Age, environmental factors and prostatic cancer

Hill, Peter; Garbaczewski, L.; Walker, Alexander

doi:10.1016/0306-9877(84)90060-4

Cited by 20 publications

(20 citation statements)

References 42 publications

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“…However, our prior findings in a nationally representative sample of US men do not support this hypothesis: we observed that serum testosterone concentration was not statistically significantly different between non-Hispanic black and non-Hispanic white men when taking into account age, percent body fat, alcohol, smoking, and physical activity [3]. Other studies also reported no statistically significant difference [4–13], including in young and adolescent males [14–16], whereas others reported higher testosterone levels in black compared with white men [17–19], including in young adult males (≥18 years) [20, 21]. Although testosterone levels did not differ, in our prior study we observed that non-Hispanic black men had a higher estradiol concentration, especially in young and mid-adulthood, than non-Hispanic white men [3].…”

Section: Introductionmentioning

confidence: 77%

“…Although testosterone levels did not differ, in our prior study we observed that non-Hispanic black men had a higher estradiol concentration, especially in young and mid-adulthood, than non-Hispanic white men [3]. Some studies in older adults [19], young adults [5], and adolescents [14–16, 22] had similar findings, whereas other studies did not find differences in estradiol level between black and white adult, young adult, and adolescent males [8, 9, 18, 20, 21]. …”

Section: Introductionmentioning

confidence: 89%

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Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males

López

Peskoe

Joshu

et al. 2013

Cancer Causes Control

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Objective Contrary to the hypothesis that the racial/ethnic disparity in prostate cancer has a hormonal basis, we did not observe a difference in serum testosterone concentration between non-Hispanic black and white men in the Third National Health and Nutrition Examination Survey (NHANES III), although non-Hispanic black men had a higher estradiol level. Unexpectedly, Mexican-American men had the highest testosterone level. Next, we evaluated whether the same patterns are observed during adolescence, the time of prostate maturation. Methods We measured serum testosterone, estradiol, and sex hormone binding globulin (SHBG) by immunoassay in 134 males aged 12–19 in NHANES III. Mean concentrations were compared by race/ethnicity adjusting for age, Tanner stage, percent body fat, waist, physical activity, tobacco smoke, and the other hormones. Results After multivariable adjustment, in the 12–15 year-old males, testosterone concentration was lower in non-Hispanic blacks than whites (P=0.043), SHBG concentration did not significantly differ between the two groups. Mexican-Americans had the highest testosterone (versus non-Hispanic black: P=0.002) and lowest SHBG (versus non-Hispanic white: P=0.010; versus non-Hispanic black: P=0.047) concentrations. Estradiol concentration was lower in non-Hispanic blacks (P=0.11) and Mexican-Americans (P=0.033) compared with non-Hispanic whites. After multivariable adjustment, in the 16–19 year-old males, testosterone, estradiol, and SHBG concentrations did not differ between non-Hispanic blacks and whites. Mexican-Americans had the highest testosterone concentration (versus non-Hispanic white: P=0.08), but did not differ from the other groups on estradiol and SHBG concentrations. In both age groups, these patterns were generally present, but less pronounced after adjusting for age and Tanner stage only. Conclusion In adolescent males, non-Hispanic blacks did not have a higher testosterone concentration than non-Hispanic whites, and Mexican-Americans had the highest testosterone concentration, patterns similar to adult males.

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Section: Introductionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 89%

Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males

López

Peskoe

Joshu

et al. 2013

Cancer Causes Control

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“…This ratio is significantly lower in African-American men (who have the highest incidence of PCa in the USA), due to higher levels of serum estrogens, compared to Caucasian-American men [23,[26][27][28]. Conversely, the T:E ratio is higher in Japanese men (who are known to have a low risk of PCa), due to lower levels of serum estrogens, compared to Caucasian-Dutch men [29].…”

Section: Estrogens and The Prostatementioning

confidence: 98%

Aromatase and regulating the estrogen:androgen ratio in the prostate gland

Ellem

Risbridger

2010

The Journal of Steroid Biochemistry and Molecular Biology

137

123

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“…21 Indeed, the mechanism of hormonal induction of PCa requires both androgens and estrogens. 36 Furthermore, increased levels of estrogens in men are linked to a higher incidence of PCa: serum levels of estrogens in African American men (who have the highest incidence of PCa in the United States) are significantly higher compared with Caucasian American men, 37 while serum levels of estrogens are lower in Japanese men (who have a low risk of PCa) compared with Caucasian-Dutch men. 38 Significantly, it is again ER␣ that mediates the development of carcinoma in response to estrogen.…”

Section: Estrogens Prostatitismentioning

confidence: 99%

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Ellem

Wang

Poutanen

et al. 2009

The American Journal of Pathology

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Prostatitis causes substantial morbidity to men, through associated urinary symptoms, sexual dysfunction, and pelvic pain; however, 90% to 95% of cases have an unknown etiology. Inflammation is associated with the development of carcinoma, and, therefore, it is imperative to identify and study the causes of prostatitis to improve our understanding of this disease and its role in prostate cancer. As estrogens cause prostatic inflammation, here we characterize the murine prostatic phenotype induced by elevated endogenous estrogens due to aromatase overexpression (AROM؉). Early-life development of the AROM؉ prostate was normal; however, progressive changes culminated in chronic inflammation and pre-malignancy. The AROM؉ prostate was smaller at puberty compared with wild-type controls. Mast cell numbers were significantly increased at puberty and preceded chronic inflammation, which emerged by 40 weeks of age and was characterized by increased mast cell, macrophage, neutrophil, and T-lymphocyte numbers. The expression of key inflammatory mediators was also significantly altered, and premalignant prostatic intraepithelial neoplasia lesions emerged by 52 weeks of age. Taken together, these data link estrogens to prostatitis and premalignancy in the prostate, further implicating a role for estrogen in prostate cancer. These data also establish the AROM؉ mouse as a novel, non-bacterial model for the study of prostatitis. Prostatitis, an exceedingly common condition in the male population worldwide, has an incidence of ϳ9% and a prevalence of ϳ14%, and, unlike benign prostatic hyperplasia and prostate cancer (PCa), which are predominantly diseases of older men, prostatitis afflicts men of all ages. It is also the most common outpatient condition seen in men under 50 years of age and accounts for more clinical visits than either PCa and/or benign prostatic hyperplasia.1,2 At present our knowledge of prostatitis is lacking, with 90% to 95% of cases having an unknown etiology. This represents a significant problem, particularly as prostatitis has also been implicated in the development of PCa.3-5 Given the prevalence of prostatitis and this putative link to PCa, it is vitally important to identify the unknown causes of prostatitis.Several causes of prostatitis have been postulated, including hormonal variation or exposure, infection due to sexually transmitted disease, 6 dietary factors, and physical trauma from urine reflux. 7 However, of particular interest is an apparent link between estrogen and prostatic inflammation, 8 which has emerged mainly from the administration of pharmacological levels of exogenous estrogen to rodents.9 Additional data obtained from further rodent studies show that the prostate gland is particularly sensitive to estrogenic exposure during development in fetal and neonatal life; transient estrogen exposure before puberty results in inflammation later in life, well after the exposure has occurred.10,11 Several decades of research from various laboratories, including our own, has demonstrated that...

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Age, environmental factors and prostatic cancer

Cited by 20 publications

References 42 publications

Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males

Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males

Aromatase and regulating the estrogen:androgen ratio in the prostate gland

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

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