Poly(ADP-Ribose) polymerase inhibition: "targeted" therapy for triple-negative breast cancer. - Wikidata - wikimedia - TriplyDB

Poly(ADP-Ribose) polymerase inhibition: "targeted" therapy for triple-negative breast cancer.

Poly(ADP-Ribose) polymerase inhibition: "targeted" therapy for triple-negative breast cancer.

http://www.wikidata.org/entity/Q34168535

about

A de novo complete BRCA1 gene deletion identified in a Spanish woman with early bilateral breast cancer Trial watch - inhibiting PARP enzymes for anticancer therapy MiRNAs and Other Epigenetic Changes as Biomarkers in Triple Negative Breast Cancer The fate of chemoresistance in triple negative breast cancer (TNBC)PARPs and the DNA damage response Use of poly ADP-ribose polymerase [PARP] inhibitors in cancer cells bearing DDR defects: the rationale for their inclusion in the clinic Dual small-molecule targeting of procaspase-3 dramatically enhances zymogen activation and anticancer activity Novel genes associated with lymph node metastasis in triple negative breast cancer Sam68 Is Required for DNA Damage Responses via Regulating Poly(ADP-ribosyl)ation Triple negative breast cancer in Moroccan women: clinicopathological and therapeutic study at the National Institute of Oncology.A colorimetric and smartphone readable method for uracil-DNA glycosylase detection based on the target-triggered formation of G-quadruplex.Poly(ADP-ribose) polymerase-1 inhibition: preclinical and clinical development of synthetic lethality.Clinicopathological, therapeutic and prognostic features of the triple-negative tumors in moroccan breast cancer patients (experience of Hassan II university hospital in Fez)Saccharomyces cerevisiae as a model system to study the response to anticancer agents.TGFβ induces "BRCAness" and sensitivity to PARP inhibition in breast cancer by regulating DNA-repair genes Stem cell-like gene expression in ovarian cancer predicts type II subtype and prognosis Differential anti-proliferative activities of poly(ADP-ribose) polymerase (PARP) inhibitors in triple-negative breast cancer cells Identification by array comparative genomic hybridization of a new amplicon on chromosome 17q highly recurrent in BRCA1 mutated triple negative breast cancer.The breast cancer susceptibility genes (BRCA) in breast and ovarian cancers.Biological and clinical significance of PARP1 protein expression in breast cancer.CpG island hypermethylation of BRCA1 and loss of pRb as co-occurring events in basal/triple-negative breast cancer.Poly(ADP-ribosyl) glycohydrolase prevents the accumulation of unusual replication structures during unperturbed S phase Management options in triple-negative breast cancer Radiosensitization with combined use of olaparib and PI-103 in triple-negative breast cancer.Inhibition of GPR30 by estriol prevents growth stimulation of triple-negative breast cancer cells by 17β-estradiol.Proteomic-based biosignatures in breast cancer classification and prediction of therapeutic response.Genetic variation in cell cycle regulatory gene AURKA and association with intrinsic breast cancer subtype.A Synthetic Lethal Screen Identifies DNA Repair Pathways that Sensitize Cancer Cells to Combined ATR Inhibition and Cisplatin Treatments.Inactivation of GPR30 reduces growth of triple-negative breast cancer cells: possible application in targeted therapy.Templated chemistry for monitoring damage and repair directly in duplex DNA Identification of BRCA1-like triple-negative breast cancers by quantitative multiplex-ligation-dependent probe amplification (MLPA) analysis of BRCA1-associated chromosomal regions: a validation study.Expanding targets of DNAzyme-based sensors through deactivation and activation of DNAzymes by single uracil removal: sensitive fluorescent assay of uracil-DNA glycosylase Direct fluorescence monitoring of DNA base excision repair 8-Amino-adenosine activates p53-independent cell death of metastatic breast cancers Predicting enhanced cell killing through PARP inhibition.Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome.mTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer.Monitoring eukaryotic and bacterial UDG repair activity with DNA-multifluorophore sensors Targeting BRCA1 localization to augment breast tumor sensitivity to poly(ADP-Ribose) polymerase inhibition.Targeting aberrant DNA double-strand break repair in triple-negative breast cancer with alpha-particle emitter radiolabeled anti-EGFR antibody.

P2860

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P2860

Poly(ADP-Ribose) polymerase inhibition: "targeted" therapy for triple-negative breast cancer.

http://www.wikidata.org/entity/Q34168535

description

2010 nî lūn-bûn

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2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Clinical Cancer Research

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Carey K Anders

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Daniel P Silver

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Eric P Winer

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George W Sledge

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Lisa A Carey

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Rebecca Dent

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P2860

High sensitivity of BRCA1-deficient mammary tumors to the PARP inhibitor AZD2281 alone and in combination with platinum drugs

Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers.

Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications

Molecular portraits of human breast tumours

Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase

Repeated observation of breast tumor subtypes in independent gene expression data sets

Roles of BRCA1 and BRCA2 in homologous recombination, DNA replication fidelity and the cellular response to ionizing radiation

Ixabepilone plus capecitabine for metastatic breast cancer progressing after anthracycline and taxane treatment

Resistance to therapy caused by intragenic deletion in BRCA2

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