Blood hormone profiles in prostate cancer patients in high-risk and low-risk populations

Abstract

Epidemiologic data reveal that the incidence rate of prostate gland carcinoma among the black population in the United States (US) is several times higher than among Nigerians. A collaborative study between the two countries was undertaken, and blood hormone (testosterone [T], dihydrotestosterone [DHT], estrone [E1], estradiol [E2], and prolactin [P1]), total acid phosphatase (TP), and prostatic acid phosphatase (PAP) profiles in the two population groups were compared. In the US groups (patients and controls) there were significantly higher levels of T (P less than 0.01) and E1 (P less than 0.05) compared with the Nigerians. Also, the US patients had significantly higher levels of T (P less than 0.05) and E1 (P less than 0.01) compared with their matched controls. In the Nigerians T but not E1 levels were significantly lower (P less than 0.05) in patients compared with controls. DHT, E2, and P1 were not significantly different in patients and controls between and within the populations. Nigerian patients had higher levels (P less than 0.001) of TP and PAP compared with US patients. It is concluded that differences in blood hormone profiles in the two population groups are based on factors other than the genetic makeup of the populations.

Vasectomy, cigarette smoking, and age at first sexual intercourse as risk factors for prostate cancer in middle-aged men

“…The growth and development of the prostate is under the control of testosterone and its metabolite dihydrotestosterone, and there is considerable evidence supporting a hormonal etiology for prostate cancer (Noble, 1982;Ghanadian et al, 1978;Ahluwalia et al, 1981;Drafta et al, 1982;Ross et al, 1986). Our data on hormone levels in vasectomized and non-vasectomized men provide limited support that the observed effect of vasectomy may have a hormonal basis.…”

Catechol-O-methyltransferase Gene Polymorphisms in Benign Prostatic Hyperplasia and Sporadic Prostate Cancer

“…Additionally, aromatase has been shown to be present in human prostate, which could provide a local source of estrogen via testosterone (6,7), and epithelial levels of estrogens are higher compared with stromal levels in normal prostates (8). Interestingly within African Americans, prostate cancer patients displayed a significantly elevated level of estrone compared with matched controls (9). In addition to the malignant form, benign prostatic hyperplasia (BPH) has also been shown to have significantly elevated estradiol and estrone levels and is correlated with age (8); and this increase seems to be associated with prostate volume (10).…”

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

“…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.…”

“…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;…”