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Chain and p56lck in T-Cells Infiltrating Human Renal Cell Carcinoma1Departments of Immunology, [J. F., J. S., S. K.], Pathology [R. T.], and Urology [E. K.] and Experimental Therapeutic Program [R. B.], Cleveland Clinic Foundation; Immunotherapy Laboratory, Program Resources, Inc./DynCorp [A. Z., A. C. O.], and Biological Response Modifiers Program [D. L. L., H. M., R. W., J. J. O.], Division of Cancer Treatment, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21702
3 To whom requests for reprints should be addressed,at Clinical Services Program, Program Resources, Inc./DynCorp, NCI-FCRDC, P. O. Box B, Frederick, MD 217021201.
Cancer patients and mice bearing tumors develop a progressive immunosuppression manifested by a decreased delayed-type hypersensitivity, decreased T-cell lytic activity, diminished production of lymphokines, and a reduced T-cell proliferative response. The mechanisms underlying these changes are incompletely understood. We recently reported the presence of marked alterations in signal transduction in T-cells from mice bearing long-term (28-day) tumors. We hypothesized that a soluble product produced by the tumor or resulting from the immune response to tumor might be responsible for inducing the changes in T-cells. Tumor-infiltrating lymphocytes from patients with renal cell carcinoma tested here showed, in 10 of 11 cases, a marked decrease in the expression of the T-cell receptor 
chain and in p56lck tyrosine kinase. The presence of major alterations in the tumor-infiltrating lymphocytes with only minor changes in the peripheral blood leukocyte T-cells supports the notion that the defects are induced by exposure to tumor. These results suggest that tumor-infiltrating lymphocytes may be compromised in their antitumor efficacy in patients with renal cell cancer.
1 Supported in part by USPHS Grants CA56937 and CA 48919 (J. F.); also supported, at least in part, by the National Cancer Institute, Department of Health and Human Services under Contract N01-C0-74102 with Program Resources, Incorporated/DynCorp, and CRADA CACR 0109 with OncoTherapeutics, Inc. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the United States Government. By acceptance of this article, the publisher or recipient acknowledges the right of the U.S. Government to retain a nonexclusive, royalty-tree license in and to any copyright covering the article.
2 Both individuals contributed equally to the work presented here.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 8/30/93. Accepted 10/20/93.
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