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Tumor antigens and tumor vaccines: Peptides as immunogens

Identifieur interne : 001650 ( Istex/Checkpoint ); précédent : 001649; suivant : 001651

Tumor antigens and tumor vaccines: Peptides as immunogens

Auteurs : Craig L. Slingluff Jr [États-Unis]

Source :

RBID : ISTEX:703FEFEDA2B71069AA61CACB6842E19B132170AD

English descriptors

Abstract

Tumor antigens recognized by human cytotoxic T lymphocytes (CTL) have been identified for multiple types of solid tumors. These include both shared and unique antigens. Unique antigens are those expressed uniquely by one patient's tumor, and shared antigens are those present on tumor cells from many different patients. Many of the shared antigens are derived from tissue‐specific differentiation antigens, oncogenes, or a set of antigens expressed only in tumors or in testis. In addition to advances in understanding tumor antigens that stimulate CTL and T‐helper cell responses, there have been advances in understanding immunity in general, including the characterization of cytokines, the recognition of the dendritic cell as an optimal antigen‐presenting cell (APC), and the characterization of costimulatory molecules as critical components of antigen presentation. Together, these developments have breathed new life into tumor immunology, and they promise to lead to a new generation of peptide‐ and cell‐based tumor vaccines. © 1996 Wiley‐Liss, Inc.

Url:
DOI: 10.1002/(SICI)1098-2388(199611/12)12:6<446::AID-SSU10>3.0.CO;2-T


Affiliations:


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ISTEX:703FEFEDA2B71069AA61CACB6842E19B132170AD

Le document en format XML

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<term>Antigenic peptides</term>
<term>Autologous</term>
<term>Autologous cytolytic</term>
<term>Autologous tumor</term>
<term>Bruggen</term>
<term>Cell lung cancers</term>
<term>Cell responses</term>
<term>Clone</term>
<term>Costimulatory</term>
<term>Costimulatory molecules</term>
<term>Cytokine</term>
<term>Cytokine secretion</term>
<term>Cytolytic</term>
<term>Cytotoxic</term>
<term>Dendritic</term>
<term>Dendritic cells</term>
<term>Encoding</term>
<term>Epitope</term>
<term>Eynde</term>
<term>Gene encoding</term>
<term>Human cytotoxic</term>
<term>Human melanoma</term>
<term>Human melanoma antigen</term>
<term>Immune</term>
<term>Immune recognition</term>
<term>Immune responses</term>
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<term>Immunology</term>
<term>Immunotherapy</term>
<term>Kawakami</term>
<term>Lymphocyte</term>
<term>Malignant melanoma</term>
<term>Melanoma</term>
<term>Melanoma cells</term>
<term>Melanoma patients</term>
<term>Metastatic melanoma</term>
<term>Natl</term>
<term>Natl cancer inst</term>
<term>Node</term>
<term>Other tumors</term>
<term>Ovarian</term>
<term>Ovarian cancer</term>
<term>Peptide</term>
<term>Peptide epitopes</term>
<term>Proc natl acad</term>
<term>Prostate cancer</term>
<term>Sarcoma</term>
<term>Solid tumors</term>
<term>Surgical oncology</term>
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<term>Tumor antigens</term>
<term>Tumor cells</term>
<term>Tumor immunology</term>
<term>Tumor vaccines</term>
<term>Tumorinfiltrating lymphocytes</term>
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<term>Vaccine</term>
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<div type="abstract" xml:lang="en">Tumor antigens recognized by human cytotoxic T lymphocytes (CTL) have been identified for multiple types of solid tumors. These include both shared and unique antigens. Unique antigens are those expressed uniquely by one patient's tumor, and shared antigens are those present on tumor cells from many different patients. Many of the shared antigens are derived from tissue‐specific differentiation antigens, oncogenes, or a set of antigens expressed only in tumors or in testis. In addition to advances in understanding tumor antigens that stimulate CTL and T‐helper cell responses, there have been advances in understanding immunity in general, including the characterization of cytokines, the recognition of the dendritic cell as an optimal antigen‐presenting cell (APC), and the characterization of costimulatory molecules as critical components of antigen presentation. Together, these developments have breathed new life into tumor immunology, and they promise to lead to a new generation of peptide‐ and cell‐based tumor vaccines. © 1996 Wiley‐Liss, Inc.</div>
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