High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.
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New Developments in Chronic Myeloid Leukemia: Implications for TherapyThe influence of subclonal resistance mutations on targeted cancer therapyBiomarkers for determining the prognosis in chronic myelogenous leukemiaResistance to tyrosine kinase inhibition therapy for chronic myelogenous leukemia: a clinical perspective and emerging treatment optionsALK kinase domain mutations in primary anaplastic large cell lymphoma: consequences on NPM-ALK activity and sensitivity to tyrosine kinase inhibitorsSecondary mutations as mediators of resistance to targeted therapy in leukemiaRandom mutagenesis reveals residues of JAK2 critical in evading inhibition by a tyrosine kinase inhibitorSensitive detection of pre-existing BCR-ABL kinase domain mutations in CD34+ cells of newly diagnosed chronic-phase chronic myeloid leukemia patients is associated with imatinib resistance: implications in the post-imatinib eraDrug resistance missense mutations in cancer are subject to evolutionary constraintsBCR-ABL SH3-SH2 domain mutations in chronic myeloid leukemia patients on imatinib.BCR-ABL1 kinase inhibits uracil DNA glycosylase UNG2 to enhance oxidative DNA damage and stimulate genomic instability.Impact of additional chromosomal aberrations and BCR-ABL kinase domain mutations on the response to nilotinib in Philadelphia chromosome-positive chronic myeloid leukemia.A TCR-mimic antibody to WT1 bypasses tyrosine kinase inhibitor resistance in human BCR-ABL+ leukemiasPredictive value of in vitro mutation data to guide second-generation tyrosine kinase inhibitor selection: ready for prime time?Practical advice for determining the role of BCR-ABL mutations in guiding tyrosine kinase inhibitor therapy in patients with chronic myeloid leukemia.Chronic myeloid leukemia: mechanisms of blastic transformationMechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia.Using functional genomics to overcome therapeutic resistance in hematological malignancies.Relapse of acute promyelocytic leukemia with PML-RARalpha mutant subclones independent of proximate all-trans retinoic acid selection pressureDynamics of mutant BCR-ABL-positive clones after cessation of tyrosine kinase inhibitor therapy.Philadelphia-positive acute lymphoblastic leukemia patients already harbor BCR-ABL kinase domain mutations at low levels at the time of diagnosisIGF-IR determines the fates of BCR/ABL leukemia.Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.Moving on up: Second-Line Agents as Initial Treatment for Newly-Diagnosed Patients with Chronic Phase CML.Coexistence of P190 and P210 BCR/ABL transcripts in chronic myeloid leukemia blast crisis resistant to imatinib.Chronic myeloid leukemia: mechanisms of resistance and treatment.Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: review and recommendations for harmonizing current methodology for detecting BCR-ABL transcripts and kinase domain mutations and for expressing results.BCR-ABL1 mutation development during first-line treatment with dasatinib or imatinib for chronic myeloid leukemia in chronic phase.Target for cancer therapy: proliferating cells or stem cells.Anticipating clinical resistance to target-directed agents : the BCR-ABL paradigm.The quantitative level of T315I mutated BCR-ABL predicts for major molecular response to second-line nilotinib or dasatinib treatment in patients with chronic myeloid leukemia.Therapeutic options for chronic myeloid leukemia: focus on imatinib (Glivec, Gleevectrade mark).Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells.Quantitative Analysis of Mutant Subclones in Chronic Myeloid Leukemia: Comparison of Different Methodological Approaches.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.Epidemiologic study on survival of chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia patients with BCR-ABL T315I mutation.Emerging therapeutic strategies for targeting chronic myeloid leukemia stem cellsBCR/ABL, DNA damage and DNA repair: implications for new treatment concepts.Pharmacologic markers and predictors of responses to imatinib therapy in patients with chronic myeloid leukemia.Suboptimal response to or failure of imatinib treatment for chronic myeloid leukemia: what is the optimal strategy?
P2860
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P2860
High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh-hant
name
High-sensitivity detection of ...... n but not response to therapy.
@en
High-sensitivity detection of ...... n but not response to therapy.
@nl
type
label
High-sensitivity detection of ...... n but not response to therapy.
@en
High-sensitivity detection of ...... n but not response to therapy.
@nl
prefLabel
High-sensitivity detection of ...... n but not response to therapy.
@en
High-sensitivity detection of ...... n but not response to therapy.
@nl
P2093
P1433
P1476
High-sensitivity detection of ...... n but not response to therapy.
@en
P2093
Byung Park
Dietger Niederwieser
Eric P Stoffregen
Ines Kovacs
Lucy Crossman
Michael W Deininger
Sandra Otto
Shadmehr Demehri
Shannon McWeeney
Stephanie G Willis
P304
P356
10.1182/BLOOD-2005-03-1036
P407
P577
2005-05-24T00:00:00Z