Abstract:
:RAD51D, a paralog of the mammalian RAD51 gene, contributes towards maintaining genomic integrity by homologous recombination DNA repair and telomere maintenance. A RAD51D variant, E233G, was initially identified as a potential susceptibility allele in high-risk, site-specific, familial breast cancer. We describe in this report that the Rad51d (E233G) genetic variant confers increased cisplatin resistance and cell growth phenotypes in human breast carcinoma cell lines with a mutant p53 gene (BT20 and T47D) but not with a wild-type p53 gene (MCF-7). Treatment with a p53 specific inhibitor, pifithrin alpha, restored this resistant phenotype in the MCF-7 cell line. Additionally, Rad51d (E233G) conferred increased cisplatin resistance of an MCF7 cell line in which p53 expression was stably knocked down by shRNAp53, indicating that the effect of this variant is dependent upon p53 status. Further study of Rad51d (E233G) will provide mechanistic insight towards the role of RAD51D in cellular response to anticancer agents and as a potential target for cancer therapy.
journal_name
Mol Carcinogjournal_title
Molecular carcinogenesisauthors
Nadkarni A,Rajesh P,Ruch RJ,Pittman DLdoi
10.1002/mc.20545subject
Has Abstractpub_date
2009-07-01 00:00:00pages
586-91issue
7eissn
0899-1987issn
1098-2744journal_volume
48pub_type
杂志文章abstract::Overexpression of Fas ligand (FasL) in cancer cells elicits potential antitumor effects via recruitment of neutrophils. Conversely, FasL-expressing tumors may counterattack tumor-infiltrating lymphocytes by delivering apoptotic death signals via Fas/FasL interactions, which may lead to tumor escape. In order to distin...
journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.21909
更新日期:2013-09-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22481
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journal_title:Molecular carcinogenesis
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journal_title:Molecular carcinogenesis
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doi:10.1002/mc.23196
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20310
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.2940080110
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.2940040405
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22379
更新日期:2016-09-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
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更新日期:2016-08-01 00:00:00
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更新日期:1996-03-01 00:00:00
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pub_type: 杂志文章
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更新日期:2015-09-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章,评审
doi:10.1002/mc.23042
更新日期:2019-09-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.21939
更新日期:2014-01-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20048
更新日期:2005-02-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22385
更新日期:2016-10-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.20591
更新日期:2010-03-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.2940010108
更新日期:1988-01-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章,多中心研究,随机对照试验
doi:10.1002/mc.23010
更新日期:2019-07-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
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更新日期:1999-02-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1002/mc.20055
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doi:10.1002/(sici)1098-2744(199903)24:3<160::aid-mc2>3
更新日期:1999-03-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
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更新日期:2012-10-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
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更新日期:2016-02-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/(sici)1098-2744(199910)26:2<69::aid-mc1>3.
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:10.1002/mc.22196
更新日期:2015-06-01 00:00:00
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journal_title:Molecular carcinogenesis
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更新日期:2017-01-01 00:00:00
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journal_title:Molecular carcinogenesis
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更新日期:2009-06-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
doi:
更新日期:1998-03-01 00:00:00
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journal_title:Molecular carcinogenesis
pub_type: 杂志文章
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更新日期:2012-10-01 00:00:00