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Titolo:
Fas receptor counterattack against tumor-infiltrating lymphocytes in vivo as a mechanism of immune escape in gastric carcinoma
Autore:
Koyama, S; Koike, N; Adachi, S;
Indirizzi:
Univ Tsukuba, Inst Clin Med, Dept Internal Med, Tsukuba, Ibaraki 3058575, Japan Univ Tsukuba Tsukuba Ibaraki Japan 3058575 sukuba, Ibaraki 3058575, Japan Univ Tsukuba, Inst Clin Med, Dept Surg, Tsukuba, Ibaraki 305, Japan Univ Tsukuba Tsukuba Ibaraki Japan 305 Surg, Tsukuba, Ibaraki 305, Japan
Titolo Testata:
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
fascicolo: 1, volume: 127, anno: 2001,
pagine: 20 - 26
SICI:
0171-5216(200101)127:1<20:FRCATL>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-MEDIATED CYTOTOXICITY; CD95 LIGAND; NECROSIS-FACTOR; DEATH FACTOR; EXPRESS FAS; APOPTOSIS; ADENOCARCINOMAS; PRIVILEGE; PERFORIN; PATHWAYS;
Keywords:
Fas receptor; Fas ligand; immune privilege; apoptosis; gastric carcinoma;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Koyama, S Univ Tsukuba, Inst Clin Med, Dept Internal Med, Tsukuba, Ibaraki3058575, Japan Univ Tsukuba Tsukuba Ibaraki Japan 3058575 araki 3058575, Japan
Citazione:
S. Koyama et al., "Fas receptor counterattack against tumor-infiltrating lymphocytes in vivo as a mechanism of immune escape in gastric carcinoma", J CANC RES, 127(1), 2001, pp. 20-26

Abstract

We investigated the presence and functional status of surface expression of the Fas receptor (FasR) and its ligand (FasL) in tumor and tumor-infiltrating lymphocytes (TIL) in gastric carcinoma (n = 36) from the primary locus, metastatic gastric carcinoma (n = 30) from malignant ascites, and benign gastric mucosa (n = 30) for the control. The quantitative analysis was based on the percentage of positive cells by a flow cytometry. The results showed that the membrane-bound FasL molecule was constitutively expressed in primary and metastatic gastric carcinomas as well as normal gastric epithelium in nearly all the patients. III particular, metastatic carcinoma proved to aberrantly express the FasL molecule. On the other hand, FasR expression ranged from minimal or absent in primary and metastatic gastric carcinomas:suggesting that the carcinoma might be rendered less sensitive toward FasL-induced killing. Apoptotic tumor cells detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTTP nick and labeling (TUNEL) were barely identified in primary and metastatic carcinomas. In the analysis of TIL, theexpression of FasR and Fast, and apoptotic TIL could not usually be observed in primary gastric carcinoma. In metastatic carcinoma, however, there was significant overexpression of FasR and FasL in immune TIL associated witha higher frequency of apoptotic cell death detected by TUNEL. The results suggest that metastatic carcinoma expressing FasL, but not FasL(+) primary carcinoma, might evade the immune attack by apoptotic depletion of activated TIL through the FasR:FasL systems. These results provide the direct and quantitative evidence of FasR counterattacks and/or paracrine fratricides asa mechanism of tumor-immune escape in vivo in human cancer.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 21:37:40