Critical evaluation of lymphocyte functions in urological cancer patients

Abstract

One hundred three patients with varying stages of urological cancer (bladder, prostate, kidney) were investigated with regard to the following lymphocyte functions. T-cells were assessed numerically (E rosettes), their blastogenic response to phytohemagglutinin (pHA) was determined, and their cytotoxic potential against heterologous target cells in short-term presence of PHA (e.i., PHA-dependent cellular cytotoxocity) was evaluated. Similarly, B cells were numerically assessed (EA rosettes), and their function was evaluated by antibody-dependent cellular cytotoxicity against antibody-coated deterologous target cells. The data on cancer patients, divided on the basis of extent of disease and prior radiation therapy, were compared to those of normal young and age-matched controls. Our investigations emphasize the importance of the following factors: (a) comparison of data with age-matched controls, since several lymphocyte functions appear to change with age; (b) use of multiple controls to compensate for the inherent variability found in certain tests; (c) minimized contamination by nonlymphoid cells in the purified cell preparation; and (d) the influence of certain treatment regimens (radiation, chemotherapy, etc.) on the results. Radiotherapy significantly depressed T-cell number with a depression of PHA blastogenic responses as well as PHA-dependent cellular cytotoxicity. When all of these conditions were taken into account, the urological cancer patients as a group were found to have a lower proportional value of E rosettes (T-cells) and a reduced PHA blastogenic responsiveness. Certain cancer patients displayed an elevated PHA-dependent cellular cytotoxicity as compared to age-matched controls, which may indicate the presence of activated cells in the presence of tumors. With this identification of a group of cancer patients with markedly depressed E rosette values and PHA responsiveness, it will now be possible to follow them clinically in comparison with a group of cancer patients with normal T-cell functions.