Plasma Steroid and Protein Hormone Concentrations in Patients With Prostatic Carcinoma, Before and During Oestrogen Therapy

Abstract

Plasma testosterone, androstenedione, oestradiol-17β, follicle stimulating hormone (FSH) and luteinizing hormone (LH) were not significantly different in patients with prostatic cancer, with benign prostatic hyperplasia or in patients without prostatic disease. Plasma prolactin concentrations were significantly lower in the patients with benign disease than those with prostatic carcinoma. Endocrine therapy in the form of stilboestrol administration significantly decreased plasma levels of testosterone, oestradiol-17β, FSH and LH within 7 days of the treatment. After 7 days therapy prolactin levels increased significantly in all patients studied. Changes in growth hormone concentrations were more varied in response to stilboestrol, being elevated in several patients and remaining unchanged in others. Treatment of a few prostatic carcinoma patients who were receiving stilboestrol therapy with CB154, an inhibitor of prolactin secretion, brought an immediate decrease in prolactin levels which was sustained. Plasma testosterone, androstenedione and growth hormone were unchanged in these patients but a significant decrease in plasma oestradiol-17β was noted in two patients during CB154 administration.

Serum pituitary and sex steroid hormone levels in the etiology of prostatic cancer – a population-based case-control study

“…In contrast to several previous studies (Harper et al, 1976;Bartsch et al, 1977b;Hammond et al, 1978;Habib, 1980;Saroff et al, 1980;H0isaeter et al, 1982;Zumoff et al, 1982;Ranikko & Adlercreutz, 1983;Hulka et al, 1987), the control group was population-based and prostate cancer was ruled out by digital rectal examination and serum analysis for prostate-specific antigen. Serum samples were drawn, stored and analysed according to highly standar- dised routines.…”

“…In general such comparisons have given conflicting results. Plasma testosterone levels in patients with prostatic cancer have been reported to be both higher than (Ghanadian et al, 1979;Jackson et al, 1980;Ahluwalia et al, 1981;Drafta et al, 1982), similar to (Young & Kent, 1968;Harper et al, 1976;Bartsch et al, 1977a;Bartsch et al, 1977b;Hammond et al, 1978;Habib, 1980;H0isaeter et al, 1982;Ranikko & Adlercreutz, 1983;Levell et al, 1985;Nomura et al, 1988;Hsing & Comstock, 1989;Barrett-Connor et al, 1990) and lower than (Jackson et al, 1980;Ahluwalia et al, 1981;Hill et al, 1982;Meikle & Stanish, 1982;Zumoff et al, 1982;Levell et al, 1985;Meikle et al, 1985) those in healthy controls. Similarly, conflicting results have been reported for estradiol (Harper et al, 1976;Bartsch et al, 1977a;Bartsch et al, 1977b;Hammond et al, 1978;Jackson et al, 1980;Jacobi et al, 1980;Ahluwalia et al, 1981;Drafta et al, 1982;Hill et al, 1982;H0isaeter et al, 1982;Meikle & Stanish, 1982;Ranikko & Adlercreutz, 1983;Hulka et al, 1987;Nomura et al, 1988;Hsing & Comstock, 1989;…”

“…In two instances, steroid hormone levels were analysed in serum samples stored for a number of years before the disease was manifested, using a nested case-control design (Nomura et al, 1988;Barrett-Connor et al, 1990). In general, however, serum samples were drawn at the time of diagnosis of the cases (Harper et al, 1976;Bartsch et al, 1977a;Bartsch et al, 1977b;Hammond et al, 1978;Ghanadian et al, 1979;Habib, 1980;Jackson et al, 1980;Saroff et al, 1980;Ahluwalia et al, 1981;Drafta et al, 1982;Hill et al, 1982;H0isaeter et al, 1982;Meikle & Stanish, 1982;Zumoff et al, 1982;Ranikko & Adlercreutz, 1983;Meikle et al, 1985;Hulka et al, 1987;Hsing & Comstock, 1989). In general such comparisons have given conflicting results.…”

A critical analysis of tumor morphology and hormone treatments in the untreated and estrogen-treated responsive and refractory human prostatic carcinoma

“…21 Recently Harper et a1. 22 concluded that the LH, FSH and testosterone levels were within normal range in the cancer patients. Tissue culture experiments have shown that the growth of cancer cells was not androgen dependent. "…”

Hormonal regulation of H19 gene expression in prostate epithelial cells

“…The PRL receptors are detected in benign prostate hyperplasia and highly synthesized in dysplasia, but only slightly in higher-grade carcinomas (Leav et al 1999). A high blood concentration of PRL in some prostate cancer patients has been reported (Harper et al 1976, Horti et al 1998. Although Stattin et al (2001) have established only a slight correlation between hyperprolactinemia and increased risk of prostate cancer in men, Ben-Jonathan et al (2002) recently reported that PRL increases prostate weight and promotes development of dysplasia and adenocarcinoma of the dorsolateral lobe of the rat prostate.…”