6-thioguanine selectively kills BRCA2-defective tumors and overcomes PARP inhibitor resistance - sprookjes - yvandenbroek - TriplyDB

6-thioguanine selectively kills BRCA2-defective tumors and overcomes PARP inhibitor resistance

6-thioguanine selectively kills BRCA2-defective tumors and overcomes PARP inhibitor resistance

http://www.wikidata.org/entity/Q24599364

about

Role of Biomarkers in the Development of PARP Inhibitors The role of PARP in DNA repair and its therapeutic exploitation Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.Overcoming Resistance of Cancer Cells to PARP-1 Inhibitors with Three Different Drug Combinations PARP inhibitor treatment in ovarian and breast cancer Poly(ADP-ribose) polymerase-1 inhibition: preclinical and clinical development of synthetic lethality.Differing clinical impact of BRCA1 and BRCA2 mutations in serous ovarian cancer.Drug repurposing screen identifies lestaurtinib amplifies the ability of the poly (ADP-ribose) polymerase 1 inhibitor AG14361 to kill breast cancer associated gene-1 mutant and wild type breast cancer cells.BRCA1, PARP, and 53BP1: conditional synthetic lethality and synthetic viability.Induction of telomere dysfunction mediated by the telomerase substrate precursor 6-thio-2'-deoxyguanosine.Secondary mutations of BRCA1/2 and drug resistance JF-305, a pancreatic cancer cell line is highly sensitive to the PARP inhibitor olaparib.A phase II clinical trial of 6-mercaptopurine (6MP) and methotrexate in patients with BRCA defective tumours: a study protocol.Drug therapy for hereditary cancers Randomized Trial of Oral Cyclophosphamide and Veliparib in High-Grade Serous Ovarian, Primary Peritoneal, or Fallopian Tube Cancers, or BRCA-Mutant Ovarian Cancer The potential for poly (ADP-ribose) polymerase inhibitors in cancer therapy.BRCA1-deficient breast cancer cell lines are resistant to MEK inhibitors and show distinct sensitivities to 6-thioguanine Cisplatin resistance: a cellular self-defense mechanism resulting from multiple epigenetic and genetic changes.Common cancer-associated imbalances in the DNA damage response confer sensitivity to single agent ATR inhibition.The role of BRCA1 in homologous recombination repair in response to replication stress: significance in tumorigenesis and cancer therapy Selective antitumor activity of roscovitine in head and neck cancer.Reverse the Resistance to PARP Inhibitors.PARP-1 and PARP-2: New players in tumour development.Recurrent ovarian cancer: when and how to treat.Systemic therapy options in BRCA mutation-associated breast cancer.PARP inhibitors: polypharmacology versus selective inhibition.Mechanisms of resistance to therapies targeting BRCA-mutant cancers.Therapeutic Targeting of Poly(ADP-Ribose) Polymerase-1 (PARP1) in Cancer: Current Developments, Therapeutic Strategies, and Future Opportunities.Distinct cellular phenotype linked to defective DNA interstrand crosslink repair and homologous recombination Dual Targeting of Epithelial Ovarian Cancer Via Folate Receptor α and the Proton-Coupled Folate Transporter with 6-Substituted Pyrrolo[2,3-d]pyrimidine Antifolates.PARP inhibitor attenuated colony formation can be restored by MAP kinase inhibitors in different irradiated cancer cell lines.Synergistic effect of hyperthermia and neferine on reverse multidrug resistance in adriamycin-resistant SGC7901/ADM gastric cancer cells.Resveratrol selectively induces DNA Damage, independent of Smad4 expression, in its efficacy against human head and neck squamous cell carcinoma.The homologous recombination protein RAD51D mediates the processing of 6-thioguanine lesions downstream of mismatch repair.ATR inhibition disrupts rewired homologous recombination and fork protection pathways in PARP inhibitor-resistant BRCA-deficient cancer cells.BRCA2 and RAD51 promote double-strand break formation and cell death in response to gemcitabine.Emerging Therapeutics to Overcome Chemoresistance in Epithelial Ovarian Cancer: A Mini-Review.Thiopurine-induced mitotic catastrophe in Rad51d-deficient mammalian cells.The promise and challenges of exploiting the proton-coupled folate transporter for selective therapeutic targeting of cancer.Modeling Therapy Resistance in BRCA1/2-Mutant Cancers.

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P2860

6-thioguanine selectively kills BRCA2-defective tumors and overcomes PARP inhibitor resistance

http://www.wikidata.org/entity/Q24599364

description

2010 nî lūn-bûn

@nan

2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

6-thioguanine selectively kill ...... omes PARP inhibitor resistance

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6-thioguanine selectively kill ...... omes PARP inhibitor resistance

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6-thioguanine selectively kill ...... omes PARP inhibitor resistance

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type

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6-thioguanine selectively kill ...... omes PARP inhibitor resistance

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6-thioguanine selectively kill ...... omes PARP inhibitor resistance

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6-thioguanine selectively kill ...... omes PARP inhibitor resistance

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prefLabel

6-thioguanine selectively kill ...... omes PARP inhibitor resistance

@ast

6-thioguanine selectively kill ...... omes PARP inhibitor resistance

@en

6-thioguanine selectively kill ...... omes PARP inhibitor resistance

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Cancer Research

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Cecilia Lundin

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Evan A Mulligan

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Ivaylo Stoimenov

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Nicholas Pedley

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Ponnari Gottipati

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P2860

The cell-cycle checkpoint kinase Chk1 is required for mammalian homologous recombination repair

Methyl methanesulfonate (MMS) produces heat-labile DNA damage but no detectable in vivo DNA double-strand breaks.

PALB2, which encodes a BRCA2-interacting protein, is a breast cancer susceptibility gene

Deficiency of human BRCA2 leads to impaired homologous recombination but maintains normal nonhomologous end joining

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

Poly(ADP-ribose) polymerase (PARP-1) has a controlling role in homologous recombination

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

A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1

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

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15

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