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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

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TLDR
The 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.
Abstract
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.

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Evidence for a tumoral immune resistance mechanism based on tryptophan degradation by indoleamine 2,3-dioxygenase

TL;DR: It is shown that most human tumors constitutively express IDO, and that expression of IDO by immunogenic mouse tumor cells prevents their rejection by preimmunized mice, suggesting that the efficacy of therapeutic vaccination of cancer patients might be improved by concomitant administration of an IDO inhibitor.
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Cancer/testis antigens, gametogenesis and cancer.

TL;DR: CT antigens are being evaluated for their role in oncogenesis — recapitulation of portions of the germline gene-expression programme might contribute characteristic features to the neoplastic phenotype, including immortality, invasiveness, immune evasion, hypomethylation and metastatic capacity.
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Immune evasion in cancer: Mechanistic basis and therapeutic strategies

TL;DR: The advances made toward understanding the basis of cancer immune evasion are discussed, the efficacy of various therapeutic measures and targets that have been developed or are being investigated to enhance tumor rejection are summarized and some natural agents and phytochemicals merit further study.
References
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Journal ArticleDOI

A gene encoding an antigen recognized by cytolytic T lymphocytes on a human melanoma

TL;DR: In this paper, a gene was identified that directed the expression of antigen MZ2-E on a human melanoma cell line, which belongs to a family of at least three genes.
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Vaccination of melanoma patients with peptide- or tumor lysate-pulsed dendritic cells.

TL;DR: Vaccination with autologous DCs generated from peripheral blood is a safe and promising approach in the treatment of metastatic melanoma and antigen-specific immunity was induced during DC vaccination.
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Immunologic and therapeutic evaluation of a synthetic peptide vaccine for the treatment of patients with metastatic melanoma

TL;DR: A synthetic peptide, designed to increase binding to HLA-A2 molecules, was used as a cancer vaccine to treat patients with metastatic melanoma and, on the basis of immunologic assays, 91% of patients could be successfully immunized with this peptide.
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Tumor-antigens recognized by T-lymphocytes

TL;DR: The identification of human tumor rejection antigens opens new possibilities for systematic approaches to the specific immune therapy of cancer.
Journal ArticleDOI

Melanoma Cell Expression of Fas(Apo-1/CD95) Ligand: Implications for Tumor Immune Escape

TL;DR: In vivo, injection of FasL+ mouse melanoma cells in mice led to rapid tumor formation and tumorigenesis was delayed in Fas-deficient lpr mutant mice in which immune effector cells cannot be killed by FasL.
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