title: Results of imatinib mesylate therapy in chronic myelogenous leukaemia with variant Philadelphia chromosome.
abstract: Five to 10 per cent of patients with Philadelphia chromosome (Ph)-positive chronic myelogenous leukaemia (CML) have variant translocations involving chromosomes other than 9 and 22. We investigated the characteristics and outcome of patients with variant translocations treated with imatinib. Among 721 patients, 44 (6%) had variant translocations, involving one (n = 39) or two (n = 4) additional chromosomes. Nineteen patients (44%) were in chronic (12 previously untreated), 24 (55%) in accelerated and one (2%) in blastic phase. A major cytogenetic response was achieved in 14 (74%) patients treated in chronic phase and in 14 (58%) treated in accelerated phase. Six of 13 (46%) evaluable patients had deletion of derivative chromosome 9, and there was a trend for a lower response rate in these patients. We compared the 43 patients in chronic or accelerated phase to 678 patients with classic Ph treated with imatinib. The only significant difference in clinical characteristics was a higher frequency of accelerated phase among those with variant translocations (56%) compared with those with classic translocations (38%). No differences in outcome were evident. In a multivariate analysis, variant Ph translocations had no impact in response rate, overall survival or duration of response. We conclude that patients with variant Ph translocations have a similar prognosis to those with classic Ph translocations when treated with imatinib.
authors.affiliation: Department of Leukaemia, M D Anderson Cancer Center, The University of Texas, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
authors.forename: Maha M T
authors.initials: MM
authors.lastname: El-Zimaity
authors.forename: Hagop
authors.initials: H
authors.lastname: Kantarjian
authors.forename: Moshe
authors.initials: M
authors.lastname: Talpaz
authors.forename: Susan
authors.initials: S
authors.lastname: O'Brien
authors.forename: Francis
authors.initials: F
authors.lastname: Giles
authors.forename: Guillermo
authors.initials: G
authors.lastname: Garcia-Manero
authors.forename: Srdan
authors.initials: S
authors.lastname: Verstovsek
authors.forename: Deborah
authors.initials: D
authors.lastname: Thomas
authors.forename: Alessandra
authors.initials: A
authors.lastname: Ferrajoli
authors.forename: Kimberly
authors.initials: K
authors.lastname: Hayes
authors.forename: B
authors.initials: B
authors.lastname: Nebiyou Bekele
authors.forename: Xian
authors.initials: X
authors.lastname: Zhou
authors.forename: Mary B
authors.initials: MB
authors.lastname: Rios
authors.forename: Armand B
authors.initials: AB
authors.lastname: Glassman
authors.forename: Jorge E
authors.initials: JE
authors.lastname: Cortes
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001549:Benzamides; D002877:Chromosomes, Human / Q000235:genetics; D005500:Follow-Up Studies; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000188:drug therapy* / Q000235:genetics; D008875:Middle Aged; D010879:Piperazines / Q000627:therapeutic use*; D011743:Pyrimidines / Q000627:therapeutic use*; D014178:Translocation, Genetic; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate