2010
DOI: 10.1016/j.ctrv.2010.03.006
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Targeting DNA repair in breast cancer: A clinical and translational update

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Cited by 54 publications
(42 citation statements)
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“…However, these are the types of cancer more susceptible to chemotherapy due to their compromised DNA repair mechanism [2]. Even triple-negative breast cancers (TNwhich have negative histochemical confirmation for ER, progesterone receptor, RP, and human epidermal growth factor receptor 2, HER2), without mutations in BRCA genes have also been described as having a BRCAness phenotype and are as sensitive to chemotherapy [3].…”
Section: Introductionmentioning
confidence: 99%
“…However, these are the types of cancer more susceptible to chemotherapy due to their compromised DNA repair mechanism [2]. Even triple-negative breast cancers (TNwhich have negative histochemical confirmation for ER, progesterone receptor, RP, and human epidermal growth factor receptor 2, HER2), without mutations in BRCA genes have also been described as having a BRCAness phenotype and are as sensitive to chemotherapy [3].…”
Section: Introductionmentioning
confidence: 99%
“…Likewise, the nucleocapsid Zn 2+ finger NCp7 protein, a protein required for the recognition and packaging of viral RNA, became attached to some platinum compounds, when its ability to bind nucleic acid was changed and prevented viral infectivity (de Paula et al, 2009;Musah, 2004 In recent years, there has been significant progress made in evaluating what happens when BRCA1 is inactivated so it cannot respond to DNA damage in cancer cells, in other words, taking advantage of the inherent weakness of the BRCA1 dysfunction in cancer cells. These cells have increased sensitivity to DNA-damaging agents that eventually result in major genomic instability and cell death (Amir et al, 2010;Ashworth, 2008;Helleday et al, 2008;Lieberman, 2008;Powell & Bindra, 2009;Quinn et al, 2009;Tassone et al, 2009;Zhu et al, 2009). Cancerous cells with inactivated BRCA1 had defects in DNA repair of double strand breaks (DSBs) (Farmer et al, 2005;Kennedy et al, 2004;Litman et al, 2008).…”
Section: Cisplatin-protein Adductsmentioning
confidence: 99%
“…This mechanism protects against uncontrolled proliferation in the context of abnormal genetic background. Disruption of these pathw a y s i n c a n c e r p r o d u c e s a n i n c r e a s e i n chromosome breaks and mutagenesis (Amir et al, 2010). Several polymorphisms in NER genes have been described.…”
Section: Nucleotide Excision Repair and Breast Cancermentioning
confidence: 99%