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Rejection antigens in chemically induced tumors

The paper of Ikeda et al. throws new light on an old problem. Four decades ago chemically induced mouse and rat tumors were found to elicit tumor-specific rejection reactions in syngeneic and even in autochtonous hosts. The tumor-specific transplantation antigens (TSTAs) that were defined by the rej... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America 10 June 1997, Vol.94(12), p.5991
Main Author: George Klein
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0027-8424 ; E-ISSN: 1091-6490
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recordid: pnas_s94_12_5991
title: Rejection antigens in chemically induced tumors
format: Article
creator:
  • George Klein
subjects:
  • Sciences (General)
ispartof: Proceedings of the National Academy of Sciences of the United States of America, 10 June 1997, Vol.94(12), p.5991
description: The paper of Ikeda et al. throws new light on an old problem. Four decades ago chemically induced mouse and rat tumors were found to elicit tumor-specific rejection reactions in syngeneic and even in autochtonous hosts. The tumor-specific transplantation antigens (TSTAs) that were defined by the rejection response were individually distinct, with no consistent cross-reactions between different tumors of the same type. In contrast, virus-induced tumors carried group-specific TSTAs, common for all tumors induced by the same virus. Immunization against both types of TSTA protected the host only against small or moderate cell doses. Resistance could be transferred with lymphocytes, but not with serum. During the following decades, much progress was made in defining the nature of the virus-induced TSTAs. With polyoma and simian virus 40 in mice and Epstein-Barr virus in humans as paradigmatic examples, major histocompatibility complex class I-associated peptides derived from vitally encoded, transformation-associated proteins were identified as being responsible for the immunogenicity and immunosensitivity of these and other virally induced tumors. The nature of the TSTAs in the chemically induced tumors and the reasons for their diversity remained enigmatic. The work of Ikeda et al. is an important advance. Following the methodology developed by Boon and his colleagues, they used a line of cytotoxic T cells (CTLs), specific for a methylcholanthrene (MC)-induced sarcoma cell. CTLs against MC-induced sarcomas have been established previously, but the target antigen has not been identified. Ikeda et al. screened a cDNA expression library prepared from the target tumor. The gene encoding the protein recognized by the CTLs was identified as a mitogen-activated protein kinase (MAPK) mutant. The target peptide differed from its normal counterpart by a single amino acid substitution. With the help of interleukin-12, the mutant peptide could elicit the tumor-specific rejection response that served as the point of departure.
language: eng
source:
identifier: ISSN: 0027-8424 ; E-ISSN: 1091-6490
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issn:
  • 0027-8424
  • 00278424
  • 1091-6490
  • 10916490
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descriptionThe paper of Ikeda et al. throws new light on an old problem. Four decades ago chemically induced mouse and rat tumors were found to elicit tumor-specific rejection reactions in syngeneic and even in autochtonous hosts. The tumor-specific transplantation antigens (TSTAs) that were defined by the rejection response were individually distinct, with no consistent cross-reactions between different tumors of the same type. In contrast, virus-induced tumors carried group-specific TSTAs, common for all tumors induced by the same virus. Immunization against both types of TSTA protected the host only against small or moderate cell doses. Resistance could be transferred with lymphocytes, but not with serum. During the following decades, much progress was made in defining the nature of the virus-induced TSTAs. With polyoma and simian virus 40 in mice and Epstein-Barr virus in humans as paradigmatic examples, major histocompatibility complex class I-associated peptides derived from vitally encoded, transformation-associated proteins were identified as being responsible for the immunogenicity and immunosensitivity of these and other virally induced tumors. The nature of the TSTAs in the chemically induced tumors and the reasons for their diversity remained enigmatic. The work of Ikeda et al. is an important advance. Following the methodology developed by Boon and his colleagues, they used a line of cytotoxic T cells (CTLs), specific for a methylcholanthrene (MC)-induced sarcoma cell. CTLs against MC-induced sarcomas have been established previously, but the target antigen has not been identified. Ikeda et al. screened a cDNA expression library prepared from the target tumor. The gene encoding the protein recognized by the CTLs was identified as a mitogen-activated protein kinase (MAPK) mutant. The target peptide differed from its normal counterpart by a single amino acid substitution. With the help of interleukin-12, the mutant peptide could elicit the tumor-specific rejection response that served as the point of departure.
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