Estrogen Receptor in Human Benign Prostatic Hyperplasia

Donnelly, Bryan J.; Lakey, William H.; McBlain, William A.

doi:10.1016/s0022-5347(17)51020-4

Cited by 40 publications

(15 citation statements)

References 22 publications

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“…In published studies on the quantitation of PgRC in human prostatic tissue, no consistent differences have been noted between the mean values for BPH and carcinoma tissue [9,11,34]. Our values are in a similar range to those formerly observed, but using the DCC method, we found that untreated carcinoma specimens with >70% malignant involvement had a significantly lower mean PgRC than the BPH specimens.…”

Section: Discussionsupporting

confidence: 48%

“…In female target organs for estrogen, the induction of progesterone receptor (PgR) synthesis is known to be a marker of estrogenic activity. Significant concentrations of PgR have been observed in human prostatic tissue [e.g., 7,9,11,, but the relationship between PgR and ER in the human prostate has not been explored. We have previously demonstrated marked increases in PgR content in response to estrogen treatment in the R3327 H and HI lines of the Dunning experimental rat prostatic tumor, which has been extensively used as a model for the human disease [ 191.…”

Section: Introductionmentioning

confidence: 99%

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Quantitation of cytosolic and nuclear estrogen and progesterone receptor in benign, untreated, and treated malignant human prostatic tissue by radioligand binding and enzyme‐immunoassays

1990

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Estrogen receptor (ER) and progesterone receptor (PgR) were quantitated in benign and malignant human prostatic tissue by using radioligand binding assays (RBA) and enzyme-immunoassays (EIA). Using a hydroxylapatite exchange method for ER, little or no nuclear ER (ERN) could be detected, but with the EIA both cytosolic (ERC) and ERN were detected in almost all specimens, although in meager concentrations. Tissue from patients with carcinoma had significantly higher ERC concentrations than tissue from patients with benign disease. Specimens from estrogen-treated patients had significantly lower ERC:ERN ratios than those from untreated patients. Progesterone receptor was detected in virtually all specimens by both methods, at concentrations higher than those of ER. Carcinoma tissue with a high malignant involvement contained significantly less PgR than benign tissue. Using either method, the highest concentrations of PgR were observed in tissue from carcinoma patients treated with estrogen. Overall, the data suggest that although human prostatic tissue contains only modest amounts of ER, this is active in that treatment with estrogen promotes association of this receptor with the nuclear fraction and increases PgR content.

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Section: Discussionsupporting

confidence: 48%

Section: Introductionmentioning

confidence: 99%

Quantitation of cytosolic and nuclear estrogen and progesterone receptor in benign, untreated, and treated malignant human prostatic tissue by radioligand binding and enzyme‐immunoassays

1990

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“…These findings are in agreement with the results of a previous investigation of normal human prostates, demonstrating very low ER content using the same DCC analysis (1). Different biochemical methods have been used in studies of ERs in the human prostate, including the hydroxyapatite (HAP) assay (6,12,13,(23)(24)(25)(26) (Table II). Generally in these studies, the samples have been small, ERs have not been detectable in all specimens, and when demonstrated, they have been found in small quantities.…”

Section: Discussionsupporting

confidence: 89%

Estrogen Receptors in the Human Male Prostatic Urethra and Prostate in Prostatic Cancer and Benign Prostatic Hyperplasia

Bødker

Bruun²,

Balslev³

et al. 1999

Scandinavian Journal of Urology and Nephrology

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Estrogen receptors (ERs) in the prostate and prostatic urethra were examined in 33 men with benign prostatic hyperplasia (BPH) and in 11 with prostate cancer (PC). The Abbot monoclonal ER-ICA assay was used for immunohistochemical investigation. In the BPH group, ERs were revealed in the prostatic stroma in eight cases and in the glandular epithelium in one. In four cases ERs were seen in the prostatic stroma and in the glandular epithelium. In the prostatic urethra, ERs were found in 19 cases located in the urothelium, lamina propria and/or periurethral glands. In the PC group, ERs were demonstrated in the prostatic stroma and/or prostatic urethra in 6 out of 11 cases. In both BPH and PC patients, immunoreactivity was weak and confined to few cells, indicating low ER content in the prostate as well as in the prostatic urethra. Dextran-coated charcoal (DCC) analysis was used for detection and quanticization of cytosolic and nuclear ERs. In the BPH group, ERs were detected once in the prostate and prostatic urethra in the nuclear and cytosol, and additionally in the prostatic urethra in the cytosol fraction in three cases. In all cases, ER content was low, ranging from 10-15 fmol/mg protein. In the PC group, ERs were detected in the prostatic urethra and/or prostate in the cytosol fraction from two patients. The contents were low, ranging from 10-13 fmol/mg protein. We conclude that in human BPH and PC, ERs can be present in the prostate and prostatic urethra. In the prostate, ERs are mainly located in the stroma, but in BPH specimens they can also be found in the glandular epithelium. Biochemically, the use of the DCC analysis is of limited value, since ER content in the human prostate and prostatic urethra is at the limit of detection with this method.

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“…Although early studies demonstrated the presence of ER in normal prostate and prostate cancer tissues in both human and rodents, no correlation between their levels and any clinicopathological parameters has been reported. 7,25,26) Estrogen's effects on the prostate have been postulated to be indirect, possibly through the hypothalamic-pituitary-testis axis, until recently. Interest in ER and its roles in the prostate gland were recently revived by the cloning and characterization of ERβ.…”

Section: Discussionmentioning

confidence: 99%

Estrogen enhancement of androgen‐responsive gene expression in hormone‐induced hyperplasia in the ventral prostate of F344 rats

et al. 2004

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It has been postulated that, in addition to the crucial role of androgens, estrogens may be involved in development of prostate hyperplasia and cancer. In rats, combined administration of estrogen and androgen synergistically increases ventral prostate weight, and continued treatment results in the development of glandular hyperplasia. Prostate adenocarcinoma can be induced by chemical carcinogens in rats, and estrogen given together with an androgen generally shortens the latent period or increases the incidence and/or multiplicity of carcinomas. However, the mechanisms responsible for these synergistic effects of estrogen and androgen are poorly understood. In the present study, we examined the combined effects of 17β β β β-estradiol (E2) and testosterone (T) on gene expression in an early stage of prostate hyperplasia in an F344 rat model. ERα α α α expression, which has been suggested to contribute to development of prostatic hyperplasia, was increased by the combined treatment with T and E2, while it was suppressed by T alone. Expression levels of two androgen-responsive genes, probasin and kallikrein S3, were increased in the ventral prostate of rats treated with T plus E2 for 4 weeks in a dose-dependent manner, while short-term treatment did not alter the expression. These results suggested that enhancing effects of E2 on transcription of androgen-responsive genes, as well as an increased level of ERα α α α may play roles in the synergistic effects of E2 on T-induced prostate hyperplasia. ndrogen plays a crucial role in development of benign prostatic hyperplasia (BPH) and prostate cancer (PC), but it has been postulated that estrogens may also be involved. In humans, BPH is known to be linked with both serum estrogen levels and urinary estrogen content.1, 2) Canine BPH is inducible by simultaneous administration of androstanediol and estradiol, 3) and in rats, administration of estrogen concomitantly with androgen promotes prostate growth. 4) Furthermore, combined estrogen and androgen treatment enhances prostate carcinogenesis in Noble rats and in chemical carcinogen-treated F344 rats.5, 6) Radioligand-binding assays and immunohistochemical studies with ERα antibodies have demonstrated the presence of ER in both BPH and prostate carcinomas, but with no apparent correlation between receptor levels and pathologic features.7) The discovery of ERβ has given rise to a new understanding of the physiological roles of ER. 8,9) In ERβ knockout mice, multiple hyperplastic foci are observed in the ventral prostate 10) and immunohistochemical studies in human prostate cancer have provided evidence of decreased ERβ expression in human BPH and PC. 11,12) These findings suggest that estrogen receptors are involved in regulating cell proliferation and in carcinogenesis in the prostate gland.In the present study, we examined the combined effects of 17β-estradiol (E2) and testosterone (T) on gene expression in an early stage of prostate hyperplasia in an F344 rat model. RNAs isolated from the ventral prostate tissue wer...

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Estrogen Receptor in Human Benign Prostatic Hyperplasia

Cited by 40 publications

References 22 publications

Quantitation of cytosolic and nuclear estrogen and progesterone receptor in benign, untreated, and treated malignant human prostatic tissue by radioligand binding and enzyme‐immunoassays

Quantitation of cytosolic and nuclear estrogen and progesterone receptor in benign, untreated, and treated malignant human prostatic tissue by radioligand binding and enzyme‐immunoassays

Estrogen Receptors in the Human Male Prostatic Urethra and Prostate in Prostatic Cancer and Benign Prostatic Hyperplasia

Estrogen enhancement of androgen‐responsive gene expression in hormone‐induced hyperplasia in the ventral prostate of F344 rats

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