title: [Treatment-free molecular remission achieved by combination therapy with imatinib and IFNα in CML with BIM deletion polymorphism relapsed after stop imatinib].
abstract: A 51-year-old man with chronic myeloid leukemia (CML) was treated with imatinib (IM). After 24 months of treatment, he achieved a complete molecular response (CMR), which he sustained for 3 years. However, 4 months after discontinuing IM treatment, the CML relapsed. The patient was treated again with IM and achieved CMR. A combination of IM and interferon-α (IFNα) was administered for the following year, and then discontinued. The patient has since sustained CMR without therapy for 24 months, to date. This patient was found to have a BCL2L11 (BIM) deletion polymorphism. CML patients with a BIM deletion polymorphism show a low response to IM, and we infer that the BIM deletion polymorphism is a negative factor for discontinuation of IM. IFNα treatment is expected to prevent relapse during immunological surveillance. Therefore, the combination of IM and IFNα might be a feasible approach for CML patients who experience difficulty with IM discontinuation.
authors.affiliation: Department of Hematology, Tokyo Medical University.
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Katagiri
authors.forename: Tetsuzo
authors.initials: T
authors.lastname: Tauchi
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Umezu
authors.forename: Yuu
authors.initials: Y
authors.lastname: Saito
authors.forename: Tamiko
authors.initials: T
authors.lastname: Suguro
authors.forename: Michiyo
authors.initials: M
authors.lastname: Asano
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Yoshizawa
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Kitahara
authors.forename: Daigo
authors.initials: D
authors.lastname: Akahane
authors.forename: Yuko
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Fujimoto
authors.forename: Seiichi
authors.initials: S
authors.lastname: Okabe
authors.forename: Moritaka
authors.initials: M
authors.lastname: Gotoh
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Ito
authors.forename: Junko H
authors.initials: JH
authors.lastname: Ohyashiki
authors.forename: Kazuma
authors.initials: K
authors.lastname: Ohyashiki
mesh_terms: D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D051017:Apoptosis Regulatory Proteins / Q000235:genetics*; D000072224:Bcl-2-Like Protein 11; D001549:Benzamides / Q000008:administration & dosage; D003131:Combined Modality Therapy; D017353:Gene Deletion; D006801:Humans; D000068877:Imatinib Mesylate; D016898:Interferon-alpha / Q000008:administration & dosage; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000175:diagnosis / Q000188:drug therapy*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D008875:Middle Aged; D010879:Piperazines / Q000008:administration & dosage; D011110:Polymorphism, Genetic; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D011743:Pyrimidines / Q000008:administration & dosage; D012008:Recurrence; D012074:Remission Induction / Q000379:methods
chemical_list: D051017:Apoptosis Regulatory Proteins; C000606775:BCL2L11 protein, human; D000072224:Bcl-2-Like Protein 11; D001549:Benzamides; D016898:Interferon-alpha; D008565:Membrane Proteins; D010879:Piperazines; D011518:Proto-Oncogene Proteins; D011743:Pyrimidines; D000068877:Imatinib Mesylate