Inhibition of DNA double-strand break repair by the dual PI3K/mTOR inhibitor NVP-BEZ235 as a strategy for radiosensitization of glioblastoma.
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New perspectives in glioblastoma antiangiogenic therapyRadioresistance of Brain TumorsGenomic landscape of human papillomavirus-associated cancersRecent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical developmentZerumbone increases oxidative stress in a thiol-dependent ROS-independent manner to increase DNA damage and sensitize colorectal cancer cells to radiation.International Differences in Treatment and Clinical Outcomes for High Grade GliomaA Potential Role for the Inhibition of PI3K Signaling in Glioblastoma Therapy.Radiation Enhancement of Head and Neck Squamous Cell Carcinoma by the Dual PI3K/mTOR Inhibitor PF-05212384.An Integrated Molecular Analysis of Lung Adenocarcinomas Identifies Potential Therapeutic Targets among TTF1-Negative Tumors, Including DNA Repair Proteins and Nrf2.Characterization of Cardiac Glycoside Natural Products as Potent Inhibitors of DNA Double-Strand Break Repair by a Whole-Cell Double Immunofluorescence Assay.Targeted Inhibition of Phosphoinositide 3-Kinase/Mammalian Target of Rapamycin Sensitizes Pancreatic Cancer Cells to Doxorubicin without Exacerbating Cardiac ToxicityDactolisib (NVP-BEZ235) toxicity in murine brain tumour models.MicroRNA-199a-3p suppresses glioma cell proliferation by regulating the AKT/mTOR signaling pathwayBEZ235 (PIK3/mTOR inhibitor) Overcomes Pazopanib Resistance in Patient-Derived Refractory Soft Tissue Sarcoma CellsTorin2 Suppresses Ionizing Radiation-Induced DNA Damage RepairOpportunities for Radiosensitization in the Stereotactic Body Radiation Therapy (SBRT) EraMicroRNA-Related Polymorphisms in PI3K/Akt/mTOR Pathway Genes Are Predictive of Limited-Disease Small Cell Lung Cancer Treatment Outcomes.New role of osteopontin in DNA repair and impact on human glioblastoma radiosensitivity.Radiation oncology in vitro: trends to improve radiotherapy through molecular targets.Management of diffuse intrinsic pontine glioma in children: current and future strategies for improving prognosis.mTOR in health and in sickness.Association of ribosomal protein S6 kinase 1 with cellular radiosensitivity of non-small lung cancer.Pediatric and adult glioblastoma radiosensitization induced by PI3K/mTOR inhibition causes early metabolic alterations detected by nuclear magnetic resonance spectroscopy.Augmented HR Repair Mediates Acquired Temozolomide Resistance in Glioblastoma.MSK1-Mediated β-Catenin Phosphorylation Confers Resistance to PI3K/mTOR Inhibitors in Glioblastoma.Targeting the VEGF and PDGF signaling pathway in glioblastoma treatment.Enhanced dependency of KRAS-mutant colorectal cancer cells on RAD51-dependent homologous recombination repair identified from genetic interactions in Saccharomyces cerevisiae.The dual PI3K/mTOR inhibitor NVP-BEZ235 inhibits proliferation and induces apoptosis of burkitt lymphoma cells.PIAS1-FAK Interaction Promotes the Survival and Progression of Non-Small Cell Lung Cancer.Combined treatment of pancreatic cancer xenograft with 90Y-ITGA6B4-mediated radioimmunotherapy and PI3K/mTOR inhibitor.Protein expression of TTF1 and cMYC define distinct molecular subgroups of small cell lung cancer with unique vulnerabilities to aurora kinase inhibition, DLL3 targeting, and other targeted therapies.Pharmacokinetics, pharmacodynamics and efficacy on pediatric tumors of the glioma radiosensitizer KU60019.The dual PI3K/mTOR inhibitor dactolisib elicits anti-tumor activity in vitro and in vivo.Radiosensitization of the PI3K inhibitor HS-173 through reduction of DNA damage repair in pancreatic cancer.Acquired resistance to tyrosine kinase inhibitors may be linked with the decreased sensitivity to X-ray irradiation.Local DNA Repair Inhibition for Sustained Radiosensitization of High-Grade Gliomas.Effects of Aptamer to U87-EGFRvIII Cells on the Proliferation, Radiosensitivity, and Radiotherapy of Glioblastoma Cells.ATR kinase inhibitors NVP-BEZ235 and AZD6738 effectively penetrate the brain after systemic administration.Dual mTOR/PI3K inhibition limits PI3K-dependent pathways activated upon mTOR inhibition in autosomal dominant polycystic kidney disease.NVP-BEZ235, a dual PI3K-mTOR inhibitor, suppresses the growth of FaDu hypopharyngeal squamous cell carcinoma and has a synergistic effect with Cisplatin.
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Inhibition of DNA double-strand break repair by the dual PI3K/mTOR inhibitor NVP-BEZ235 as a strategy for radiosensitization of glioblastoma.
description
article científic
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article scientifique
@fr
articolo scientifico
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artigo científico
@pt
bilimsel makale
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scientific article published on 23 December 2013
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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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name
Inhibition of DNA double-stran ...... sensitization of glioblastoma.
@en
Inhibition of DNA double-stran ...... sensitization of glioblastoma.
@nl
type
label
Inhibition of DNA double-stran ...... sensitization of glioblastoma.
@en
Inhibition of DNA double-stran ...... sensitization of glioblastoma.
@nl
prefLabel
Inhibition of DNA double-stran ...... sensitization of glioblastoma.
@en
Inhibition of DNA double-stran ...... sensitization of glioblastoma.
@nl
P2093
P2860
P1476
Inhibition of DNA double-stran ...... sensitization of glioblastoma.
@en
P2093
Amyn A Habib
Bipasha Mukherjee
Carlos Rodrigo Gil del Alcazar
Jingsheng Yan
Molly Catherine Hardebeck
Nozomi Tomimatsu
Robert Bachoo
Sandeep Burma
Xian-Jin Xie
P2860
P304
P356
10.1158/1078-0432.CCR-13-1607
P407
P577
2013-12-23T00:00:00Z