title: Discontinuation of imatinib therapy after achievement of complete molecular response in a Ph(+) CML patient treated while in long lasting complete cytogenetic remission (CCR) induced by interferon.
abstract: Imatinib has become the gold standard therapy for Ph(+) CML, as it induces complete cytogenetic remission (CCR) in 75-90% of patients in chronic phase (CP), and up to 40% of these patients obtain at least a 3 log reduction of BCR/ABL transcript [Kantarjian HM, Cortes JE, O'Brien S, Luthra R, Giles F, Verstovsek S, et al. Long-term survival benefit and improved complete cytogenetic and molecular response rates with imatinib mesylate in Philadelphia chromosome-positive chronic-phase chronic myeloid leukemia after failure of interferon-alpha. Blood. 2004;104:1979-1988]. However, it is not yet stated whether continued therapy is required to maintain this response or whether imatinib may be discontinued after confirmation of a prolonged complete molecular remission (CMR). We here report on a Ph(+) CML case in long lasting CCR following interferon-alpha treatment (IFN) which reached CMR with imatinib but soon relapsed at molecular level after this latter drug discontinuation; we considered the present observation also in the light of previously reported data.
authors.affiliation: Department of Cellular Biotechnologies and Hematology, University La Sapienza, Rome, Italy. breccia@bce.uniroma1.it
authors.forename: M
authors.initials: M
authors.lastname: Breccia
authors.forename: D
authors.initials: D
authors.lastname: Diverio
authors.forename: F
authors.initials: F
authors.lastname: Pane
authors.forename: M
authors.initials: M
authors.lastname: Nanni
authors.forename: E
authors.initials: E
authors.lastname: Russo
authors.forename: F
authors.initials: F
authors.lastname: Biondo
authors.forename: A
authors.initials: A
authors.lastname: Frustaci
authors.forename: F
authors.initials: F
authors.lastname: Gentilini
authors.forename: G
authors.initials: G
authors.lastname: Alimena
mesh_terms: D000230:Adenocarcinoma / Q000175:diagnosis / Q000628:therapy*; D001549:Benzamides; D020732:Cytogenetic Analysis / Q000379:methods*; D005500:Follow-Up Studies; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D020869:Gene Expression Profiling; D015973:Gene Expression Regulation, Leukemic; D006801:Humans; D000068877:Imatinib Mesylate; D016898:Interferon-alpha / Q000009:adverse effects* / Q000627:therapeutic use; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000175:diagnosis / Q000188:drug therapy* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D016609:Neoplasms, Second Primary / Q000175:diagnosis / Q000628:therapy*; D010879:Piperazines; D011743:Pyrimidines; D012004:Rectal Neoplasms / Q000175:diagnosis / Q000628:therapy*; D012008:Recurrence; D012074:Remission Induction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014158:Transcription, Genetic; D016896:Treatment Outcome
chemical_list: D001549:Benzamides; D016898:Interferon-alpha; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate; D016044:Fusion Proteins, bcr-abl