Genomic characterization of Imatinib resistance in CD34+ cell populations from chronic myeloid leukaemia patients.
Leuk Res, 2011/4;35(4):448-58.
Joha S[1], Dauphin V, Leprêtre F, Corm S, Nicolini FE, Roumier C, Nibourel O, Grardel N, Maguer-Satta V, Idziorek T, Figeac M, Laï JL, Quesnel B, Etienne G, Guilhot F, Lippert E, Preudhomme C, Roche-Lestienne C
Affiliations
PMID: 20684991DOI: 10.1016/j.leukres.2010.07.012
Impact factor: 3.715
Abstract
To ascertain genomic alterations associated with Imatinib resistance in chronic myeloid leukaemia, we performed high resolution genomic analysis of CD34(+) cells from 25 Imatinib (IM) resistant and 11 responders CML patients. Using patients' T-cells as reference, we found significant association between number of acquired cryptic copy number alterations (CNA) and disease phase (p=0.036) or loss of IM response for patients diagnosed in chronic phase (CP) (p=0.04). Recurrent cryptic losses were identified on chromosomes 7, 12 and 13. On chromosome 7, recurrent deletions of the IKZF1 locus were detected, for the first time, in 4 patients in CP.
MeSH terms
Antigens, CD34; Antineoplastic Agents; Benzamides; Chromosomes, Human, Pair 12; Chromosomes, Human, Pair 13; Chromosomes, Human, Pair 7; Comparative Genomic Hybridization; Drug Resistance, Neoplasm; Gene Dosage; Genes, abl; Genome-Wide Association Study; Humans; Ikaros Transcription Factor; Imatinib Mesylate; In Situ Hybridization, Fluorescence; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mutation; Piperazines; Pyrimidines; T-Lymphocytes
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