MCL-1 and BCL-xL-dependent resistance to the BCL-2 inhibitor ABT-199 can be overcome by preventing PI3K/AKT/mTOR activation in lymphoid malignancies.
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TCL1 transgenic mouse model as a tool for the study of therapeutic targets and microenvironment in human B-cell chronic lymphocytic leukemiaRegulation of Bim in Health and DiseaseKnow the enemy as well as the weapons in hand: the aberrant death pathways and therapeutic agents in chronic lymphocytic leukemiaTargeted therapies in CLL: mechanisms of resistance and strategies for managementThe potential of venetoclax (ABT-199) in chronic lymphocytic leukemiaThe biology behind B-cell lymphoma 2 as a target in chronic lymphocytic leukemiaExploitation of the Apoptosis-Primed State of MYCN-Amplified Neuroblastoma to Develop a Potent and Specific Targeted Therapy CombinationBcl-2high mantle cell lymphoma cells are sensitized to acadesine with ABT-199.Phase Ib trial of the PI3K/mTOR inhibitor voxtalisib (SAR245409) in combination with chemoimmunotherapy in patients with relapsed or refractory B-cell malignancies.PI3Kδ inhibition elicits anti-leukemic effects through Bim-dependent apoptosisPharmacological and Protein Profiling Suggests Venetoclax (ABT-199) as Optimal Partner with Ibrutinib in Chronic Lymphocytic LeukemiaCyclin E/Cdk2-dependent phosphorylation of Mcl-1 determines its stability and cellular sensitivity to BH3 mimeticsmiR-377-dependent BCL-xL regulation drives chemotherapeutic resistance in B-cell lymphoid malignancies.MCL-1-independent mechanisms of synergy between dual PI3K/mTOR and BCL-2 inhibition in diffuse large B cell lymphoma.Attacking cancer's Achilles heel: antagonism of anti-apoptotic BCL-2 family membersCombination of galectin inhibitor GCS-100 and BH3 mimetics eliminates both p53 wild type and p53 null AML cells.Targeting MCL-1/BCL-XL Forestalls the Acquisition of Resistance to ABT-199 in Acute Myeloid Leukemia.Defining specificity and on-target activity of BH3-mimetics using engineered B-ALL cell lines.Idelalisib therapy of indolent B-cell malignancies: chronic lymphocytic leukemia and small lymphocytic or follicular lymphomasIdelalisib for the treatment of non-Hodgkin lymphoma.A New G-Quadruplex with Hairpin Loop Immediately Upstream of the Human BCL2 P1 Promoter Modulates Transcription.Synergistic anti-leukemic interactions between ABT-199 and panobinostat in acute myeloid leukemia ex vivoHigh efficacy of the BCL-2 inhibitor ABT199 (venetoclax) in BCL-2 high-expressing neuroblastoma cell lines and xenografts and rational for combination with MCL-1 inhibition.Atg5-dependent autophagy contributes to the development of acute myeloid leukemia in an MLL-AF9-driven mouse model.Improving nelarabine efficacy in T cell acute lymphoblastic leukemia by targeting aberrant PI3K/AKT/mTOR signaling pathway.Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells.Down-Regulation of MicroRNA-133b Suppresses Apoptosis of Lens Epithelial Cell by Up-Regulating BCL2L2 in Age-Related Cataracts.Identification of myeloproliferative neoplasm drug agents via predictive simulation modeling: assessing responsiveness with micro-environment derived cytokines.PNT2258, a novel deoxyribonucleic acid inhibitor, induces cell cycle arrest and apoptosis via a distinct mechanism of action: a new class of drug for non-Hodgkin's lymphoma.MLL-AF4 binds directly to a BCL-2 specific enhancer and modulates H3K27 acetylationDevelopment of venetoclax for therapy of lymphoid malignancies.Mcl-1 expression and JNK activation induces a threshold for apoptosis in Bcl-xL-overexpressing hematopoietic cells.Ibrutinib in B lymphoid malignancies.Non-Hodgkin and Hodgkin lymphomas select for overexpression of BCLW.Rational combination strategies to enhance venetoclax activity and overcome resistance in hematologic malignancies.ABT-199 (venetoclax) and BCL-2 inhibitors in clinical development.Learning from the failures of drug discovery in B-cell non-Hodgkin lymphomas and perspectives for the future: chronic lymphocytic leukemia and diffuse large B-cell lymphoma as two ends of a spectrum in drug development.Targeting mTOR for the treatment of B cell malignancies.Targeting BET proteins improves the therapeutic efficacy of BCL-2 inhibition in T-cell acute lymphoblastic leukemia.The Development and Current Use of BCL-2 Inhibitors for the Treatment of Chronic Lymphocytic Leukemia.
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P2860
MCL-1 and BCL-xL-dependent resistance to the BCL-2 inhibitor ABT-199 can be overcome by preventing PI3K/AKT/mTOR activation in lymphoid malignancies.
description
2015 nî lūn-bûn
@nan
2015 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2015 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
name
MCL-1 and BCL-xL-dependent res ...... tion in lymphoid malignancies.
@ast
MCL-1 and BCL-xL-dependent res ...... tion in lymphoid malignancies.
@en
type
label
MCL-1 and BCL-xL-dependent res ...... tion in lymphoid malignancies.
@ast
MCL-1 and BCL-xL-dependent res ...... tion in lymphoid malignancies.
@en
prefLabel
MCL-1 and BCL-xL-dependent res ...... tion in lymphoid malignancies.
@ast
MCL-1 and BCL-xL-dependent res ...... tion in lymphoid malignancies.
@en
P2093
P2860
P50
P356
P1476
MCL-1 and BCL-xL-dependent res ...... tion in lymphoid malignancies.
@en
P2093
P2860
P2888
P356
10.1038/CDDIS.2014.525
P577
2015-01-15T00:00:00Z
P5875
P6179
1017708540