Transient potent BCR-ABL inhibition is sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis.
about
The proximal signaling network of the BCR-ABL1 oncogene shows a modular organizationChemotherapeutic agents circumvent emergence of dasatinib-resistant BCR-ABL kinase mutations in a precise mouse model of Philadelphia chromosome-positive acute lymphoblastic leukemiaAP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistanceOncogene Overdose: Too Much of a Bad Thing for Oncogene-Addicted Cancer CellsCombination Therapies to Inhibit the RAF/MEK/ERK Pathway in Melanoma: We are not Done YetThe growing arsenal of ATP-competitive and allosteric inhibitors of BCR-ABLWill kinase inhibitors make it as glioblastoma drugs?Targeting the SH2-Kinase Interface in Bcr-Abl Inhibits LeukemogenesisAxitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformationA common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.c-Abl Inhibitors Enable Insights into the Pathophysiology and Neuroprotection in Parkinson's DiseaseDual targeting of p53 and c-MYC selectively eliminates leukaemic stem cellsIntracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cellsThe Synthetic β-Nitrostyrene Derivative CYT-Rx20 Inhibits Esophageal Tumor Growth and Metastasis via PI3K/AKT and STAT3 PathwaysSensitive and selective plasmon ruler nanosensors for monitoring the apoptotic drug response in leukemia.A bead-based activity screen for small-molecule inhibitors of signal transduction in chronic myelogenous leukemia cells.Dasatinib: a review of its use in the treatment of chronic myeloid leukaemia and Philadelphia chromosome-positive acute lymphoblastic leukaemia.The kinase Mirk is a potential therapeutic target in osteosarcoma.Phase 1 dose-finding study of rebastinib (DCC-2036) in patients with relapsed chronic myeloid leukemia and acute myeloid leukemia.Therapeutic sensitivity to Rac GTPase inhibition requires consequential suppression of mTORC1, AKT, and MEK signaling in breast cancerA chemical and phosphoproteomic characterization of dasatinib action in lung cancerIsocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic CholangiocarcinomaSurface engineering on mesoporous silica chips for enriching low molecular weight phosphorylated proteinsThe phosphatase and tensin homolog regulates epidermal growth factor receptor (EGFR) inhibitor response by targeting EGFR for degradationAmplification of EGFR T790M causes resistance to an irreversible EGFR inhibitorTargeting the cancer kinome through polypharmacology.Inhibition of the insulin-like growth factor-1 receptor (IGF1R) tyrosine kinase as a novel cancer therapy approachChronic myeloid leukemia: mechanisms of blastic transformationDasatinib 100 mg once daily minimizes the occurrence of pleural effusion in patients with chronic myeloid leukemia in chronic phase and efficacy is unaffected in patients who develop pleural effusionAssessing the efficacy of molecularly targeted agents on cell line-based platforms by using system identification.Phase I/II study of the Src inhibitor dasatinib in combination with erlotinib in advanced non-small-cell lung cancer.MEK-dependent negative feedback underlies BCR-ABL-mediated oncogene addictionHigh Id1 expression, a generally negative prognostic factor, paradoxically predicts a favorable prognosis for adjuvant paclitaxel plus cisplatin therapy in surgically treated lung cancer patients.Model system to define pharmacokinetic requirements for antimalarial drug efficacy.cml biology for the clinician in 2011: six impossible things to believe before breakfast on the way to cure.Galectin-3 (Gal-3) induced by leukemia microenvironment promotes drug resistance and bone marrow lodgment in chronic myelogenous leukemiaMultiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors."Pulsatile" high-dose weekly erlotinib for CNS metastases from EGFR mutant non-small cell lung cancer.(124)I-iodopyridopyrimidinone for PET of Abl kinase-expressing tumors in vivo.NCI's provocative questions on cancer: some answers to ignite discussion.
P2860
Q24294830-0919A584-E28D-4A2C-A314-04030C1FD398Q24622397-8127D713-29F6-46A7-8B52-295B2E349CA4Q24648017-94EBBEA2-A622-451E-B1E3-ADB76A17FE1DQ26774625-AADA79E1-785A-4AF4-B1C6-6222C14E4736Q26799864-682154A8-26C0-43B2-99B3-71BC89F5243CQ26866312-89C883C0-C20E-4020-83BF-03B29F9A26D6Q27012684-EFCBCC0C-1618-4241-86CD-8502BA7F5AA6Q27675049-56B9EE1F-D069-4932-8E15-4A7101889055Q27698001-A4920691-7152-4223-AFF5-F90939593CDAQ27851729-D6F0C2B4-673B-4ABF-B7DC-F1F2423ACCDEQ28070292-BC639E31-3D98-4809-8D8D-2903B029F022Q28276260-28B86FCE-52E4-49EA-B46A-7948398510E0Q28481327-CB5C7E90-E3F8-4158-AF5B-388836E95F71Q28553655-10C8F2DB-8A2E-4534-87BB-050C7CAD2086Q30587590-5A651307-D160-4FBF-B2D6-F6FBB017CA99Q30981853-FBE1BA33-00AE-4AB9-966D-258493C00200Q33397085-C84F7C10-1764-4330-990D-AB55CCF9C1F8Q33521423-BB9C9124-8062-41B9-9715-2CF751FCDF68Q33573760-81258FE5-5CD1-4DD1-BB73-2858F9F74DA9Q33591690-A14D9A19-3611-40A0-8D97-8E558DC96741Q33742159-832D3370-E57C-4489-938F-F5D90C98C9D4Q33763540-DA89B820-6CB6-47B5-9C78-A0CACA18D2EFQ33764263-20083158-12AE-4113-BD60-FC88C7EB876AQ33778905-83EA74C7-D795-4882-84B4-F82E81D10583Q33810574-D02AF184-D395-4C1B-A7F9-1A44377B1A0EQ33893019-8B3E82B9-34CA-4DA2-98E4-7C85866625D3Q33925323-4913FC38-D70E-489A-B6E5-440568D200C5Q33968037-AEF2E008-5262-4764-955A-FC37D613F021Q34289635-8D0C5BDE-9EA0-441A-AC9F-6B87833C9A7AQ34470371-8E66D553-C457-413F-AD52-8FCD27A8A93CQ34578584-154D667C-EFCE-4197-96B3-4827A75A1183Q34588920-75B14F5B-2679-4BA6-8FB0-B3C125E4B4C6Q34956692-4888D06A-820A-47FF-82B0-365BF9071CB6Q35007051-E44ABD5A-4E8F-44C3-8AEA-90B82BF19CE1Q35145688-E60ED784-8524-46A6-BAC1-E6328662CC89Q35409569-9FC0355B-FE0B-4FBF-A3F7-14C931E31BF8Q35525305-F5D10D15-CDC7-4A15-A75C-D40E37296C36Q35570245-6261E80C-7CB7-4F9A-9E71-629E4D3A0712Q35609644-E6A712D3-057B-482E-930A-739A070706A8Q35764401-C1BBA50E-986D-496E-B4F7-D75386F7B27C
P2860
Transient potent BCR-ABL inhibition is sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
Transient potent BCR-ABL inhib ...... lls irreversibly to apoptosis.
@en
Transient potent BCR-ABL inhib ...... lls irreversibly to apoptosis.
@nl
type
label
Transient potent BCR-ABL inhib ...... lls irreversibly to apoptosis.
@en
Transient potent BCR-ABL inhib ...... lls irreversibly to apoptosis.
@nl
prefLabel
Transient potent BCR-ABL inhib ...... lls irreversibly to apoptosis.
@en
Transient potent BCR-ABL inhib ...... lls irreversibly to apoptosis.
@nl
P2093
P921
P1433
P1476
Transient potent BCR-ABL inhib ...... lls irreversibly to apoptosis.
@en
P2093
Charles L Sawyers
Christopher Weier
Claude Nicaise
Corynn Kasap
Eric Bleickardt
John M Nicoll
Minna Balbas
Neil P Shah
P304
P356
10.1016/J.CCR.2008.11.001
P577
2008-12-01T00:00:00Z