Abstract
Preferentially expressed antigen of melanoma (PRAME) was first isolated using cDNA expression cloning techniques as a gene encoding a human melanoma antigen recognized by melanoma reactive cytotoxic T-cells (CTL) (1). This gene codes for a 509-amino-acid protein whose function has not yet been identified. PRAME is expressed in various types of cancer, including melanoma (97%), sarcoma (80%), small-cell lung cancer (70%), renal cell carcinoma (40%), and head and neck cancer (29%) (1,2). PRAME is also found in limited normal tissues, including endometrium and adrenal glands, and found highly expressed in testis.
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References
Ikeda, H., Lethe, B., Lehmann, F., et al. (1997) Characterization of an antigen that is recognized on a melanoma showing partial HLA loss by CTL expressing an NK inhibitory receptor. Immunity 6, 199–208.
Neumann, E., Engelsberg, A., Decker, J., et al. (1998) Heterogeneous expression of the tumor-associated antigens RAGE-1, PRAME, and glycoprotein 75 in human renal cell carcinoma: candidates for T-cell-based immunotherapies? Cancer Res. 58, 4090–4095.
Matsushita, M., Ikeda, H., Kizaki, M., et al. (2001) Quantitative monitoring of the PRAME gene for the detection of minimal residual disease in leukemia. Br. J. Haematol. 112, 916–926.
van Baren, N., Brasseur, F., Godelaine, D., et al. (1999) Genes encoding tumor-specific antigens are expressed in human myeloma cells. Blood 94, 1156–1164.
Kessler, J. H., Beekman, N. J., Bres-Vloemans, S. A., et al. (2001) Efficient identification of novel HLA-A(*)0201-presented cytotoxic T lymphocyte epitopes in the widely expressed tumor antigen PRAME by proteasome-mediated digestion analysis. J. Exp. Med. 193, 73–88.
Lin, F., van Rhee, F., Goldman, J. M., et al. (1996) Kinetics of increasing BCR-ABL transcript numbers in chronic myeloid leukemia patients who relapse after bone marrow transplantation. Blood 87, 4473–4478.
Lion, T., Gaiger, A., Henn, T., et al. (1995) Use of quantitative polymerase chain reaction to monitor residual disease in chronic myelogenous leukemia during treatment with interferon. Leukemia 9, 1353–1360.
Muto, A., Mori, S., Matsushita, H., et al. (1996) Serial quantification of minimal residual disease of t(8;21) acute myelogenous leukemia with RT-competitive PCR assay. Br. J. Haematol. 95, 85–94.
Roberts, W. M., Estrov, Z., Ouspenskaia, M. V., et al. (1997) Measurement of residual leukemia during remission in childhood acute lymphoblastic leukemia. N. Engl. J. Med. 336, 317–323.
Seriu, T., Hansen-Hagge, T. E., Erz, D. H., et al. (1995) Improved detection of minimal residual leukemia through modifications of polymerase chain reaction analyses based on clonospecific T cell receptor junctions. Leukemia 9, 316–320.
Inoue, K., Ogawa, H., Yamagami, T., et al. (1996) Long-term follow-up of minimal residual disease in leukemia patients by monitoring WT1 (Wilms tumor gene) expression levels. Blood 88, 2267–2278.
Mensink, E., van de Locht, A., Schattenberg, A., et al. (1998) Quantitation of minimal residual disease in Philadelphia chromosome positive chronic myeloid leukemia patients using real-time quantitative RT-PCR. Br. J. Haematol. 102, 768–774.
Dolken, G. (2001) Detection of minimal residual disease. Adv. Cancer Res. 82, 133–185.
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© 2004 Humana Press Inc., Totowa, NJ
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Matsushita, M., Yamazaki, R., Kawakami, Y. (2004). Quantitative Analysis of PRAME for Detection of Minimal Residual Disease in Leukemia. In: Roulston, J.E., Bartlett, J.M.S. (eds) Molecular Diagnosis of Cancer. Methods in Molecular Medicine, vol 97. Humana Press. https://doi.org/10.1385/1-59259-760-2:267
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DOI: https://doi.org/10.1385/1-59259-760-2:267
Publisher Name: Humana Press
Print ISBN: 978-1-58829-160-8
Online ISBN: 978-1-59259-760-4
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