Modulatory effects of oestrogen on immunologic responsiveness. I. Inhibition of DNA synthesis in peripheral blood lymphocytes from patients with Peyronie's disease, prostatic cancer and transsexuals and a commentary.

A reduction in the phytohaemagglutinin-induced transformation of peripheral blood lymphocytes from patients with Peyronie's disease and prostate cancer and transsexuals cultured in autologous and homologous serum following the receipt of oestrogen therapy has been observed. Reduction of lymphocyte transformation in patients with prostatic cancer and without malignancy receiving oestrogen, i.e., Peyronie's disease and transsexuals, suggests that this reduction is related to the mode of therapy rather than to malignancy or a particular pathologic state. No direct evidence exists that the observed in vitro aberrations of lymphocytic responsiveness are reflective of host compromise, but these observations are of potential relevance in terms of their implications in the therapeutic management of patients with prostatic cancer and other hormonally-dependent tumours, e.g., of the breast, as well as responsive diseases, through their effect on cellular immunocompetence and suitability of hormonally treated patients as prospective candidates for adjuvant immunotherapy. The possible relevance of the present observations to the suggested association between uterine cancer and prolonged administration of diethylstilboesterol, as well as that between development of vaginal tumours in offspring and maternal ingestion during pregnancy, also remains of potential concern, pending further investigation.

Hormonal therapy and alteration of lymphocyte proliferation.

Suppression of the blastogenic response of phytohemagglutinin-stimulated peripheral blood lymphocytes in autologous serum obtained from patients with prostatic cancer. Peyronie's disease, and transsexuals following estrogen therapy has been observed. Observations of suppression of blastogenesis in patients with prostatic cancer and without malignancy receiving estrogen suggests that this suppression would appear not to be associated with a particular pathologic state or malignancy per se but, rather, the given mode of therapy. The relevance of these observations to the effect of estrogen on cell-mediated responsiveness in patients with hormonally dependent tumors and to the suggested association between uterine cancer and prolonged administration of diethylstilbesterol and the development of vaginal tumors in offspring found in association with material ingestion during pregnancy remains speculative.