Dynamics of mutant BCR-ABL-positive clones after cessation of tyrosine kinase inhibitor therapy.
about
Dynamics of resistance development to imatinib under increasing selection pressure: a combination of mathematical models and in vitro dataPatients with Philadelphia-positive leukemia with BCR-ABL kinase mutations before allogeneic transplantation predominantly relapse with the same mutation.Characterizing of Four Common BCR-ABL Kinase Domain Mutations (T315I, Y253H, M351T and E255K) in Iranian Chronic Myelogenous Leukemia Patients With Imatinib ResistanceOptimization of dosing for EGFR-mutant non-small cell lung cancer with evolutionary cancer modeling.The impact of multiple low-level BCR-ABL1 mutations on response to ponatinib.Quantitative Analysis of Mutant Subclones in Chronic Myeloid Leukemia: Comparison of Different Methodological Approaches.BCR-ABL1 kinase domain mutations may persist at very low levels for many years and lead to subsequent TKI resistanceThe BCR-ABLT315I mutation compromises survival in chronic phase chronic myelogenous leukemia patients resistant to tyrosine kinase inhibitors, in a matched pair analysisOxidative stress downstream of mTORC1 but not AKT causes a proliferative defect in cancer cells resistant to PI3K inhibitionSelection of therapy: rational decisions based on molecular events.Advances in treatment of chronic myeloid leukemia with tyrosine kinase inhibitors: the evolving role of Bcr-Abl mutations and mutational analysis.Imatinib resistance: a review of alternative inhibitors in chronic myeloid leukemia.Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients.Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.Novel BCR-ABL1 fusion and leukemic mutations of SETBP1, PAX5, and TP53 detected by next generation sequencing in chronic myeloid leukemia.Return of the malingering mutants.Mutant BCR-ABL clones in chronic myeloid leukemia.Prospective analysis of low-level BCR-ABL1 T315I mutation in CD34 + cells of patients with de novo chronic myeloid leukemia.Imatinib and beyond--targeting activated tyrosine kinases in myeloproliferative disorders.Dynamics of the emergence of dasatinib and nilotinib resistance in imatinib-resistant CML patients
P2860
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P2860
Dynamics of mutant BCR-ABL-positive clones after cessation of tyrosine kinase inhibitor therapy.
description
2010 nî lūn-bûn
@nan
2010 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年学术文章
@wuu
2010年学术文章
@zh-cn
2010年学术文章
@zh-hans
2010年学术文章
@zh-my
2010年学术文章
@zh-sg
2010年學術文章
@yue
name
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@ast
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@en
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@nl
type
label
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@ast
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@en
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@nl
prefLabel
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@ast
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@en
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@nl
P2093
P2860
P1433
P1476
Dynamics of mutant BCR-ABL-pos ...... sine kinase inhibitor therapy.
@en
P2093
Armin Leitner
Benjamin Hanfstein
Christian Lorentz
Martin C Müller
Rüdiger Hehlmann
Sebastian Kreil
Thomas Ernst
Thomas Schenk
Uwe Schwindel
P2860
P304
P356
10.3324/HAEMATOL.2010.030999
P577
2010-12-06T00:00:00Z