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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Loss of T-cell receptor zeta chain and p56lck in T-cells infiltrating human renal cell carcinoma.

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) tumours. 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 zeta 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]

References

  1. Loss of T-cell receptor zeta chain and p56lck in T-cells infiltrating human renal cell carcinoma. Finke, J.H., Zea, A.H., Stanley, J., Longo, D.L., Mizoguchi, H., Tubbs, R.R., Wiltrout, R.H., O'Shea, J.J., Kudoh, S., Klein, E. Cancer Res. (1993) [Pubmed]
 
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