title: WT1 peptide vaccine induces reduction in minimal residual disease in an Imatinib-treated CML patient.
abstract: How to treat CML patients who are resistant to inhibitors of BCR-ABL tyrosine kinase such as Imatinib is a very important and urgent issue in clinical hematology. Here, we report a case of Imatinib-treated CML in which intradermally administered WT1 peptide vaccine elicited WT1-specific immune responses and the resultant reduction in the persistent residual disease in co-administration of Imatinib. BCR-ABL mRNA levels were being maintained under the detection limit for 8 months since week 77 of vaccination. No adverse effects except local erythema at the injection sites were observed. The tetramer assay revealed that the decrease in BCR-ABL mRNA levels was associated with the increase in frequency of WT1-specific cytotoxic T lymphocytes, notably effector-memory type of that, in the patient's peripheral blood. The case presented here indicates that WT1 peptide vaccine may become a safe and cure-oriented therapy for CML patients who have residual disease regardless of the treatment with Imatinib.
authors.affiliation: Department of Cancer Stem Cell Biology Respiratory Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Oji
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Oka
authors.forename: Sumiyuki
authors.initials: S
authors.lastname: Nishida
authors.forename: Akihiro
authors.initials: A
authors.lastname: Tsuboi
authors.forename: Manabu
authors.initials: M
authors.lastname: Kawakami
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Shirakata
authors.forename: Kazuko
authors.initials: K
authors.lastname: Takahashi
authors.forename: Ayako
authors.initials: A
authors.lastname: Murao
authors.forename: Hiroko
authors.initials: H
authors.lastname: Nakajima
authors.forename: Miwako
authors.initials: M
authors.lastname: Narita
authors.forename: Masuhiro
authors.initials: M
authors.lastname: Takahashi
authors.forename: Satoshi
authors.initials: S
authors.lastname: Morita
authors.forename: Junichi
authors.initials: J
authors.lastname: Sakamoto
authors.forename: Toshio
authors.initials: T
authors.lastname: Tanaka
authors.forename: Ichiro
authors.initials: I
authors.lastname: Kawase
authors.forename: Naoki
authors.initials: N
authors.lastname: Hosen
authors.forename: Haruo
authors.initials: H
authors.lastname: Sugiyama
mesh_terms: D000368:Aged; D000970:Antineoplastic Agents / Q000627:therapeutic use; D001549:Benzamides; D019496:Cancer Vaccines / Q000737:chemistry / Q000276:immunology / Q000627:therapeutic use*; D003131:Combined Modality Therapy; D019008:Drug Resistance, Neoplasm; D005260:Female; D016044:Fusion Proteins, bcr-abl / Q000037:antagonists & inhibitors; D006801:Humans; D000068877:Imatinib Mesylate; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000276:immunology / Q000473:pathology* / Q000628:therapy*; D018365:Neoplasm, Residual; D010879:Piperazines / Q000627:therapeutic use; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D011743:Pyrimidines / Q000627:therapeutic use; D012333:RNA, Messenger; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D022223:Vaccines, Subunit / Q000276:immunology / Q000627:therapeutic use; D025721:WT1 Proteins / Q000737:chemistry / Q000276:immunology*
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D019496:Cancer Vaccines; D010879:Piperazines; D011743:Pyrimidines; D012333:RNA, Messenger; D022223:Vaccines, Subunit; D025721:WT1 Proteins; D000068877:Imatinib Mesylate; D011505:Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl