Identification of a SART-1-derived peptide capable of inducing HLA-A24-restricted and tumor-specific cytotoxic T lymphocytes

Kikuchi, Megumi; Nakao, Motoki; Inoue, Yosuke; Matsunaga, Kazuko; Shichijo, Shigeki; Yamana, Hideaki; Itoh, Kyogo

doi:10.1002/(sici)1097-0215(19990505)81:3<459::aid-ijc21>3.0.co;2-6

Cited by 66 publications

(70 citation statements)

References 24 publications

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“…Recent technical advances have enabled the identification of various tumor-associated antigens (TAAs) [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21]; however, few of their epitopes are inducers of cytotoxic T lymphocyte (CTL) responses against tumors [22]. Several kinds of epitope have also been identified in patients with pancreatic adenocarcinoma [23,24].…”

Section: Introductionmentioning

confidence: 99%

P53, hTERT, WT-1, and VEGFR2 are the most suitable targets for cancer vaccine therapy in HLA-A24 positive pancreatic adenocarcinoma

Terashima

Mizukoshi

Arai

et al. 2014

Cancer Immunol Immunother

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Cancer vaccine therapy is one of the most attractive therapies as a new treatment procedure for pancreatic adenocarcinoma. Recent technical advances have enabled the identification of cytotoxic T lymphocyte (CTL) epitopes in various tumor-associated antigens (TAAs). However, little is known about which TAA and its epitope are the most immunogenic and useful for a cancer vaccine for pancreatic adenocarcinoma. We

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Section: Introductionmentioning

confidence: 99%

P53, hTERT, WT-1, and VEGFR2 are the most suitable targets for cancer vaccine therapy in HLA-A24 positive pancreatic adenocarcinoma

Terashima

Mizukoshi

Arai

et al. 2014

Cancer Immunol Immunother

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“…The low frequency of SART3 expression in tissue specimens could be due in part to the contamination of the specimens by normal cells or lion-proliferating cells, including dead tumor cells. A similarly low frequency of SART3 expression in tissue specimens was also observed in other histological types of tumors [11,12,24,29]. The SART3 protein may play an important role in cellular proliferation, given its exclusive expression in proliferating cells, phosphorylation of tyrosine residue at position 3 16 (unpublished observation), RNA-binding capacity [4], and regulatory function in alternative splicing of pre-mRNA (Harada et al, manuscript in preparation).…”

Section: Discussionmentioning

confidence: 72%

Expression of a newly defined tumor‐rejection antigen SART3 in musculoskeletal tumors and induction of HLA class I‐restricted cytotoxic T lymphocytes by SART3‐derived peptides

Tsuda

Murayama

Ishida

et al. 2001

Journal Orthopaedic Research

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We recently reported that a SART3 tumor-rejection antigen possessing tumor epitopes is capable of inducing HLA class I-restricted and tumor-specific cytotoxic T lymphocytes in cancer patients. We studied the expression of the SART3 protein in mrtsculo.rkeleta/ tumors to find a molecule for potential use in tumor-specific immunotherapy. The SART3 was detected at protein levels in 10004 of the osteosarcoma cell lines (n = 70), in 50% of the musculuslieletal tumor tissue specimens ( n = 37). and at notable levels in 67% of osteosarcoma tissues ( n = 9) and malignant fibrous histiocytosis tissues ( n = 9), respectively. SART3-derived peptides at positions 109-1 18 and 315-313 induced HLA-A?4-restricted tumor-specific cytoxic T lymphocytes from peripheral blood mononuclear cells of patients with osteosarconia or m d i g m n t fibrous histiocytosis. These peptide-induced cytotoxic T lymphocytes recognized HLA-A14+ SART3+ osteosarcoma cells but not H L A -A X or SART3-cells. These results suggest that the SART3 protein and its derived peptides could be molecules appropriate for use in specific immunotherapies for approximately 60% of HLA-A74-patients with osteosarcoma or malignant fibrous histiocytosis. 0 300 1 Orthopaedic Research Society. Published by

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“…This situation limits the broad applicability of this approach. To improve the situation, efforts have been made to identify TAAs expressed in multiple cell types (van den Burg et al, 1995;Tanaka et al, 1997;Fujie et al, 1999;Kikuchi et al, 1999;Oiso et al, 1999). As the same time, new tumour antigenic peptides restricted to other HLA class I alleles have been explored (van den Burg et al, 1996;Nestle et al, 1998;Maric and Liu, 1999;Wang et al, 1999;Yang et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Generation of cytotoxic T cell responses to an HLA-A24 restricted epitope peptide derived from wild-type p53

et al. 2001

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Mutations in the p53 gene are the most common genetic alterations found in human tumours, and these mutations result in high levels of p53 protein in the tumour cells. Since the expression levels of wild-type p53 in nonmalignant tissue are usually much lower in contrast, the p53 protein is an attractive target for cancer immunotherapy. We tested p53 encoded HLA-A24 binding peptides for their capacity to elicit anti-tumour cytotoxic T lymphocytes (CTL) in vitro. These peptides were in murine p53-derived cytotoxic peptides, which were being presented to CTL by H-2K d and H-2K b molecules, because the HLA-A24 peptide binding motifs were similar to the H-2K d and H-2K b . For CTL induction, we used CD8 + T lymphocytes from the peripheral blood mononuclear cells (PBMC) of healthy donors and the peptides from pulsed dendritic cells as antigen-presenting cells. We identified the peptide, p53-161 (AIYKQSQHM), which was capable of eliciting CTL lines that lysed tumour cells expressing HLA-A24 and p53. The effectors lysed C1RA24 cells (p53 + , HLA-A*2402 transfectant), but not their parental cell lines C1R (p53 + , HLA-A,B null cell). These results strongly indicate that the CTL exerts cytotoxic activity in HLA-A24's restricted manner. The identification of this novel p53 epitope for CTL offers the possibility to design and develop specific immunotherapeutic approaches for treating tumours with p53 mutation in HLA-A24-positive patients. © 2001 Cancer Research Campaign http://www.bjcancer.com

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Identification of a SART-1-derived peptide capable of inducing HLA-A24-restricted and tumor-specific cytotoxic T lymphocytes

Cited by 66 publications

References 24 publications

P53, hTERT, WT-1, and VEGFR2 are the most suitable targets for cancer vaccine therapy in HLA-A24 positive pancreatic adenocarcinoma

P53, hTERT, WT-1, and VEGFR2 are the most suitable targets for cancer vaccine therapy in HLA-A24 positive pancreatic adenocarcinoma

Expression of a newly defined tumor‐rejection antigen SART3 in musculoskeletal tumors and induction of HLA class I‐restricted cytotoxic T lymphocytes by SART3‐derived peptides

Generation of cytotoxic T cell responses to an HLA-A24 restricted epitope peptide derived from wild-type p53

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