The relationship between Fas-mediated apoptosis and Type 1 diabetes is currently under investigation. Fas/Fas ligand interaction could be involved both in the insulitis process and in beta-cell death. Nevertheless, different mechanisms appear to be involved in human Type 1 diabetes and in NOD mice.
Fas/Fas ligand system and apoptosis induction in testicular carcinoma
β Scribed by Hans U. Schmelz; Michael Abend; Klaus Kraft; Ekkehard W. Hauck; Wolfgang Weidner; Dirk van Beuningen; Christoph Sparwasser
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 135 KB
- Volume
- 95
- Category
- Article
- ISSN
- 0008-543X
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
BACKGROUND
Tumorβinfiltrating, Fas ligand (FasL)βexpressing lymphocytes are able to eliminate Fasβbearing tumor cells by apoptosis induction. Activated cytotoxic Tβcells 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;95:73β81. Β© 2002 American Cancer Society.
DOI 10.1002/cncr.10649
π SIMILAR VOLUMES
Adult sexual dimorphism in neuronal cell number is controlled by estrogen exposure during a tightly defined period of rat brain development. The mechanisms of estrogen's effect are unknown; one possibility is regulation of programmed cell death (apoptosis). In this study we have shown that estradiol
Background and Objectives: Fas (APO-1) induces apoptosis after binding Fas ligand (FasL). Evidence suggests that tumors may use this interaction to evade the host immune response. Fas/FasL expression has not been reported in esophageal cancer. We hypothesized that Fas expression would render esophag