The Bcr-Abl mutations T315I and Y253H do not confer a growth advantage in the absence of imatinib.
about
Chemotherapeutic agents circumvent emergence of dasatinib-resistant BCR-ABL kinase mutations in a precise mouse model of Philadelphia chromosome-positive acute lymphoblastic leukemiaCks1 is required for tumor cell proliferation but not sufficient to induce hematopoietic malignanciesDynamics of mutant BCR-ABL-positive clones after cessation of tyrosine kinase inhibitor therapy.Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.Janus kinase inhibition by ruxolitinib extends dasatinib- and dexamethasone-induced remissions in a mouse model of Ph+ ALL.GP130 activation induces myeloma and collaborates with MYC.Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib.Impact of FLT3-ITD location on sensitivity to TKI-therapy in vitro and in vivo.Laboratory practice guidelines for detecting and reporting BCR-ABL drug resistance mutations in chronic myelogenous leukemia and acute lymphoblastic leukemia: a report of the Association for Molecular Pathology.Targeting survival cascades induced by activation of Ras/Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways for effective leukemia therapy.The role of mitochondrial DNA damage and repair in the resistance of BCR/ABL-expressing cells to tyrosine kinase inhibitorsAurora A Kinase Inhibitor AKI603 Induces Cellular Senescence in Chronic Myeloid Leukemia Cells Harboring T315I Mutation.Preclinical approaches in chronic myeloid leukemia: from cells to systemsAdvances in treatment of chronic myeloid leukemia with tyrosine kinase inhibitors: the evolving role of Bcr-Abl mutations and mutational analysis.Grb10 is involved in BCR-ABL-positive leukemia in mice.Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.BCR-ABL mutants spread resistance to non-mutated cells through a paracrine mechanism.In vivo hematopoietic Myc activation directs a transcriptional signature in endothelial cells within the bone marrow microenvironment.Quantifying mutated and unmutated BCR-ABL transcripts confirms suitability of direct sequencing sensitivity in mutation analysis of patients with chronic myeloid leukemia with secondary resistance to tyrosine kinase inhibitors, regardless of ratio vNovel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-gamma1-driven activation of mTOR/p70S6-kinase pathway.Cks1 is a critical regulator of hematopoietic stem cell quiescence and cycling, operating upstream of Cdk inhibitors.
P2860
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P2860
The Bcr-Abl mutations T315I and Y253H do not confer a growth advantage in the absence of imatinib.
description
2006 nî lūn-bûn
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2006年の論文
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2006年論文
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2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
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2006年論文
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2006年论文
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2006年论文
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2006年论文
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name
The Bcr-Abl mutations T315I an ...... ge in the absence of imatinib.
@en
The Bcr-Abl mutations T315I an ...... ge in the absence of imatinib.
@nl
type
label
The Bcr-Abl mutations T315I an ...... ge in the absence of imatinib.
@en
The Bcr-Abl mutations T315I an ...... ge in the absence of imatinib.
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prefLabel
The Bcr-Abl mutations T315I an ...... ge in the absence of imatinib.
@en
The Bcr-Abl mutations T315I an ...... ge in the absence of imatinib.
@nl
P2093
P2860
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The Bcr-Abl mutations T315I an ...... age in the absence of imatinib
@en
P2093
Grundler R
von Bubnoff N
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P304
P356
10.1038/SJ.LEU.2404151
P577
2006-04-01T00:00:00Z
P5875
P6179
1038692361