Exploiting cellular pathways to develop new treatment strategies for AML.
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Targeting mTOR for the treatment of AML. New agents and new directionsDistinct patterns of DNA damage response and apoptosis correlate with Jak/Stat and PI3kinase response profiles in human acute myelogenous leukemiaAcid ceramidase is upregulated in AML and represents a novel therapeutic target.Targeting tumor suppressor networks for cancer therapeutics.The Nrf2 transcription factor is a positive regulator of myeloid differentiation of acute myeloid leukemia cellsTreatment of FLT3-ITD acute myeloid leukemia.Dual mTORC2/mTORC1 targeting results in potent suppressive effects on acute myeloid leukemia (AML) progenitors.Low expression of PP2A regulatory subunit B55α is associated with T308 phosphorylation of AKT and shorter complete remission duration in acute myeloid leukemia patients.Overexpression of SET is a recurrent event associated with poor outcome and contributes to protein phosphatase 2A inhibition in acute myeloid leukemia.Phosphorylation of GSK3α/β correlates with activation of AKT and is prognostic for poor overall survival in acute myeloid leukemia patients.Inhibition of the receptor tyrosine kinase Axl impedes activation of the FLT3 internal tandem duplication in human acute myeloid leukemia: implications for Axl as a potential therapeutic target.Small-molecule inhibition of BRD4 as a new potent approach to eliminate leukemic stem- and progenitor cells in acute myeloid leukemia AML.CXCR4 chemokine receptor signaling induces apoptosis in acute myeloid leukemia cells via regulation of the Bcl-2 family members Bcl-XL, Noxa, and BakImmunotherapy with histamine dihydrochloride for the prevention of relapse in acute myeloid leukemia.New agents for acute myeloid leukemia: is it time for targeted therapies?SAR103168: a tyrosine kinase inhibitor with therapeutic potential in myeloid leukemias.Amsacrine-induced apoptosis of human leukemia U937 cells is mediated by the inhibition of AKT- and ERK-induced stabilization of MCL1.FLT3 inhibition as therapy in acute myeloid leukemia: a record of trials and tribulations.Peripheral T cell lymphoma: new model + new insight.The Association Between p38 MAPK-Mediated TNF-α/TNFR2 up-Regulation and 2-(4-Aminophenyl)-7-Methoxybenzothiazole-Induced Apoptosis in Human Leukemia U937 Cells.Cell-Type-Specific Effects of Silibinin on Vitamin D-Induced Differentiation of Acute Myeloid Leukemia Cells Are Associated with Differential Modulation of RXRα Levels.The CXCR4 inhibitor BL-8040 induces the apoptosis of AML blasts by downregulating ERK, BCL-2, MCL-1 and cyclin-D1 via altered miR-15a/16-1 expression.X-linked inhibitor of apoptosis inhibition sensitizes acute myeloid leukemia cell response to TRAIL and chemotherapy through potentiated induction of proapoptotic machinery.Enhancement of chemosensitivity by simultaneously silencing of Mcl-1 and Survivin genes using small interfering RNA in human myelomonocytic leukaemia.
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Exploiting cellular pathways to develop new treatment strategies for AML.
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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 06 January 2010
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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
Exploiting cellular pathways to develop new treatment strategies for AML.
@en
Exploiting cellular pathways to develop new treatment strategies for AML.
@nl
type
label
Exploiting cellular pathways to develop new treatment strategies for AML.
@en
Exploiting cellular pathways to develop new treatment strategies for AML.
@nl
prefLabel
Exploiting cellular pathways to develop new treatment strategies for AML.
@en
Exploiting cellular pathways to develop new treatment strategies for AML.
@nl
P2093
P2860
P1476
Exploiting cellular pathways to develop new treatment strategies for AML.
@en
P2093
Amir T Fathi
Judith E Karp
Steven Grant
P2860
P304
P356
10.1016/J.CTRV.2009.12.004
P577
2010-01-06T00:00:00Z