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Tumor regressions observed in patients with metastatic melanoma treated with an antigenic peptide encoded by gene MAGE‐3 and presented by HLA‐A1
Author(s) -
Marchand Marie,
van Baren Nicolas,
Weynants Patrick,
Brichard Vincent,
Dréno Brigitte,
Tessier MarieHélène,
Rankin Elaine,
Parmiani Giorgio,
Arienti Flavio,
Humblet Yves,
Bourlond André,
Vanwijck Romain,
Liénard Danielle,
Beauduin Marc,
Dietrich PierreYves,
Russo Vincenzo,
Kerger Joseph,
Masucci Giuseppe,
Jäger Elke,
De Greve Jacques,
Atzpodien Jens,
Brasseur Francis,
Coulie Pierre G.,
van der Bruggen Pierre,
Boon Thierry
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990118)80:2<219::aid-ijc10>3.0.co;2-s
Subject(s) - ctl* , medicine , melanoma , metastatic melanoma , cytolysis , peptide , regression , human leukocyte antigen , antigen , immunology , immunotherapy , oncology , t lymphocyte , immune system , cytotoxic t cell , cancer research , biology , psychology , biochemistry , psychoanalysis , cd8 , in vitro
Thirty‐nine tumor‐bearing patients with metastatic melanoma were treated with 3 subcutaneous injections of the MAGE‐3.A1 peptide at monthly intervals. No significant toxicity was observed. Of the 25 patients who received the complete treatment, 7 displayed significant tumor regressions. All but one of these regressions involved cutaneous metastases. Three regressions were complete and 2 of these led to a disease‐free state, which persisted for more than 2 years after the beginning of treatment. No evidence for a cytolytic T lymphocyte (CTL) response was found in the blood of the 4 patients who were analyzed, including 2 who displayed complete tumor regression. Our results suggest that injection of the MAGE‐3.A1 peptide induced tumor regression in a significant number of the patients, even though no massive CTL response was produced. Int. J. Cancer 80:219–230, 1999. © 1999 Wiley‐Liss, Inc.