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Your search keyword '"Itoh, Kyogo"' showing total 24 results
Start Over Author "Itoh, Kyogo" Journal international journal of cancer
24 results on '"Itoh, Kyogo"'

1. T‐cell receptor Vβ gene usage by T cells reactive with the tumor‐rejection antigen SART‐1 in oral squamous cell carcinoma

Author

Kumamaru, Wataru, primary, Nakamura, Seiji, additional, Kadena, Tsutomu, additional, Yamada, Akira, additional, Kawamura, Eiji, additional, Sasaki, Masanori, additional, Ohyama, Yukiko, additional, Toyoshima, Takeshi, additional, Hayashida, Jun‐nosuke, additional, Itoh, Kyogo, additional, and Shirasuna, Kanemitsu, additional

Published
2003
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2. Cleavage and polyadenylation specificity factor (CPSF)‐derived peptides can induce HLA‐A2‐restricted and tumor‐specific CTLs in the majority of gastrointestinal cancer patients

Author

Maeda, Yoshiaki, primary, Ito, Masaaki, additional, Harashima, Nanae, additional, Nakatsura, Tetsuya, additional, Hida, Naoya, additional, Imai, Nobue, additional, Sato, Yuuji, additional, Shichijo, Shigeki, additional, Todo, Satoru, additional, and Itoh, Kyogo, additional

Published
2002
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16. Detection of mage-4 protein in lung cancers

Author

Shichijo, Shigeki, primary, Hayashi, Akihiro, additional, Takamori, Shinzo, additional, Tsunosue, Rika, additional, Hoshino, Tomoaki, additional, Sakata, Motoko, additional, Kuramoto, Terukazu, additional, Oizumi, Kotaro, additional, and Itoh, Kyogo, additional

Published
1995
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23. A newly identified <TOGGLE>MAGE-3</TOGGLE>-derived epitope recognized by HLA-A24-restricted cytotoxic T lymphocytes

Author

Oiso, Masatake, Eura, Masao, Katsura, Fumihiro, Takiguchi, Masafumi, Sobao, Yuji, Masuyama, Keisuke, Nakashima, Manabu, Itoh, Kyogo, and Ishikawa, Takeru

Abstract

Five MAGE-3-derived peptides carrying an HLA-A24-binding motif were synthesized. Binding capacity of these peptides was analyzed by an HLA-class-I stabilization assay. Two of the 5 peptides bound to HLA-A*2402 molecule with high affinity, and 3 peptides with low affinity. Peripheral-blood mononuclear cells (PBMC) depleted of CD4+T cells were stimulated with the peptides to determine whether these peptides would induce cytotoxic T lymphocytes (CTL) from PBMCs obtained from 7 healthy HLA-A*2402+ donors. Peptide M3-p97 (TFPDLESEF; corresponding to amino-acid residues 97–105 of MAGE-3), with high binding capacity to the HLA-A*2402 molecule, elicited the peptide-specific and HLA-A24-restricted CD8+CTL lines in 2 of the 7 donors, while none of the 4 other peptides induced CTL specific for the corresponding peptide in any of the donors. CTL lines induced by stimulation with peptide M3-p97 exhibited cytolytic activities against HLA-A*2402 transfectant cell lines (C1R-A*2402) in the presence of peptide M3-p97, but not in unloaded or irrelevant peptide-pulsed C1R-A*2402 cells. The CTL lines and a cloned CD8+CTL isolated from one of the bulk populations by limiting dilution could lyse MAGE-3+/HLA-A*2402+ squamous-cell-carcinoma(SCC) lines but neither MAGE-3−/HLA-A*2402+ nor MAGE-3+/HLA-A*2402− SCC lines, indicating that M3-p97 can be naturally processed and presented on the tumor-cell surface in association with HLA-A*2402 molecules. Combined with the 4 currently reported CTL epitopes derived from MAGE-3 and presented by HLA-A1, HLA-A2, HLA-A24 or HLA-B44, identification of this CTL epitope presented by the HLA-A*2402 molecule will extend the application of MAGE-3-derived peptides for immunotherapy for cancer patients. Int. J. Cancer 81:387–394, 1999. © 1999 Wiley-Liss, Inc.

Published
1999
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24. T-cell receptor Vbeta gene usage by T cells reactive with the tumor-rejection antigen SART-1 in oral squamous cell carcinoma.

Author

Kumamaru W, Nakamura S, Kadena T, Yamada A, Kawamura E, Sasaki M, Ohyama Y, Toyoshima T, Hayashida JN, Itoh K, and Shirasuna K

Subjects
Antigens, Neoplasm pharmacology, HLA-A Antigens metabolism, HLA-A24 Antigen, Humans, Lymphocyte Activation, Neoplasm Proteins pharmacology, Tumor Cells, Cultured, Antigens, Neoplasm metabolism, Carcinoma, Squamous Cell metabolism, Genes, T-Cell Receptor beta, Mouth Neoplasms metabolism, Neoplasm Proteins metabolism, Ribonucleoproteins, Small Nuclear, T-Lymphocytes, Cytotoxic metabolism
Abstract

We recently described that the SART-1(690-698) peptide could induce HLA-A24-restricted cytotoxic T lymphocytes (CTLs), which recognize the SART-1(259) (+) tumor cells from peripheral blood mononuclear cells (PBMCs) of HLA-A24(+) cancer patients. In our study, in 5 of 14 HLA-A24(+) patients with oral squamous cell carcinomas (SCCs), CTLs could be induced with the SART-1(690-698) peptide from the PBMCs. In 2 of the patients from whom the highest CTL activities were induced, the T-cell receptor (TCR) Vbeta repertoire expressed by the SART-1(690-698)-specific CTLs was found to be restricted and multiple Vbeta families were predominantly expressed in each patient. Although the predominant Vbeta families were different between the 2 patients, Vbeta7 was highly and commonly predominant. The same predominant Vbeta families were also detected in the tumor-infiltrating lymphocytes (TILs) from each patient, and each Vbeta family contained one or more unique T-cell clonotypes. The unique T-cell clonotypes were found to be common between the TILs and SART-1(690-698)-specific CTLs from each patient, and especially 2 T-cell clonotypes with Vbeta7 were identical even in the 2 patients. One of the 2 T-cell clonotypes with Vbeta7 was detected in the TILs from 11 of 14 HLA-A24(+) patients and another was found in those from 8 of HLA-A24(+) patients, while none of 10 HLA-A24(-) patients demonstrated both T-cell clonotypes. These results strongly suggest that the T-cell clonotypes with Vbeta7 are major TCR Vbeta genes expressed by SART-1(690-698)-specific CTLs. Furthermore, autologous tumor cells from one of the HLA-A24(+) patients stimulated the PBMCs and regional lymph node cells (LNCs) to expand the same T-cell clonotypes as those in the SART-1(690-698)-specific CTLs. These results strongly suggest that the SART-1(690-698)-specific CTLs clearly accumulate in vivo, especially in the TILs, as a consequence of in situ antigenic stimulation by autologous tumor cells. The identification of the unique TCR Vbeta genes used by SART-1(259)-specific CTLs should help to improve the diagnosis of the specific immune response in patients with SART-1(259) (+) cancers, especially during anticancer immunotherapy., (Copyright 2003 Wiley-Liss, Inc.)

Published
2004
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