[1] Ikeda H, Lethé B, Lehmann F, et al. Characterization of an antigen that is recognized on a melanoma showing partial HLA loss by CTL expressing an NK inhibitory receptor[J]. Immunity,1997, 6(2): 199-208.
[2] Schenk T, Stengel S, Goellner S, et al. Hypomethylation of PRAME is responsible for its aberrant overexpression in human malignancies[J]. Genes Chromosomes Cancer, 2007, 46(9): 796-804.
[3] Epping MT, Wang L, Edel MJ, et al. The human tumor antigen PRAME is a dominant repressor of retinoic acid receptor signaling[J]. Cell, 2005, 122(6): 835-847.
[4] Matsushita M, Ikeda H, Kizaki M, et al. Quantitative monitoring of the PRAME gene for the detection of minimal residual disease in leukaemia[J]. Br J Haematol, 2001, 112(4): 916-926.
[5] ProtoSiqueira R, FigueiredoPontes LL, Panepucci RA, et al. PRAME is a membrane and cytoplasmic protein aberrantly expressed in chronic lymphocytic leukemia and mantle cell lymphoma[J]. Leuk Res, 2006, 30(11): 1333-1339.
[6] Spanaki A, Perdikogianni C, Linardakis E, et al. Quantitative assessment of PRAME expression in diagnosis of childhood acute leukemia[J]. Leuk Res, 2007, 31(5): 639-642.
[7] Steinbach D, Viehmann S, Zintl F, et al. PRAME gene expression in childhood acute lymphoblastic leukemia[J]. Cancer Genetics Cytogenet, 2002, 138(1): 89-91.
[8] van den Ancker W, Ruben JM, Westers TM, et al. Priming of PRAME and WT1specific CD8+ T cells in healthy donors but not in AML patients in complete remission: implications for immunotherapy[J]. Oncoimmunology, 2013, 2(4): e23971.
[9] Lynch RG, Graff RJ, Sirisinha S, et al. Myeloma proteins as tumorspecific transplantation antigens[J]. Proc Natl Acad Sci USA, 1972, 69(6): 1540-1544.
[10] Crainie M, Belch AR, Mant MJ, et al. Overexpression of the receptor for hyaluronanmediated motility (RHAMM) characterizes the malignant clone in multiple myeloma: identification of three distinct RHAMM variants[J]. Blood, 1999, 93(5): 1684-1696.
[11] Qian J, Xie J, Hong S, et al. Dickkopf1 (DKK1) is a widely expressed and potent tumorassociated antigen in multiple myeloma[J]. Blood, 2007, 110(5): 1587-1594.
[12] Abramenko IV, Belous NI, Kriachok IA, et al. Expression of PRAME gene in multiple myeloma[J]. Ter Arkh, 2004, 76(7): 77-81.
[13] Qin YZ, Zhu HH, Liu YR, et al. PRAME and WT1 transcripts constitute a good molecular marker combination for monitoring minimal residual disease in myelodysplastic syndromes[J]. Leuk Lymphoma, 2013, 54(7): 1442-1449.
[14] Staege MS, BanningEichenseer U, Weissflog G, et al. Gene expression profiles of Hodgkin′s lymphoma cell lines with different sensitivity to cytotoxic drugs[J]. Exp Hematol, 2008, 36(7): 886-896.
[15] Kewitz S, Staege MS. Knockdown of PRAME increases retinoic acid signaling and cytotoxic drug sensitivity of Hodgkin lymphoma cells[J]. PLoS One, 2013, 8(2): e55897.
[16] Beà S, Salaverria I, Armengol L, et al. Uniparental disomies, homozygous deletions, amplifications, and target genes in mantle cell lymphoma revealed by integrative high-resolution wholegenome profiling[J]. Blood, 2009, 113(13): 3059-3069.
[17] Paydas S, Tanriverdi K, Yavuz S, et al. PRAME mRNA levels in cases with acute leukemia: clinical importance and future prospects[J]. Am J Hematol, 2005, 79(4): 257-261.
[18] Perna SK, De Angelis B, Pagliara D, et al. Interleukin 15 provides relief to CTLs from regulatory T cellmediated inhibition: implications for adoptive T cellbased therapies for lymphoma[J]. Clin Cancer Res, 2013, 19(1): 106-117.
[19] Dudley ME, Wunderlich JR, Yang JC, et al. Adoptive cell transfer therapy following nonmyeloablative but lymphodepleting chemotherapy for the treatment of patients with refractory metastatic melanoma[J]. J Clin Oncol, 2005, 23(10): 2346\-2357.
[20] Colombo MP, Piconese S. RegulatoryTcell inhibition versus depletion: the right choice in cancer immunotherapy[J]. Nat Rev Cancer, 2007, 7(11): 880-887.
[21] Cerundolo V, Hermans IF, Salio M. Dendritic cells: a journey from laboratory to clinic[J]. Nat Immunol, 2004, 5(1): 7-10.
[22] Li L, Giannopoulos K, Reinhardt P, et al. Immunotherapy for patients with acute myeloid leukemia using autologous dendritic cells generated from leukemic blasts[J]. Int J Oncol, 2006, 28(4): 855-861.
[23] Weber G, Caruana I, Rouce RH, et al. Generation of tumor antigenspecific T cell lines from pediatric patients with acute lymphoblastic leukemiaimplications for immunotherapy[J]. Clin Cancer Res, 2013, 19(18): 5079-5091.
[24] Yong AS, Keyvanfar K, Eniafe R, et al. Hematopoietic stem cells and progenitors of chronic myeloid leukemia express leukemiaassociated antigens: implications for the graftversusleukemia effect and peptide vaccinebased immunotherapy[J]. Leukemia, 2008, 22(9): 1721-1727.
[25] Kessler JH, Khan S, Seifert U, et al. Antigen processing by nardilysin and thimet oligopeptidase generates cytotoxic T cell epitopes[J]. Nat Immunol, 2011, 12(1): 45-67.
[26] Tabarkiewicz J, Giannopoulos K. Definition of a target for immunotherapy and results of the first Peptide vaccination study in chronic lymphocytic leukemia[J]. Transplant Proc, 2010, 42(8): 3293-3296.
[27] Griffioen M, Kessler JH, Borghi M, et al. Detection and functional analysis of CD8+ T cells specific for PRAME: a target for Tcell therapy[J]. Clin Cancer Res, 2006, 12(10): 3130-3136.
[28] Weber JS, Vogelzang NJ, Ernstoff MS, et al. A Phase 1 study of a vaccine targeting preferentially expressed antigen in melanoma and prostatespecific membrane antigen in patients with advanced solid tumors[J]. J Immunother, 2011, 34(7): 556-567.
[29] Bullinger L, Schlenk RF, Gtz M, et al. PRAMEinduced inhibition of retinoic acid receptor signalingmediated differentiationa possible target for ATRA response in AML without t(15;17)[J]. Clin Cancer Res, 2013, 19(9): 2562-2571. |