The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKCs-mediated DNA damage responses.
about
Molecular characterizations of glioblastoma, targeted therapy, and clinical results to dateDeciphering the link between PI3K and PAK: An opportunity to target key pathways in pancreatic cancer?Predicting mTOR inhibitors with a classifier using recursive partitioning and Naïve Bayesian approachesRe-purposing clinical kinase inhibitors to enhance chemosensitivity by overriding checkpointsPhosphorylation of EXO1 by CDKs 1 and 2 regulates DNA end resection and repair pathway choice.NVP-BEZ235, a dual PI3K/mTOR inhibitor synergistically potentiates the antitumor effects of cisplatin in bladder cancer cells.Targeting DNA repair pathways for cancer treatment: what's new?Combining targeted agents with modern radiotherapy in soft tissue sarcomas.Connection between Tumor Suppressor BRCA1 and PTEN in Damaged DNA RepairPotential anti-aging agents suppress the level of constitutive mTOR- and DNA damage- signalingNVP-BEZ235, a novel dual PI3K/mTOR inhibitor, enhances the radiosensitivity of human glioma stem cells in vitro.Efficacy of dual PI-3K and mTOR inhibitors in vitro and in vivo in acute lymphoblastic leukemiaComparative analysis of radiosensitizers for K-RAS mutant rectal cancersTumor cells, but not endothelial cells, mediate eradication of primary sarcomas by stereotactic body radiation therapyRadiation Enhancement of Head and Neck Squamous Cell Carcinoma by the Dual PI3K/mTOR Inhibitor PF-05212384.mTORC1 and DNA-PKcs as novel molecular determinants of sensitivity to Chk1 inhibitionCharacterization 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 ToxicityInhibition of human positive cofactor 4 radiosensitizes human esophageal squmaous cell carcinoma cells by suppressing XLF-mediated nonhomologous end joiningInhibition of autophagy as a strategy to augment radiosensitization by the dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235Discovering new mTOR inhibitors for cancer treatment through virtual screening methods and in vitro assays.Combined inhibition of PI3K-related DNA damage response kinases and mTORC1 induces apoptosis in MYC-driven B-cell lymphomasSynergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.Torin2 Suppresses Ionizing Radiation-Induced DNA Damage RepairPhosphoproteomic characterization of DNA damage response in melanoma cells following MEK/PI3K dual inhibitionCancer subclonal genetic architecture as a key to personalized medicine.Strategies for optimizing the response of cancer and normal tissues to radiation.Doubling down on the PI3K-AKT-mTOR pathway enhances the antitumor efficacy of PARP inhibitor in triple negative breast cancer model beyond BRCA-nessInhibition of DNA double-strand break repair by the dual PI3K/mTOR inhibitor NVP-BEZ235 as a strategy for radiosensitization of glioblastoma.Novel PI3K and mTOR Inhibitor NVP-BEZ235 Radiosensitizes Breast Cancer Cell Lines under Normoxic and Hypoxic Conditions.Support for phosphoinositol 3 kinase and mTOR inhibitors as treatment for lupus using in-silico drug-repurposing analysis.Extracellular Vesicles Mediate Radiation-Induced Systemic Bystander Signals in the Bone Marrow and Spleen.Targeting the PI3K/AKT/mTOR signaling pathway in glioblastoma: novel therapeutic agents and advances in understanding.Targeting PI3K in Cancer: Any Good News?The emergence of targeted drugs in breast cancer to prevent resistance to endocrine treatment and chemotherapy.NF-κB drives acquired resistance to a novel mutant-selective EGFR inhibitor.Clinical relevance of autophagic therapy in cancer: Investigating the current trends, challenges, and future prospects.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.Simultaneous perturbation of the MAPK and the PI3K/mTOR pathways does not lead to increased radiosensitization.
P2860
Q26822717-0FA69605-1D96-4F77-A07A-5BF87CD9EBA0Q28079848-CDC98CC1-D91F-4C4B-A349-960B320E1D55Q28538732-B14F6F7D-E768-4137-8A7A-FBB11AA9CE5BQ30584974-0770602C-4E20-4E61-B2D9-91E18E512533Q33697447-B5E2E0D5-9C7B-4B55-9D36-B16653B35D2FQ34000632-13438E2E-937C-4FEC-B549-53C8BAB3AF99Q34015040-3D243AD5-4301-4FF3-A820-64BB400E5FBDQ34396047-D794631B-966D-49AA-9866-5B4522DD0327Q34481443-54614415-2C55-4642-9BAC-9B9EC9FD8A20Q34567724-D6B98B74-D8C4-47FE-BF49-BB2B6372B6FEQ34679652-2A5FD079-8FA4-4474-8903-16041FB66A58Q34786480-A408F6AD-0D24-4765-B41E-23715F8CD623Q35070685-21BC5DD3-C55B-482C-8F19-8C0E0CB434ADQ35178834-1C68D216-075A-4064-93BE-A99E04E7EECDQ35751948-68AF2DCB-F09E-40DD-8E85-E4FE1746334AQ35809470-2CD04CC8-B3EF-44DD-B66F-15C4682751D4Q35940003-50525C03-E04B-4A06-BE2E-37AEFADD5DD9Q35999766-39526B73-616C-4599-9420-8CA4DD1E2CE6Q36291148-89549F99-CA15-4BE2-B158-9A5672E4CAB3Q36412815-197973A9-9EE7-4E14-9531-CE54B2E174B2Q36432654-8A6409FA-F20C-46FF-9117-973F47804E36Q36761564-609F6D24-CFB2-4A0A-A112-157F343DEE07Q36984507-B14FFDEE-88BE-4722-B407-93E37F18C71BQ37041046-14BF6113-C1BC-4C5E-AA60-8C4B959F271DQ37353168-1852EC4B-A114-4FCA-B8FF-06579E01CE24Q37448116-5D0B6A3E-DE0D-482F-BCA5-3A01131C3BCBQ37531724-F8AD6FA4-19F2-40B0-90F8-94BACCF2C053Q37584321-4B9E3C66-2CFF-45DE-A6AC-85564CA9DCA7Q37626600-1356C825-1622-4257-ACA5-4C9EDAECF07CQ37660260-B1BF9002-3088-480C-8ADE-8DEB7DA5CF8DQ37694044-257184D5-0BBE-4109-B216-D3249A0FC980Q37721689-3B16278E-9075-4A58-B0DC-450B95724AC9Q38102636-BE967C95-9F50-41E5-9379-FC889D9AA5A8Q38105322-6D2DB761-2795-408E-8C5C-0E142E2A6FADQ38192017-BD91A7FF-31C3-4916-9EB4-8FD7FBCF3A95Q38631853-B55192CC-0139-49F5-B5A6-C1A849874684Q38689955-918B5603-F7FD-4D40-9EB0-39CB75BEE23FQ38720885-BC925C90-52F2-40C6-A404-4BE132EFC8C5Q38760793-A62AE86F-F7B6-4FE2-A284-06FBE1BB07DBQ38825141-B9E3466A-703E-4CCA-B04C-B78130C159F4
P2860
The dual PI3K/mTOR inhibitor NVP-BEZ235 is a potent inhibitor of ATM- and DNA-PKCs-mediated DNA damage responses.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
The dual PI3K/mTOR inhibitor N ...... mediated DNA damage responses.
@ast
The dual PI3K/mTOR inhibitor N ...... mediated DNA damage responses.
@en
type
label
The dual PI3K/mTOR inhibitor N ...... mediated DNA damage responses.
@ast
The dual PI3K/mTOR inhibitor N ...... mediated DNA damage responses.
@en
prefLabel
The dual PI3K/mTOR inhibitor N ...... mediated DNA damage responses.
@ast
The dual PI3K/mTOR inhibitor N ...... mediated DNA damage responses.
@en
P2093
P2860
P356
P1433
P1476
The dual PI3K/mTOR inhibitor N ...... mediated DNA damage responses.
@en
P2093
Bipasha Mukherjee
Cristel V Camacho
Kaushik Amancherla
Nandini Pichamoorthy
Nozomi Tomimatsu
Sandeep Burma
P2860
P356
10.1593/NEO.111512
P577
2012-01-01T00:00:00Z