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Title:
Advances in using PARP inhibitors to treat cancer | BMC Medicine
Description:
The poly (ADP-ribose) polymerase (PARP) family of enzymes plays a critical role in the maintenance of DNA integrity as part of the base excision pathway of DNA repair. PARP1 is overexpressed in a variety of cancers, and its expression has been associated with overall prognosis in cancer, especially breast cancer. A series of new therapeutic agents that are potent inhibitors of the PARP1 and PARP2 isoforms have demonstrated important clinical activity in patients with breast or ovarian cancers that are caused by mutations in either the BRCA1 or 2 genes. Results from such studies may define a new therapeutic paradigm, wherein simultaneous loss of the capacity to repair DNA damage may have antitumor activity in itself, as well as enhance the antineoplastic potential of cytotoxic chemotherapeutic agents.
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Keywords {π}
parp, dna, cancer, article, repair, inhibitors, pubmed, google, scholar, clinical, cas, patients, brca, polymerase, damage, inhibition, inhibitor, adpribose, activity, ovarian, phase, pathway, breast, development, tumors, olaparib, tumor, polyadpribose, trial, central, poly, agents, proteins, trials, research, access, doroshow, ber, pathways, nature, oncol, par, oral, carmichael, parchment, abstract, excision, defects, cells, national,
Topics {βοΈ}
asco-nci-eortc annual meeting pre-publication history recurrent high-grade serous triple-negative breast cancer open access article radiation-induced dna damage article download pdf dna protein kinase poly-adp-ribosylated macromolecules homologous recombination-deficient cells purifying padpr-binding proteins single-strand intermediate nonhomologous end joining double-strand break privacy choices/manage cookies pyrophosphohydrolase nudix enzymes quantify drug-induced inhibition decreased parp1/2-specific activity single-strand break termed 'synthetic lethality' recurrent ovarian cancer nuclear localization signal intramural research program homologous end joining nucleotide excision repair net negative charge dense negative charge dna excision repair early breast cancer recent reports evaluate base excision repair poly-adp-ribose standard dna damaging therapies single strand annealing mononuclear cell samples recent clinical trials ataxia telangiectasia-mutated recently reported lack integrated genomic analyses developmental therapeutics program dna repair process repair dna damage dna damage repair article kummar /ii multicenter trial phase ii trial domchek sm biomed central nat rev cancer measurable colorectal cancer
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- Sharova NP: How does a cell repair damaged DNA?
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headline:Advances in using PARP inhibitors to treat cancer
description:The poly (ADP-ribose) polymerase (PARP) family of enzymes plays a critical role in the maintenance of DNA integrity as part of the base excision pathway of DNA repair. PARP1 is overexpressed in a variety of cancers, and its expression has been associated with overall prognosis in cancer, especially breast cancer. A series of new therapeutic agents that are potent inhibitors of the PARP1 and PARP2 isoforms have demonstrated important clinical activity in patients with breast or ovarian cancers that are caused by mutations in either the BRCA1 or 2 genes. Results from such studies may define a new therapeutic paradigm, wherein simultaneous loss of the capacity to repair DNA damage may have antitumor activity in itself, as well as enhance the antineoplastic potential of cytotoxic chemotherapeutic agents.
datePublished:2012-03-09T00:00:00Z
dateModified:2012-03-09T00:00:00Z
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DNA repair
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headline:Advances in using PARP inhibitors to treat cancer
description:The poly (ADP-ribose) polymerase (PARP) family of enzymes plays a critical role in the maintenance of DNA integrity as part of the base excision pathway of DNA repair. PARP1 is overexpressed in a variety of cancers, and its expression has been associated with overall prognosis in cancer, especially breast cancer. A series of new therapeutic agents that are potent inhibitors of the PARP1 and PARP2 isoforms have demonstrated important clinical activity in patients with breast or ovarian cancers that are caused by mutations in either the BRCA1 or 2 genes. Results from such studies may define a new therapeutic paradigm, wherein simultaneous loss of the capacity to repair DNA damage may have antitumor activity in itself, as well as enhance the antineoplastic potential of cytotoxic chemotherapeutic agents.
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