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Exploiting synthetic lethal interactions for targeted cancer therapy.

Exploiting synthetic lethal interactions for targeted cancer therapy.

http://www.wikidata.org/entity/Q37597842

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Trial Watch: Targeting ATM-CHK2 and ATR-CHK1 pathways for anticancer therapy Targeting ATM-deficient CLL through interference with DNA repair pathways Dynamics of p53 and NF-κB regulation in response to DNA damage and identification of target proteins suitable for therapeutic intervention.Detection of COPB2 as a KRAS synthetic lethal partner through integration of functional genomics screens.Kinase requirements in human cells: V. Synthetic lethal interactions between p53 and the protein kinases SGK2 and PAK3 Mechanism-based screen establishes signalling framework for DNA damage-associated G1 checkpoint response.The stress phenotype makes cancer cells addicted to CDT2, a substrate receptor of the CRL4 ubiquitin ligase.Synthetic lethal compound combinations reveal a fundamental connection between wall teichoic acid and peptidoglycan biosyntheses in Staphylococcus aureus Knockdown of Slingshot 2 (SSH2) serine phosphatase induces Caspase3 activation in human carcinoma cell lines with the loss of the Birt-Hogg-Dubé tumour suppressor gene (FLCN).Identification and evaluation of a potent novel ATR inhibitor, NU6027, in breast and ovarian cancer cell lines DNA repair mechanisms in cancer development and therapy Cooperative effects of Akt-1 and Raf-1 on the induction of cellular senescence in doxorubicin or tamoxifen treated breast cancer cells.Recent progress in targeting cancer.NCI's provocative questions on cancer: some answers to ignite discussion.A chemical-genetic screen reveals a mechanism of resistance to PI3K inhibitors in cancer.MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition Enhanced cytotoxicity of PARP inhibition in mantle cell lymphoma harbouring mutations in both ATM and p53 Metabolic vulnerability of KRAS-driven cancer cells.Targeting SOD1 induces synthetic lethal killing in BLM- and CHEK2-deficient colorectal cancer cells.Caffeine Suppresses Apoptosis of Bladder Cancer RT4 Cells in Response to Ionizing Radiation by Inhibiting Ataxia Telangiectasia Mutated-Chk2-p53 Axis Synthetic lethal targeting of PTEN-deficient cancer cells using selective disruption of polynucleotide kinase/phosphatase Targeting an Achilles' heel of cancer with a WRN helicase inhibitor MicroRNA-based screens for synthetic lethal interactions with c-Myc Mutant ras elevates dependence on serum lipids and creates a synthetic lethality for rapamycin Exploration of synthetic lethal interactions as cancer drug targets.Posttranscriptional regulation of gene expression-adding another layer of complexity to the DNA damage response.Complex DNA repair pathways as possible therapeutic targets to overcome temozolomide resistance in glioblastoma.DNA repair and cell cycle checkpoint defects as drivers and therapeutic targets in melanoma.Revisiting p53 for cancer-specific chemo- and radiotherapy: ten years after.Triple-negative breast cancer: investigating potential molecular therapeutic target.Antitumor mechanisms when pRb and p53 are genetically inactivated.The Bcl-2 repertoire of mesothelioma spheroids underlies acquired apoptotic multicellular resistance A reversible gene-targeting strategy identifies synthetic lethal interactions between MK2 and p53 in the DNA damage response in vivo.Molecular inhibitors of DNA repair: searching for the ultimate tumor killing weapon.The changing landscape of phase I trials in oncology.Antinuclear antibodies defining autoimmunity pathways.Cell cycle-tailored targeting of metastatic melanoma: Challenges and opportunities.Molecularly targeted therapies for p53-mutant cancers.Genome evolution predicts genetic interactions in protein complexes and reveals cancer drug targets.Oxidative stress as a therapeutic perspective for ATM-deficient chronic lymphocytic leukemia patients.

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P2860

Exploiting synthetic lethal interactions for targeted cancer therapy.

http://www.wikidata.org/entity/Q37597842

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on October 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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Exploiting synthetic lethal interactions for targeted cancer therapy.

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Exploiting synthetic lethal interactions for targeted cancer therapy.

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Exploiting synthetic lethal interactions for targeted cancer therapy.

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Exploiting synthetic lethal interactions for targeted cancer therapy.

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Exploiting synthetic lethal interactions for targeted cancer therapy.

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Exploiting synthetic lethal interactions for targeted cancer therapy.

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Exploiting synthetic lethal interactions for targeted cancer therapy.

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H Christian Reinhardt

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

Hai Jiang

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

Michael B Yaffe

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

Michael T Hemann

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P2860

The Hallmarks of Cancer

TAO kinases mediate activation of p38 in response to DNA damage

MAPKAP kinase-2 is a cell cycle checkpoint kinase that regulates the G2/M transition and S phase progression in response to UV irradiation

Synapsis of DNA ends by DNA-dependent protein kinase

Chk1 is an essential kinase that is regulated by Atr and required for the G(2)/M DNA damage checkpoint

Core signaling pathways in human pancreatic cancers revealed by global genomic analyses

A genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene

Somatic mutations affect key pathways in lung adenocarcinoma

An integrated genomic analysis of human glioblastoma multiforme

Essential role for DNA-PKcs in DNA double-strand break repair and apoptosis in ATM-deficient lymphocytes

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3112-3119

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scholarly article

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10.4161/CC.8.19.9626

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19

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8

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2009-10-01T00:00:00Z

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26813676

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19755856

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3057180

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