Steroid Hormones and the Pathogenesis of
Benign Prostatic Hyperplasia

Griffiths, K.; Eaton, Colby L.; Harper, M. E.; Peeling, B; Davies, P.

doi:10.1159/000471750

Cited by 50 publications

(32 citation statements)

References 39 publications

(49 reference statements)

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“…Prostatic hyperplasia in dogs appears to be pure proliferation of epithelial cells (7,9,18). Our findings are also supported by Isaacs (9), who states that hyperplasia in the canine prostate involves more the glandular compartment than the stroma.…”

Section: Discussionmentioning

confidence: 99%

“…The results of some studies show that canine BPH is present either grossly or microscopically in almost 100% of sexually-intact adult male dogs over the age of seven years (9,10,13). The peripheral region of the canine prostate is little different from the periurethral region (5,7,13). The acini in the peripheral region are grosser and more abundant than in the periurethral region, the ducts here are narrower and longer, and aberrant ducts can be found in this region.…”

Section: Introductionmentioning

confidence: 99%

“…The canine prostate is grossly and microscopically homogeneous (16). It has been theorised that because of different tissue sensitivity to sexual hormones and various growth factors, BPH in the canine prostate involves the peripheral region more (6,7). Strong relationships between some pathologies and prostate regions have not been established.…”

Section: Introductionmentioning

confidence: 99%

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Histomorphometric study of the canine prostate during ageing and in cases of benign prostate hyperplasia

Juodžiukynienė

Aniulienė

2016

Journal of Veterinary Research

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Introduction: The aim of the study was to examine the percentage volume of epithelium, acini, and interstitial collagen in the nonhyperplastic canine prostate and in cases of epithelial and epithelial cystic hyperplasia. Material and Methods: A histomorphometric study of 39 prostates was performed using computer image analysis. Results: The highest percentage volume of epithelium was found in cases of epithelial hyperplasia (47.8 %) and epithelial cystic hyperplasia was the correlate for acini (48.97 %). Epithelium decreased with dogs' age (P < 0.01), whereas acini increased (P < 0.01). Interstitial collagen varied only insignificantly across age groups, but collagen was higher (12.1 %) in the nonhyperplastic prostates. With age cystic formation progressed in the canine prostate, the percentage volume of epithelium decreased and that of acini increased, but this same parameter in prostatic collagen did not change distinctly. The epithelium percentage volume increased in cases of epithelial hyperplasia but the cystic variant caused an increase in acinar volume. Conclusion: As dogs age, cystic formation progresses in the prostate, therefore the volume of epithelium decreases and that of acini increases. The volume of prostatic collagen did not change distinctly with age, and was higher in normal prostates than in both epithelial and epithelial cystic hyperplastic glands.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Histomorphometric study of the canine prostate during ageing and in cases of benign prostate hyperplasia

Juodžiukynienė

Aniulienė

2016

Journal of Veterinary Research

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“…One assumes that only prostate tissue DHT levels are critical in the causation of BPH, and that these levels are poorly associated with plasma DHT levels; this as sumption has considerable empirical support [3,10,11]. The other possible explanation is that DHT, or its precur sor T, could have a permissive role and that other hor mones, growth factors, or physiologic processes are needed to interact with DHT for the development of BPH [12,13],…”

Section: Kargermentioning

confidence: 99%

Serum Steroids in Relation to Benign Prostatic Hyperplasia

Λάγιου

Mantzoros²,

Τζώνου³

et al. 1997

Oncology

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In order to investigate the endocrine etiology of benign prostatic hyperplasia (BPH), we conducted a case-control study in Athens, Greece using 52 patients with histologically confirmed BPH and 52 healthy controls matched according to age and town of residence. Blood samples were collected from all participants and analyzed blindly in Boston, Mass. regarding testosterone (T), dihydrotestosterone, estradiol (E2), sex hormone-binding globulin, and dehydroepiandrosterone sulfate (DHEAS). Results from logistic regression models, adjusting for age, height, body mass index, years of schooling, and mutually among the measured hormones, indicate that DHEAS is significantly positively associated with the risk of BPH [odds ratio = 3.10 per standard deviation (60 ixg/dl), 95% confidence interval (1.28,7.50)]. T and E2 were not significantly related to the risk of BPH.

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“…Androgens play a key role in prostate development, maturation, homeostasis, and pathogenesis including benign prostatic hyperplasia (BPH) and prostate cancer [1][2][3][4]. Androgen action is mediated through the androgen receptor (AR), a ligand-regulated transcription factor that regulates the expression of many androgen-responsive genes [5,6].…”

Section: Introductionmentioning

confidence: 99%

Gene Expression Profiling Reveals Regulation of ERK Phosphorylation by Androgen-Induced Tumor Suppressor U19/EAF2 in the Mouse Prostate

Corrêa

Luo

et al. 2013

Cancer Microenvironment

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U19/EAF2 is regulated by androgens in the prostate and capable of regulating transcriptional elongation of RNA Pol II via interaction with the ELL family proteins. Inactivation of U19/EAF2 induces tumorigenesis in multiple organs; however the mechanism of U19/EAF2 tumor suppression remains unclear. To elucidate potential mechanisms of U19/EAF2 action, we performed cDNA microarray analysis and identified 164 mRNA transcripts regulated by U19/EAF2 in the mouse ventral prostate. Bioinformatics analysis indicated that U19/EAF2 knockout activates the RAS-BRAF-ERK signaling pathway, which is known to play important roles in carcinogenesis. qPCR verified increased expression of BRAF mRNA, and immunostaining and Western blot analysis demonstrated increased expression of p-ERK at the protein level suggested U19/EAF2 knockout activates this important pathway. These findings indicate that loss of EAF2 up-regulates transcription of RAS cascade genes including Grb2, PI3K, and BRAF, leading to elevated p-ERK levels, which may represent a major functional role of U19/EAF2 in the prostate. Furthermore, these observations suggest that U19/EAF2 is a key player in crosstalk between androgen receptor and the RAS-BRAF-ERK signaling pathway.

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Steroid Hormones and the Pathogenesis of Benign Prostatic Hyperplasia

Cited by 50 publications

References 39 publications

Histomorphometric study of the canine prostate during ageing and in cases of benign prostate hyperplasia

Histomorphometric study of the canine prostate during ageing and in cases of benign prostate hyperplasia

Serum Steroids in Relation to Benign Prostatic Hyperplasia

Gene Expression Profiling Reveals Regulation of ERK Phosphorylation by Androgen-Induced Tumor Suppressor U19/EAF2 in the Mouse Prostate

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