Prognostic impact of apoptosis marker Fas (CD95) and its ligand (FasL) on bladder cancer in Egypt: Study of the effect of schistosomiasis

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Abstract

Objective: The Fas-Fas ligand (FasL) system has been recognized as a major pathway for the induction of apoptosis in cells and tissues. Fas-mediated apoptosis is deeply involved in cancer cell death brought about by the immune system. This study was performed to determine the Fas and FasL expression in human bladder cancer and the impact of schistosomiasis infection. Material and methods: Of the 75 patients, 25 with chronic bilharzial cystitis and 50 with bladder cancer were included in this study. Ten control patients were included in the study, following their consent. Fas and FasL expressions in bladder tissue were determined by indirect immunohistochemistry using avidin-biotin-peroxidase complex (ABC) method. Results: The association of bilharziasis with malignancy raised the incidence of Fas positive immunoreactivity to 100%. The number of malignant cases positive for Fas decreased with progress of tumour grade and stage. All control cases were negative for FasL expression. The percentage of positive FasL malignant cases increased with increasing tumour grade or stage. Conclusion: Malignant bladder lesions express high levels of Fas and decreased expression of Fas is associated with disease progression. Urinary bladder carcinoma acquires the functional FasL during tumour progression that may induce apoptosis of anti tumour T lymphocytes. Fas and FasL are recommended to be considered important tumour markers to define aggressive bladder cancer and may be included in defining the surveillance protocol for superficial bladder cancer. © the authors; licensee ecancermedicalscience.

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Elmansy, H. M., Kotb, A. F., Hammam, O., AbdelRaouf, H., Salem, H. K., Onsi, M., & ElLeithy, T. (2012). Prognostic impact of apoptosis marker Fas (CD95) and its ligand (FasL) on bladder cancer in Egypt: Study of the effect of schistosomiasis. Ecancermedicalscience, 6(1). https://doi.org/10.3332/ecancer.2012.278

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