Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition. - Test2 - elhamkhani - TriplyDB

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

http://www.wikidata.org/entity/Q35737613

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Cyclin-dependent kinase inhibitor therapy for hematologic malignancies STRUCTURE-FUNCTION OF THE TUMOR SUPPRESSOR BRCA1 Trial watch - inhibiting PARP enzymes for anticancer therapy Homologous Recombination Deficiency: Exploiting the Fundamental Vulnerability of Ovarian Cancer PARP inhibitors in the management of breast cancer: current data and future prospects Exploiting the Fanconi Anemia Pathway for Targeted Anti-Cancer Therapy New molecular targets in mantle cell lymphoma Novel treatment strategies in triple-negative breast cancer: specific role of poly(adenosine diphosphate-ribose) polymerase inhibition CDK1 Is a Synthetic Lethal Target for KRAS Mutant Tumours.Use of poly ADP-ribose polymerase [PARP] inhibitors in cancer cells bearing DDR defects: the rationale for their inclusion in the clinic Strategies for the Use of Poly(adenosine diphosphate ribose) Polymerase (PARP) Inhibitors in Cancer Therapy.Targeting tumor suppressor networks for cancer therapeutics.Sublethal concentrations of 17-AAG suppress homologous recombination DNA repair and enhance sensitivity to carboplatin and olaparib in HR proficient ovarian cancer cells.Histone deacetylase inhibitor treatment induces 'BRCAness' and synergistic lethality with PARP inhibitor and cisplatin against human triple negative breast cancer cells miR-9 regulation of BRCA1 and ovarian cancer sensitivity to cisplatin and PARP inhibition.The history and future of targeting cyclin-dependent kinases in cancer therapy.Subtyping of triple-negative breast cancer: implications for therapy APC/C(Cdh1) controls CtIP stability during the cell cycle and in response to DNA damage.Regulators of homologous recombination repair as novel targets for cancer treatment.Inactivating UBE2M impacts the DNA damage response and genome integrity involving multiple cullin ligases.Histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), enhances anti-tumor effects of the poly (ADP-ribose) polymerase (PARP) inhibitor olaparib in triple-negative breast cancer cells.Killing cells by targeting mitosis Nanoparticle-mediated measurement of target-drug binding in cancer cells Poly (ADP-ribose) polymerase inhibitors: recent advances and future development.Tumor-Targeted Synergistic Blockade of MAPK and PI3K from a Layer-by-Layer Nanoparticle.Cdk1 protein-mediated phosphorylation of receptor-associated protein 80 (RAP80) serine 677 modulates DNA damage-induced G2/M checkpoint and cell survival.PARP inhibition selectively increases sensitivity to cisplatin in ERCC1-low non-small cell lung cancer cells.AZD5438, an inhibitor of Cdk1, 2, and 9, enhances the radiosensitivity of non-small cell lung carcinoma cells.Polo-like kinase 1 mediates BRCA1 phosphorylation and recruitment at DNA double-strand breaks Mammalian interphase cdks: dispensable master regulators of the cell cycle.Therapeutic applications of PARP inhibitors: anticancer therapy and beyond Identifying novel genes and chemicals related to nasopharyngeal cancer in a heterogeneous network.mTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer.Inhibiting the DNA damage response as a therapeutic manoeuvre in cancer.Evaluation of rucaparib and companion diagnostics in the PARP inhibitor landscape for recurrent ovarian cancer therapy.Comparative antiproliferative effects of iniparib and olaparib on a panel of triple-negative and non-triple-negative breast cancer cell lines Centrosomal protein FOR20 is essential for S-phase progression by recruiting Plk1 to centrosomes.Genetically-defined novel oral squamous cell carcinoma cell lines for the development of molecular therapies.Grading breast cancer tissues using molecular portraits.Inhibition of CDK4/6 protects against radiation-induced intestinal injury in mice.

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P2860

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

http://www.wikidata.org/entity/Q35737613

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2011年論文

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2011年论文

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2011年论文

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2011年论文

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name

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

@ast

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

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type

label

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

@ast

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

@en

prefLabel

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

@ast

Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition.

@en

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Nature Medicine

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Compromised CDK1 activity sensitizes BRCA-proficient cancers to PARP inhibition

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Alan D D'Andrea

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Christine Unitt

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Danan Li

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David R Newell

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Geoffrey I Shapiro

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Huw D Thomas

http://www.w3.org/2001/XMLSchema#string

Katherine A Cheng

http://www.w3.org/2001/XMLSchema#string

Lisa A Moreau

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Neil Johnson

http://www.w3.org/2001/XMLSchema#string

Roderick T Bronson

http://www.w3.org/2001/XMLSchema#string

P2860

CDK-dependent phosphorylation of BRCA2 as a regulatory mechanism for recombinational repair

Cell cycle, CDKs and cancer: a changing paradigm

XRCC3 promotes homology-directed repair of DNA damage in mammalian cells

The impact of human EGFR kinase domain mutations on lung tumorigenesis and in vivo sensitivity to EGFR-targeted therapies.

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

DNA end resection, homologous recombination and DNA damage checkpoint activation require CDK1

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

Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway

Cyclin-dependent kinase pathways as targets for cancer treatment

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10.1038/NM.2377

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21706030

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