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Fas/Fas ligand system and apoptosis induction in testicular carcinoma
Author(s) -
Schmelz Hans U.,
Abend Michael,
Kraft Klaus,
Hauck Ekkehard W.,
Weidner Wolfgang,
van Beuningen Dirk,
Sparwasser Christoph
Publication year - 2002
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.10649
Subject(s) - fas ligand , apoptosis , immune system , cytotoxic t cell , cancer research , fas receptor , cell , medicine , biology , programmed cell death , pathology , immunology , in vitro , biochemistry
Abstract BACKGROUND Tumor‐infiltrating, Fas ligand (FasL)‐expressing lymphocytes are able to eliminate Fas‐bearing tumor cells by apoptosis induction. Activated cytotoxic T‐cells that express Fas may enter apoptosis in the presence of FasL tumor cells. To date, no studies of patients with testicular carcinoma have correlated the differential expression of Fas and FasL in both cell types with the corresponding apoptotic index (AI). METHODS Fas and FasL were investigated immunohistochemically in paraffin embedded tissue sections from 25 patients with nonseminomatous testicular tumors. The percentages of positive cells and the ratios of Fas cells to FasL cells were correlated with the AI of tumor cells and lymphocytes, respectively, using Spearman correlations. RESULTS No association was found between the rate of FasL positive cells and AI of the other cell type or between the rate of Fas positive cells and the AI of the same cell type. Ratios between Fas positive cells and FasL positive cells were not correlated with the AI; however, a significant positive correlation was found between the AI of tumor cells and the AI of lymphocytes. CONCLUSIONS It seems unlikely that the Fas/FasL system is responsible for immune escape of the tumor in testicular carcinoma. Rather, the significant positive correlation between the AIs of tumor cells and lymphocytes implicate a previously unknown mechanism of apoptosis induction in both cell types. Cancer 2002;95:73–81. © 2002 American Cancer Society. DOI 10.1002/cncr.10649