Histopathological evidence for an association of inflammation with ductal pin‐like lesions but not with ductal adenocarcinoma in the prostate of the noble rat

Bernoulli, Jenni; Yatkin, Emrah; Laakso, Arto; Anttinen, Mikael; Bosland, Maarten C.; Vega, Katherine; Kallajoki, Markku; Santti, Risto; Pylkkänen, Liisa

doi:10.1002/pros.20719

Cited by 32 publications

(30 citation statements)

References 43 publications

(58 reference statements)

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“…In agreement with these findings, concomitantly, both inflammatory infiltrations and obstructive voiding with hormonal treatments have also been observed in Nakano model [50]. More recently, Santti's group has been able to demonstrate that elevated estrogens, moreover, T-to-E2 ratio are essential for induction and maintenance of prostatic inflammation and obstructive voiding [55][56][57] in a Noble rat model. Although mechanisms of BOO and non-bacterial prostatitis have not been thoroughly studied, these data demonstrate that exposure of estrogens is closely linked to prostatic inflammation and obstructive voiding.…”

Section: Estrogen Prostatitis and Boosupporting

confidence: 51%

“…Capacity of the bladder, bladder stones and urinary retention had been shown to be increased in adult male mice after a 3-month treatment with DES in some other studies [76,77]. Recently, Santti's group has been able to demonstrate that combination of T and estradiol treatment in Noble rat induces prostatic inflammation and obstructive voiding [55][56][57]. Their findings support the rationale that increased E, moreover, T-to-E ratio is essential for the development of BOO.…”

Section: Steroids Exposed Animalsmentioning

confidence: 96%

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Estrogens and bladder outlet obstruction

Rahman

2010

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Estrogen Prostatitis and Boosupporting

confidence: 51%

Section: Steroids Exposed Animalsmentioning

confidence: 96%

Estrogens and bladder outlet obstruction

Rahman

2010

The Journal of Steroid Biochemistry and Molecular Biology

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“…Early-life BPA exposure was reported to induce persistent immunological effects including augmented T H 2 cytokine production in adult mice [41]. It is known that chronic inflammatory cell infiltration in the prostate leads to proliferative reactions in the epithelium and is suspected to play a role in the process of carcinogenesis itself [42, 43]. The involvement of the immune axis in BPA-treated rats and the role of inflammatory cells in prostate carcinogenesis is an area of active investigation in several laboratories and the specific interactions between BPA, estradiol, inflammatory responses and prostatic carcinogenesis warrants detailed examination in future studies.…”

Section: 4 Discussionmentioning

confidence: 99%

Serum bisphenol A pharmacokinetics and prostate neoplastic responses following oral and subcutaneous exposures in neonatal Sprague–Dawley rats

Prins

Birch

et al. 2011

Reproductive Toxicology

132

103

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The present study examines BPA pharmacokinetics in neonatal rats following s.c. injection or oral delivery of 10μg BPA/kg BW and compares susceptibility to estrogen-induced prostate intraepithelial neoplasia (PIN) following either exposure route. Serum BPA in PND3 rats was measured using HPLC-MS-MS. Free and total BPA at Cmax were 1.77 and 2.0 ng/ml, respectively following injection and 0.26 and 1.02 ng/ml, respectively following oral exposure. The AUC0-2 for free and total BPA was 4.1-fold and 1.8-fold greater, respectively, in s.c. versus oral delivery. While exposure route affected BPA metabolism, internal dosimetry following s.c. injection of 10μg BPA/kg BW is similar to BPA levels observed in humans. Prostates from aged rats given s.c. or oral BPA neonatally and T+E implants as adults exhibited nearly identical, heightened susceptibility to PIN incidence and score as compared to neonatal oil-controls. These findings on prostate health are directly relevant to humans at current BPA exposure levels.

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“…56-58 Another potential culprit associated with estrogen-induced/promoted PCa is hormone-induced chronic inflammation, 38;59-61 although this view is not uniformly supported by all studies. 62 …”

Section: Epidemiologic and Animal-model Studies Of The Relationship Bmentioning

confidence: 99%

Estrogens and Prostate Cancer: Etiology, Mediators, Prevention, and Management

Lee

Lam

et al. 2011

Endocrinology and Metabolism Clinics of North America

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The relationship between hormones and the pathogenesis of prostate cancer (PCa) has been studied extensively. All the mainstay targets for hormonal PCa therapies are based on negating androgen action. Recent epidemiologic and experimental data have clearly pinpointed the key roles of estrogens in PCa development and progression. Racial and geographical differences, as well as age-associated changes, in estrogen synthesis and metabolism contribute significantly to the etiology by increasing the ratio of circulating estrogen to androgen, sex hormone binding globulin synthesis, and aromatase activity and reducing androgen glucuronidation and tissue bioactivation. Promotion of aberrant cell growth, evasion of apoptosis, increased oxidative stress and inflammation, and gains in adiposity and bioactivation to genotoxic carcinogens during adulthood are probable mechanisms of estrogen carcinogenicity, while “estrogen imprinting” via epigenetics in early-life also determines PCa risk. Although the effects of estrogens are known to be mediated by genomic actions of the two estrogen receptor (ER) subtypes (ERα and ERβ), other non-canonical mediators, including the different ERβ isoforms, membrane and mitochondrial ERs, and G protein-coupled receptor 30, may have major actions diverging from classical ER actions. These new discoveries have led to renewed interest among the public and the medicinal field in estrogens and antiestrogens as singular and adjuvant PCa treatment and prevention regimens. This review summarizes current knowledge on how different estrogens/antiestrogens/estrogen mimics contribute to prostate carcinogenesis, the roles of the different mediators of estrogen in the process, and the potentials of new estrogenic/antiestrogenic compounds as targeted therapies for prevention and treatment of PCa.

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Histopathological evidence for an association of inflammation with ductal pin‐like lesions but not with ductal adenocarcinoma in the prostate of the noble rat

Cited by 32 publications

References 43 publications

Estrogens and bladder outlet obstruction

Estrogens and bladder outlet obstruction

Serum bisphenol A pharmacokinetics and prostate neoplastic responses following oral and subcutaneous exposures in neonatal Sprague–Dawley rats

Estrogens and Prostate Cancer: Etiology, Mediators, Prevention, and Management

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