Abstract: . . .  system. J. Urol., 1999, 162, 1246-1258. ____________________ SUMMARY Mechanisms of local immune tolerance in renal cancers . Many arguments suggest that renal tumours are immunogenic. However, the immune cells present around or within the tumour are unable to induce tumour rejection and the results of immu - notherapy in metastatic renal cancer remain disappointing regardless of the protocols used. The objective of this study was to review the main mechanisms by which a renal tumour can escape immune destruction. These mechanisms can concern: tumour antigens, antigen-pre - senting molecules on the cell surface or defects of the cell machi - nery leading to the preparation of these molecules. Defects may also concern intercellular communications, especially adhesion and co-stimulation molecules. The immune cells present may also be defective, presenting qualitative or quantitative deficits, abnor - malities of the T receptor, defect of cytokine production and these defects may concern both effector . . .
. . .  205-207. 72. WURTZEN P.A., PEDERSEN L.O., POULSEN H.S., CLAESSON M.H.: Specific killing of P53 mutated tumor cell lines by a cross- reactive human HLA-A2-restricted P53-specific CTL line. Int. J. Cancer , 2001, 93, 855-861. 73. ZAMBRANO N.R., LUBENSKY I.A., MERINO M.J., LINEHAN W.M., WALTHER M.M.: Histopathology and molecular genetics of renal tumors toward unification of a classification system. J. Urol., 1999, 162, 1246-1258. ____________________ SUMMARY Mechanisms of local immune tolerance in renal cancers . Many arguments suggest that renal tumours are immunogenic. However, the immune cells present around or within the tumour are unable to induce tumour rejection and the results of immu - notherapy in metastatic renal cancer remain disappointing regardless of the protocols used. The objective of this study was to review the main mechanisms by which a renal tumour can escape immune destruction. These mechanisms can concern: tumour antigens, antigen-pre - senting molecules on the cell surface . . .
. . .  ROBBINS PF., ROSENBERG SA.: Utilization of an alternative open reading frame of a normal gene in generating a novel human cancer antigen. J. Exp. Med., 1996, 183, 1131-1140 70. WOLFEL T., HAUER, M., SCHNEIDER J., SERRANO M., WOL- FEL C., KLEHMANN-HIEB E., DE PLAEN E., HANKELN T., MEYER ZUM BUSCHENFELDE K. H., BEACH D.A.: p16INK4a- insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma. Science, 1995, 269, 1281-1284. 71. WUNDERLICH H., STEINER T., KOSMEHL H., JUNKER U., REINHOLD D., REICHELT O., ZERMANN D.H., SCHUBERT J.: Increased transforming growth factor beta1 plasma level in patients with renal cell carcinoma: a tumor-specific marker? Urol. Int., 1998, 60, 205-207. 72. WURTZEN P.A., PEDERSEN L.O., POULSEN H.S., CLAESSON M.H.: Specific killing of P53 mutated tumor cell lines by a cross- reactive human HLA-A2-restricted P53-specific CTL line. Int. J. Cancer , 2001, 93, 855-861. 73. ZAMBRANO N.R., LUBENSKY I.A., MERINO M.J., LINEHAN W.M., WALTHER M.M.: Histopathology . . .
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