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dc.contributor.authorChen, Junjie
dc.contributor.authorSilver, Daniel P.
dc.contributor.authorCantor, Sharon B.
dc.contributor.authorLivingston, David M.
dc.contributor.authorScully, Ralph
dc.date2022-08-11T08:08:01.000
dc.date.accessioned2022-08-23T15:39:32Z
dc.date.available2022-08-23T15:39:32Z
dc.date.issued1999-04-10
dc.date.submitted2008-12-10
dc.identifier.citationCancer Res. 1999 Apr 1;59(7 Suppl):1752s-1756s.
dc.identifier.issn0008-5472 (Print)
dc.identifier.pmid10197592
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26193
dc.description.abstractThe two major hereditary breast cancer susceptibility genes, BRCA1 and BRCA2, are associated with early-onset breast and/or ovarian cancer and encode products that each interact with the product of the eukaryotic RecA homologue, hRad51. We have recently found that BRCA1 and BRCA2 coexist in a common biochemical complex. The two proteins also colocalize in subnuclear foci in somatic cells as well as on the axial elements of developing synaptonemal complexes in meiotic cells. Thus, BRCA1 and BRCA2 participate in a common DNA damage response pathway associated with the activation of homologous recombination and double-strand break repair. Dysfunction of this pathway may be a general phenomenon in the majority of cases of hereditary breast and/or ovarian cancer. The BRCA1/BRCA2 complex may function in postreplicational repair processes activated during the DNA synthesis stage of the cell cycle.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10197592&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://cancerres.aacrjournals.org/cgi/content/abstract/59/7_Supplement/1752s
dc.subjectBRCA2 Protein
dc.subjectBreast Neoplasms
dc.subject*DNA Damage
dc.subjectDNA Repair
dc.subjectDNA-Binding Proteins
dc.subject*Genes, BRCA1
dc.subjectGenetic Predisposition to Disease
dc.subjectHumans
dc.subjectNeoplasm Proteins
dc.subjectRad51 Recombinase
dc.subjectRecombination, Genetic
dc.subjectTranscription Factors
dc.subjectCancer Biology
dc.subjectNeoplasms
dc.titleBRCA1, BRCA2, and Rad51 operate in a common DNA damage response pathway
dc.typeArticle
dc.source.journaltitleCancer research
dc.source.volume59
dc.source.issue7 Suppl
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cancerbiology_pp/10
dc.identifier.contextkey679288
html.description.abstract<p>The two major hereditary breast cancer susceptibility genes, BRCA1 and BRCA2, are associated with early-onset breast and/or ovarian cancer and encode products that each interact with the product of the eukaryotic RecA homologue, hRad51. We have recently found that BRCA1 and BRCA2 coexist in a common biochemical complex. The two proteins also colocalize in subnuclear foci in somatic cells as well as on the axial elements of developing synaptonemal complexes in meiotic cells. Thus, BRCA1 and BRCA2 participate in a common DNA damage response pathway associated with the activation of homologous recombination and double-strand break repair. Dysfunction of this pathway may be a general phenomenon in the majority of cases of hereditary breast and/or ovarian cancer. The BRCA1/BRCA2 complex may function in postreplicational repair processes activated during the DNA synthesis stage of the cell cycle.</p>
dc.identifier.submissionpathcancerbiology_pp/10
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages1752s-1756s


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