Selective FLT3 inhibition of FLT3-ITD+ acute myeloid leukaemia resulting in secondary D835Y mutation: a model for emerging clinical resistance patterns
about
Aurora Kinase Inhibitors: Current Status and OutlookProgress in acute myeloid leukemiaOptimization of Imidazo[4,5- b ]pyridine-Based Kinase Inhibitors: Identification of a Dual FLT3/Aurora Kinase Inhibitor as an Orally Bioavailable Preclinical Development Candidate for the Treatment of Acute Myeloid LeukemiaEmergence of polyclonal FLT3 tyrosine kinase domain mutations during sequential therapy with sorafenib and sunitinib in FLT3-ITD-positive acute myeloid leukemia.Targeting oncoprotein stability overcomes drug resistance caused by FLT3 kinase domain mutationsUsing functional genomics to overcome therapeutic resistance in hematological malignancies.Pharmacological targeting of miR-155 via the NEDD8-activating enzyme inhibitor MLN4924 (Pevonedistat) in FLT3-ITD acute myeloid leukemia.SU11652 Inhibits tyrosine kinase activity of FLT3 and growth of MV-4-11 cellsFLT3 kinase inhibitor TTT-3002 overcomes both activating and drug resistance mutations in FLT3 in acute myeloid leukemia.Targeting CDK1 promotes FLT3-activated acute myeloid leukemia differentiation through C/EBPα.Targeting oncogenic Ras signaling in hematologic malignancies.The Dual MEK/FLT3 Inhibitor E6201 Exerts Cytotoxic Activity against Acute Myeloid Leukemia Cells Harboring Resistance-Conferring FLT3 Mutations.Crenolanib is active against models of drug-resistant FLT3-ITD-positive acute myeloid leukemia.FLT3/D835Y mutation knock-in mice display less aggressive disease compared with FLT3/internal tandem duplication (ITD) mice.MUC1-C oncoprotein promotes FLT3 receptor activation in acute myeloid leukemia cellsTTT-3002 is a novel FLT3 tyrosine kinase inhibitor with activity against FLT3-associated leukemias in vitro and in vivo.Inhibition of Aurora B by CCT137690 sensitizes colorectal cells to radiotherapy.Discovery of BPR1K871, a quinazoline based, multi-kinase inhibitor for the treatment of AML and solid tumors: Rational design, synthesis, in vitro and in vivo evaluationFLT3 inhibition: a moving and evolving target in acute myeloid leukaemia.Children's Oncology Group's 2013 blueprint for research: acute myeloid leukemiaNovel therapies for children with acute myeloid leukaemia.Will FLT3 inhibitors fulfill their promise in acute meyloid leukemia?The evolving role of FLT3 inhibitors in acute myeloid leukemia: quizartinib and beyond.Targeting FLT3 to treat leukemia.Mutations in tyrosine kinase and tyrosine phosphatase and their relevance to the target therapy in hematologic malignancies.Perspectives for therapeutic targeting of gene mutations in acute myeloid leukaemia with normal cytogenetics.Novel Therapies for Acute Myeloid Leukemia: Are We Finally Breaking the Deadlock?Identifying high-risk adult AML patients: epigenetic and genetic risk factors and their implications for therapy.The Aurora kinase inhibitors in cancer research and therapy.Facile identification of dual FLT3-Aurora A inhibitors: a computer-guided drug design approach.Reversal of acquired drug resistance in FLT3-mutated acute myeloid leukemia cells via distinct drug combination strategies.The role of FLT3 inhibitors in the treatment of FLT3-mutated acute myeloid leukemia.Activation of protein phosphatase 2A in FLT3+ acute myeloid leukemia cells enhances the cytotoxicity of FLT3 tyrosine kinase inhibitors.The secondary FLT3-ITD F691L mutation induces resistance to AC220 in FLT3-ITD+ AML but retains in vitro sensitivity to PKC412 and Sunitinib.Gene Mutations as Emerging Biomarkers and Therapeutic Targets for Relapsed Acute Myeloid Leukemia.Targeted therapies in Acute Myeloid Leukemia: a focus on FLT-3 inhibitors and ABT199.Cabozantinib is well tolerated in acute myeloid leukemia and effectively inhibits the resistance-conferring FLT3/tyrosine kinase domain/F691 mutation.MYC-dependent downregulation of telomerase by FLT3 inhibitors is required for their therapeutic efficacy on acute myeloid leukemia.Therapeutic targeting of leukemic stem cells in acute myeloid leukemia - the biological background for possible strategies.A novel, dual pan-PIM/FLT3 inhibitor SEL24 exhibits broad therapeutic potential in acute myeloid leukemia.
P2860
Q26770583-7B7D3728-72B1-4C0D-9333-E2F9F77382F6Q27024006-9E4ED54B-A8D6-42FD-90E7-8C55A4CE652DQ27674324-4510BF27-FD22-44F0-AF26-AF5AA40E10CAQ27852520-7DC5B5E4-6330-475B-8505-32CC9E10A887Q28539032-131518EC-B88F-4190-BDDE-B243F705CCAEQ34401328-7E2D75CE-CFD8-4E83-B1E0-657D51026DDCQ34476246-6B930299-85BE-4A9C-9685-BD115728B6C9Q34502608-B94CD81F-ACB0-41D0-AA7A-ED08186E3C39Q34993145-CB6AAE32-E25F-425D-8F5C-C4E5D052D512Q36129030-1577D2A1-0EFE-4398-BD66-389915931DFDQ36352506-752AB2CB-7384-4565-8F1F-9144F31AFD57Q36693252-4AE4D2B0-A32F-4E1D-B8B7-D24B501C9773Q37334711-A46076E2-BEDF-4137-BF3C-EF68A8301572Q37421401-5D07644C-2A5B-486D-999F-934C7353F500Q37535249-DD450368-DE47-4459-8FFB-EF2A1A5F78F0Q37623535-690CB322-7E87-438E-8F7D-8D25D22DE7E0Q37685338-322DF4D7-4727-4DFE-926E-7BE2EC60EE75Q37699220-63AF0D33-FA64-49C1-BE4F-727E32D28731Q38026453-F220FF52-98E1-49BA-8EC4-CE66EAACDBA4Q38068816-48DEEDBC-870C-49F1-B190-0E185B437C53Q38096798-75A036C1-643B-4068-830F-21CC6D52F6DBQ38182335-E91AB391-8D1C-4719-8718-A57DFA515C09Q38216649-31F30E6E-249A-4FF7-8169-17E15028086AQ38251339-AFF77E3F-89F3-41F3-AE76-034578CADA31Q38357132-4C24A4E9-B011-4DDA-8D44-4D1E27282135Q38428692-F6DF3CDC-F250-4DB9-A728-B1B4DE162F82Q38664735-FF82C919-38EA-4F42-AA5E-6F5E0F29A215Q38694866-9476E61F-E545-4357-A64C-F17B47A46EDFQ38756932-9DB8EFE7-04FC-46A9-94FA-01CC6F309016Q39012096-153D9C4E-A735-445A-9E39-07DE4A2D10B9Q39016415-E4DAFEE9-4C3E-4DB0-B740-C73264C09DD5Q39045272-3B941992-B297-45BF-B2F9-842893304FA0Q40859498-4D7ABF0E-BA35-427B-87BE-F9CE65050A91Q44688617-38A3C6B2-A6AE-49F4-8448-F3E0AB1EECBAQ47136441-BE91C36E-7C8E-4F78-99B2-D1816D9565D9Q47965108-F3B1628C-FDBB-404F-B7DC-8A5AA6BB494DQ48273276-C4D00A65-C149-46A8-BF44-40A2B907246CQ49722374-41DCBF45-248A-41B2-B20E-3F4948D2DE5CQ51818965-B234F6B3-4218-43F1-BC5B-6FECCA77DA9CQ52571251-B287B6BC-B8E8-4867-AD0B-01DBA4AD9BC9
P2860
Selective FLT3 inhibition of FLT3-ITD+ acute myeloid leukaemia resulting in secondary D835Y mutation: a model for emerging clinical resistance patterns
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
2012年學術文章
@zh
2012年學術文章
@zh-hant
name
Selective FLT3 inhibition of F ...... g clinical resistance patterns
@ast
Selective FLT3 inhibition of F ...... g clinical resistance patterns
@en
type
label
Selective FLT3 inhibition of F ...... g clinical resistance patterns
@ast
Selective FLT3 inhibition of F ...... g clinical resistance patterns
@en
prefLabel
Selective FLT3 inhibition of F ...... g clinical resistance patterns
@ast
Selective FLT3 inhibition of F ...... g clinical resistance patterns
@en
P2093
P2860
P50
P356
P1433
P1476
Selective FLT3 inhibition of F ...... g clinical resistance patterns
@en
P2093
A D J Pearson
A de Haven Brandon
D Gonzalez de Castro
J Swansbury
P2860
P2888
P304
P356
10.1038/LEU.2012.52
P577
2012-02-22T00:00:00Z