BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.
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Chronic myeloid leukemia: reminiscences and dreamsAxitinib effectively inhibits BCR-ABL1(T315I) with a distinct binding conformationStructural insight into selectivity and resistance profiles of ROS1 tyrosine kinase inhibitors.Current developments in molecular monitoring in chronic myeloid leukemiaSecondary mutations as mediators of resistance to targeted therapy in leukemiaIdentification of small molecules that disrupt signaling between ABL and its positive regulator RIN1Molecular Determinants Underlying Binding Specificities of the ABL Kinase Inhibitors: Combining Alanine Scanning of Binding Hot Spots with Network Analysis of Residue Interactions and CoevolutionKnockout Serum Replacement Promotes Cell Survival by Preventing BIM from Inducing Mitochondrial Cytochrome C ReleaseInterferon-α Revisited: Individualized Treatment Management Eased the Selective Pressure of Tyrosine Kinase Inhibitors on BCR-ABL1 Mutations Resulting in a Molecular Response in High-Risk CML PatientsTreating adults with acute lymphocytic leukemia: new pharmacotherapy options.Targeting kinase signaling pathways with constrained peptide scaffolds.Clonal distribution of BCR-ABL1 mutations and splice isoforms by single-molecule long-read RNA sequencing.Janus kinase inhibition by ruxolitinib extends dasatinib- and dexamethasone-induced remissions in a mouse model of Ph+ ALL.How we will treat chronic myeloid leukemia in 2016.Erk Negative Feedback Control Enables Pre-B Cell Transformation and Represents a Therapeutic Target in Acute Lymphoblastic Leukemia.Discovery of a small molecule targeting SET-PP2A interaction to overcome BCR-ABLT315I mutation of chronic myeloid leukemia.Design of substrate-based BCR-ABL kinase inhibitors using the cyclotide scaffold.In chronic myeloid leukemia patients on second-line tyrosine kinase inhibitor therapy, deep sequencing of BCR-ABL1 at the time of warning may allow sensitive detection of emerging drug-resistant mutants.Ponatinib as first-line treatment for patients with chronic myeloid leukaemia in chronic phase: a phase 2 study.A coiled-coil mimetic intercepts BCR-ABL1 dimerization in native and kinase-mutant chronic myeloid leukemiaEfficacy of the polo-like kinase inhibitor rigosertib, alone or in combination with Abelson tyrosine kinase inhibitors, against break point cluster region-c-Abelson-positive leukemia cells.The impact of multiple low-level BCR-ABL1 mutations on response to ponatinib.Best Practices in Chronic Myeloid Leukemia Monitoring and ManagementExtreme mutational selectivity of axitinib limits its potential use as a targeted therapeutic for BCR-ABL1-positive leukemia.The chimeric ubiquitin ligase SH2-U-box inhibits the growth of imatinib-sensitive and resistant CML by targeting the native and T315I-mutant BCR-ABLA role for FOXO1 in BCR-ABL1-independent tyrosine kinase inhibitor resistance in chronic myeloid leukemiaOpportunities and challenges in combination gene cancer therapy.Depletion of γ-catenin by Histone Deacetylase Inhibition Confers Elimination of CML Stem Cells in Combination with ImatinibSensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatmentAurora A Kinase Inhibitor AKI603 Induces Cellular Senescence in Chronic Myeloid Leukemia Cells Harboring T315I Mutation.Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both Bcr/Abl-dependent and Bcr/Abl-independent mechanisms.Exploiting Temporal Collateral Sensitivity in Tumor Clonal Evolution.Molecular techniques for the personalised management of patients with chronic myeloid leukaemia.Individualizing kinase-targeted cancer therapy: the paradigm of chronic myeloid leukemia.Detecting and targetting oncogenic fusion proteins in the genomic era.Chronic myeloid leukemia: advances in understanding disease biology and mechanisms of resistance to tyrosine kinase inhibitors.The role of ponatinib in Philadelphia chromosome-positive acute lymphoblastic leukemia.Causes of resistance and treatment choices of second- and third-line treatment in chronic myelogenous leukemia patients.Management of advanced-phase chronic myeloid leukemia.Heat-shock protein 90 (Hsp90) as anticancer target for drug discovery: an ample computational perspective.
P2860
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P2860
BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
2014年论文
@zh
2014年论文
@zh-cn
name
BCR-ABL1 compound mutations co ...... chromosome-positive leukemia.
@en
type
label
BCR-ABL1 compound mutations co ...... chromosome-positive leukemia.
@en
prefLabel
BCR-ABL1 compound mutations co ...... chromosome-positive leukemia.
@en
P2093
P2860
P50
P1433
P1476
BCR-ABL1 compound mutations co ...... chromosome-positive leukemia.
@en
P2093
Anthony D Pomicter
Charles Chuah
Christopher A Eide
Elias J Jabbour
Franck E Nicolini
Francois-Xavier Mahon
Gabriel Etienne
Gert J Ossenkoppele
Gisela Barbany
Hanna J Khoury
P2860
P304
P356
10.1016/J.CCR.2014.07.006
P50
P577
2014-08-14T00:00:00Z