BRCA1 CpG island hypermethylation predicts sensitivity to poly(adenosine diphosphate)-ribose polymerase inhibitorsBRCA1 CpG island hypermethylation predicts sensitivity to poly(adenosine diphosphate)-ribose polymerase inhibitors

Recently, Fong et al reported the antitumor activity of the poly(adenosine diphosphate)-ribose polymerase (PARP) inhibitor olaparib (AZD2281; KU-0059436) in patients with BRCA1/BRCA2 germline mutated ovarian cancer. Female BRCA1 and BRCA2 mutation carriers have a significantly elevated lifetime risk...

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Detalhes bibliográficos
Autores: Veeck, Jürgen, Ropero, Santiago, Setién, Fernando, Gonzalez-Suarez, Eva, Osorio, Ana, Benitez, Javier, Herman, James G., Esteller, Manel
Tipo de documento: artigo
Estado:Versão publicada
Data de publicação:2010
País:España
Recursos:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositório:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/198525
Acesso em linha:https://hdl.handle.net/2445/198525
Access Level:Acceso aberto
Palavra-chave:Proteïnes supressores de tumors
ADN
Malalties de l'ovari
Genètica
Tumor suppressor protein
DNA
Ovary diseases
Genetics
Descrição
Resumo:Recently, Fong et al reported the antitumor activity of the poly(adenosine diphosphate)-ribose polymerase (PARP) inhibitor olaparib (AZD2281; KU-0059436) in patients with BRCA1/BRCA2 germline mutated ovarian cancer. Female BRCA1 and BRCA2 mutation carriers have a significantly elevated lifetime risk of breast and ovarian cancer. BRCA1 and BRCA2 proteins play major roles in DNA double-strand break repair through homologous recombination, and inhibition of DNA single-strand break repair leads to the accumulation of double-strand breaks. These potentially lethal events in homologous recombination-deficient cells could be exploited for therapeutic purposes. The PARP-1 protein is essential for single-strand break repair, and inhibition of PARP leads to persistence of DNA lesions normally repaired by homologous recombination.