Prostaglandin E2 Affects the Tumor Immune Response in Prostatic Carcinoma
- 1 July 1981
- journal article
- research article
- Published by Wolters Kluwer Health in Journal of Urology
- Vol. 126 (1) , 65-70
- https://doi.org/10.1016/s0022-5347(17)54384-0
Abstract
Antitumor immunity to prostatic carcinoma was assayed by the tube leukocyte adherence inhibition assay. Peripheral blood leukocytes from 37 patients with prostatic carcinoma and 128 patients without prostatic carcinoma were incubated separately with extracts from prostatic carcinoma and from an unrelated control cancer, and the non-adherence index was calculated. The number of patients with prostatic carcinoma who had a positive response (non-adherence index .gtoreq. 30) was small. The mean non-adherence index (11) of the patients with prostatic a carcinoma was statistically different (P < 0.02) from the mean non-adherence index (2) of the subjects without prostatic carcinoma. Of patients with prostatic carcinoma, 14% (5 of 37) had positive leukocyte adherence inhibition responses compared to 1.5% of control subjects (2 of 128) (P < 0.05). Sixty patients diagnosed clinically as having benign prostatic hyperplasia were screened by the leukocyte adherence inhibition test and the non-adherence index results were evaluated with the histopathological diagnosis of the surgical specimen. Of the patients with benign prostatic hyperplasia, 3 (5%) had stage A prostatic carcinoma and 1 of these 3 patients (33%) had a positive leukocyte adherence inhibition test. After in vitro treatment of the peripheral blood leukocytes with 10-6 M. prostaglandin E2, 11 of 18 patients with prostatic carcinoma (61%) and 1 of 35 subjects without prostatic carcinoma (3%) had positive leukocyte adherence inhibition responses. The ability of prostaglandin E2 to heighten the leukocyte adherence inhibition response of the peripheral blood leukocytes from patients with prostatic carcinoma suggests that there is a functional defect in the antitumor response of the peripheral blood leukocytes, possibly caused in part by an excess of circulating tumor antigen. This is supported by the high mean non-adherence index (19) in patients with prostatic carcinoma who serum prostatic acid phosphatase within normal limits whereas patients with an elevated prostatic acid phosphatase had a low mean non-adherence index (0.2). Patients with prostatic carcinoma are apparently expressing an antitumor response to prostatic carcinoma but this response is weak even when the clinical stage of the disease seems to be early.This publication has 22 references indexed in Scilit:
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