi Anemia / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008957:Models, Genetic; D009154:Mutation; D009386:Neoplastic Syndromes, Hereditary / Q000235:genetics* / Q000378:metabolism; D053484:RecQ Helicases
D024682:BRCA2 Protein; D045647:DNA Glycosylases; C061738:mutY adenine glycosylase; D000251:Adenosine Triphosphatases; C097151:Bloom syndrome protein; D004265:DNA Helicases; D053484:RecQ Helicases