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Uro-Oncology Group of the Norris Cotton Cancer Center [J. A. H., A. R. S., M. S. E.], Sections of Medical Hematology/Oncology [M. S. E.] and Urology [J. A. H.], and Department of Pathology [A. R. S.], Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire 03756-0001; Division of Medical Oncology, Allegheny University of the Health Sciences, Philadelphia, Pennsylvania 19102 [G. C.]; and Istituto Nazionale per la Ricerca sul Cancro di Genova Sezione di Roma, 00100 Rome, Italy [G. C.]
The functional expression of Fas-ligand on tumor cells reported in a variety of neoplasms has been proposed by several groups as a mechanism of tumor escape from immunological detection. To better support this hypothesis, we have evaluated and quantified for the first time the presence of the Fas(CD95)-R molecule on tumor-infiltrating lymphocytes and on matched peripheral blood lymphocytes (PBLs) of renal cell cancer patients. By two-color flow cytometry we have detected a significant increase in the Fas(CD95)-R expression on tumor-infiltrating lymphocytes compared with matched patient and normal volunteer PBLs. We also observed a decreased expression of the Fas(CD95)-R expression on PBLs from renal cell cancer patients compared with normal healthy controls. The Fas(CD95)-R expression was observed predominantly on the CD4+ subset in all three groups. These different distributions of the Fas(CD95)-R molecule support the hypothesis that the Fas(CD95)-R/Fas(CD95)-L pathway and tumor microenvironment play a major role in the modulation of T-cell function and differentiation to either memory and activation or apoptosis.
1 Supported in part by NIH Grants CA 49002 and CA 23108.
2 To whom requests for reprints should be addressed, at Allegheny University of the Health Sciences, Broad and Vine Streets, Mail Stop 299, Philadelphia, PA 19102. Phone: (215) 762-3118; Fax: (215) 762-7701.
Received 2/23/98. Accepted 3/30/98.
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