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Evaluation of cellular immunologic responsiveness in the clinical management of patients with prostatic cancer. I. Thymic-dependent lymphocytic blastogenesis.

作者信息

Ablin R J, Bruns G R, Guinan P D, Bush I M

出版信息

Urol Int. 1976;31(5):374-82. doi: 10.1159/000280074.

Abstract

Thymic-dependent lymphocytic blastogenesis of peripheral blood lymphocytes of 59 patients with varying stages of prostatic cancer to the non-specific plant mitogen, phytohaemagglutinin (PHA) and the correlation of their responsiveness with the clinical stage of malignancy and level of alpha2-globulin have been evaluated. Patients within each of the four stages of malignancy possessed statistically significant extrinsic (noted in 40 (68%) of 59 patients) and intrinsic (noted in 21 (47%) of 45 patients) aberrations of their lymphocytic responsiveness to PHA compared with the responsiveness of a control population of non-cancer patients. The observed aberrations were, however, not significantly different between each stage nor did they correlate with the stage of disease. Similarly, levels of alpha2-globulin, while significantly elevated within each stage, as compared with the levels in the control population, no significant differences or correlation with the stage of disease was observed. Of interest, perhaps pending further study, were observations of the increased frequency of the number of patients with a significant elevation of alpha2 with a progression of malignancy from localized to invasive and metastatic disease. A similar trend in the incidence of the association of aberrations of lymphocytic reactivity with elevated levels of alpha2 were also noted with a progression of disease. The present confirmatory observations of a recent study in this laboratory of diminished cellular responsiveness in patients with prostatic cancer may be of considerable relevance in directing the therapeutic management of the patient - lest the therapy selected be further debilitating providing reduced surveillance - metastization of tumour cells, and alteration of tumour-host homeostasis.

摘要

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