[Immunological evaluation for CML and its possibility for an immunotherapy].
Chronic myelogenous leukemia (CML) is associated with the Ph1 chromosome translocation, which produces a chimeric tyrosine-specific kinase gene, the product of the fusion of the BCR gene and the ABL gene. The immune system has long been implicated in the control of CML. We found oligoclonal T cell responses in treated patients with IFN-alpha or leukemic dendritic cells. Also other groups treated chronic phase CML (CP-CML) patients with various leukemic antigen peptides, resulted in apparent immune response and clinical response. Imatinib mesylate is currently used as the first line therapy for CP-CML patients. Although it selectively targets the ABL portion of BCR-ABL protein as a reversible tyrosine kinase inhibitor, it cannot kill the leukemic stem cells of CML. To find a possibility to enhance the immunity in imatinib-treated CML patients by combining it with immunotherapy, we summarized the immune response of innate and adaptive immunity in CML. Development of such immunotherapeutic strategies would be a promising approach to treat the imatinib-treated CML-CP patients.
Fujii
Shin-ichiro
S
Research Unit for Cellular Immunotherapy, Research Center for Allergy and Immunology, RIKEN.
D000951:Antigens, Neoplasm / Q000276:immunology; D000970:Antineoplastic Agents / Q000627:therapeutic use; D001549:Benzamides; D003713:Dendritic Cells / Q000502:physiology; D016503:Drug Delivery Systems; D006801:Humans; D000068877:Imatinib Mesylate; D007167:Immunotherapy / Q000379:methods; D007694:Killer Cells, Natural / Q000502:physiology; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000276:immunology* / Q000628:therapy*; D010879:Piperazines / Q000627:therapeutic use; D011743:Pyrimidines / Q000627:therapeutic use
D000951:Antigens, Neoplasm; D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D011743:Pyrimidines; D000068877:Imatinib Mesylate