Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment.
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Expression of the leukemic prognostic marker CD7 is linked to epigenetic modifications in chronic myeloid leukemiaImplications of genetic heterogeneity in cancerThe T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATPTwo different point mutations in ABL gene ATP-binding domain conferring primary imatinib resistance in a chronic myeloid leukemia (CML) patient: A case reportNew Developments in Chronic Myeloid Leukemia: Implications for TherapyThe influence of subclonal resistance mutations on targeted cancer therapyGenetic instability in the tumor microenvironment: a new look at an old neighborCancer heterogeneity--a multifaceted viewKinase-independent mechanisms of resistance of leukemia stem cells to tyrosine kinase inhibitorsTumour heterogeneity and the evolution of polyclonal drug resistanceClonal evolution in hematological malignancies and therapeutic implicationsSciClone: inferring clonal architecture and tracking the spatial and temporal patterns of tumor evolutionDissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling.Ponatinib is a pan-BCR-ABL kinase inhibitor: MD simulations and SIE studyIntratumor Heterogeneity and Branched Evolution Revealed by Multiregion SequencingImproving anticancer drug development begins with cell culture: misinformation perpetrated by the misuse of cytotoxicity assaysSecondary mutations as mediators of resistance to targeted therapy in leukemiaCauses and consequences of microRNA dysregulation in cancerSensitive 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 eraInhibition of Aurora kinase B is important for biologic activity of the dual inhibitors of BCR-ABL and Aurora kinases R763/AS703569 and PHA-739358 in BCR-ABL transformed cellsDose-Dependent Mutation Rates Determine Optimum Erlotinib Dosing Strategies for EGFR Mutant Non-Small Cell Lung Cancer PatientsComparative chemical array screening for p38γ/δ MAPK inhibitors using a single gatekeeper residue difference between p38α/β and p38γ/δThe cancer genomeEvolution of BCR/ABL gene mutation in CML is time dependent and dependent on the pressure exerted by tyrosine kinase inhibitor.Eradication of chronic myeloid leukemia stem cells: a novel mathematical model predicts no therapeutic benefit of adding G-CSF to imatinibImatinib mesylate and nilotinib (AMN107) exhibit high-affinity interaction with ABCG2 on primitive hematopoietic stem cells.Development and validation of a sensitive assay for the quantification of imatinib using LC/LC-MS/MS in human whole blood and cell culture.Cellular and genetic diversity in the progression of in situ human breast carcinomas to an invasive phenotype.Tumor heterogeneity: causes and consequencesLimited impact of intratumour heterogeneity on molecular risk assignment in endometrial cancer.Patan hospital experience in treating philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukemia patients with gleevec (imatinib mesylate); the first generation specific tyrosine kinase inhibitor.Structural and mechanistic underpinnings of the differential drug sensitivity of EGFR mutations in non-small cell lung cancer.Zebrafish as a model to assess cancer heterogeneity, progression and relapse.Molecular mechanisms of acquired resistance to tyrosine kinase targeted therapyNovel pyrrolo-1,5-benzoxazepine compounds display significant activity against resistant chronic myeloid leukaemia cells in vitro, in ex vivo patient samples and in vivo.Oncogenic activity of epidermal growth factor receptor kinase mutant alleles is enhanced by the T790M drug resistance mutationSecondary somatic mutations restoring BRCA1/2 predict chemotherapy resistance in hereditary ovarian carcinomas.Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC.Practical management of patients with chronic myeloid leukemia who develop tyrosine kinase inhibitor-resistant BCR-ABL1 mutations.Relapse of acute promyelocytic leukemia with PML-RARalpha mutant subclones independent of proximate all-trans retinoic acid selection pressure
P2860
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P2860
Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
@wuu
2002年学术文章
@zh-cn
2002年学术文章
@zh-hans
2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
@yue
2002年學術文章
@zh
2002年學術文章
@zh-hant
name
Several types of mutations of ...... ist to the onset of treatment.
@en
Several types of mutations of ...... ist to the onset of treatment.
@nl
type
label
Several types of mutations of ...... ist to the onset of treatment.
@en
Several types of mutations of ...... ist to the onset of treatment.
@nl
prefLabel
Several types of mutations of ...... ist to the onset of treatment.
@en
Several types of mutations of ...... ist to the onset of treatment.
@nl
P2093
P50
P921
P1433
P1476
Several types of mutations of ...... xist to the onset of treatment
@en
P2093
Jean-Luc Laï
Nathalie Philippe
Pierre Fenaux
Thierry Facon
Valerie Soenen-Cornu
P304
P356
10.1182/BLOOD.V100.3.1014
P407
P577
2002-08-01T00:00:00Z