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Hart From the Haematology/Immunology Research Group, Christchurch Hospital, Christchurch, New Zealand. Chronic myeloid leukemia (CML) is characterized by a specific translocation of the c-abl oncogene on chromosome 9 to the break point cluster region (bcr) on chromosome 22, t(9; 22) (q34; q11). This translocation results in the expression of a 210-kD bcr-abl protein fusion gene product. The juxtaposition of the bcr and abl genes produces a novel junctional amino acid sequence, which may be presented by antigen-presenting cells and recognized specifically by human T lymphocytes. We have generated a CD4+ T lymphocyte line (NG-1) which recognizes the peptide epitope (GFKQSSKALQR) in association with HLA-DR1*0101-02. A comparison of antigen-presenting cells showed that CMRF-44+ blood dendritic cell presented a 12mer b3a2 peptide effectively. The b3a2 peptide was able to generate specific primary T-lymphocyte responses in other HLA-DR1 donors. We also show that bcr-abl, b3a2 peptide-specific T-lymphocyte lines proliferate in response to bcr-abl b3a2 containing cell lysates (K562 or CML PBMC derived) but not control (including b2a2 CML PBMC) lysates. Blood, Vol. 90 No. 1 (July 1), 1997: pp. 290-297 © 1997 by The American Society of Hematology. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. J. Barrett Leukemia Vaccines to Boost the Graft-versus-Leukemia Effect after Allogeneic Stem Cell Transplantation ASCO Educational Book, January 1, 2008; 2008(1): 330 - 333. [Abstract] [Full Text] [PDF] Y.-X. Chen, K. Man, G. S. Ling, Y. Chen, B.-S. Sun, Q. Cheng, O. H. Wong, C.-K. Lo, I. O.-L. Ng, L. C. Chan, et al. A Crucial Role for Dendritic Cell (DC) IL-10 in Inhibiting Successful DC-Based Immunotherapy: Superior Antitumor Immunity against Hepatocellular Carcinoma Evoked by DC Devoid of IL-10 J. Immunol., November 1, 2007; 179(9): 6009 - 6015. 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