Inflammatory mediators in the development and progression of benign prostatic hyperplasia

Nunzio, Cosimo De; Presicce, Fabrizio; Tubaro, Andrea

doi:10.1038/nrurol.2016.168

Cited by 164 publications

(167 citation statements)

References 102 publications

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“…Inflammation also seems to have a role in the development of BPH 106 , but BPH does not display substantial telomere shortening in contrast to HGPIN and prostate cancer 39,47 . Presumably, the telomerase activity in the postulated epithelial progenitor cells and stem-like cells in BPH would not safeguard against genomic insults from ROS.…”

Section: Telomeres and Genomic Alterationsmentioning

confidence: 99%

Telomeres and telomerase in prostate cancer development and therapy

Graham

Meeker

2017

Nat Rev Urol

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Aberrations in telomere biology are among the earliest events in prostate cancer tumorigenesis and continue during tumour progression. Substantial telomere shortening occurs in prostate cancer cells and high-grade prostatic intraepithelial neoplasia. Not all mechanisms of telomere shortening are understood, but oxidative stress from local inflammation might accelerate prostatic telomere loss. Critically short telomeres can drive the accumulation of tumour-promoting genomic alterations; however, continued telomere erosion is unsustainable and must be mitigated to ensure cancer cell survival and unlimited replication potential. Prostate cancers predominantly maintain telomeres by activating telomerase, but alternative mechanisms of telomere extension can occur in metastatic disease. Telomerase activity and telomere length assessment might be useful in prostate cancer diagnosis and prognosis. Telomere shortening in normal stromal cells has been associated with prostate cancer, whereas variable telomere lengths in prostate cancer cells and telomere shortening in cancer-associated stromal cells correlated with lethal disease. Single-agent telomerase-targeted treatments for solid cancers were ineffective in clinical trials but have not been investigated in prostate cancer and might be useful in combination with established regimens. Telomere-directed strategies have not been explored as extensively. Telomere deprotection strategies have the advantage of being effective in both telomerase-dependent and telomerase-independent cancers. Disruption of androgen receptor function in prostate cancer cells results in telomere dysfunction, indicating telomeres and telomerase as potential therapeutic targets in prostate cancer.

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Section: Telomeres and Genomic Alterationsmentioning

confidence: 99%

Telomeres and telomerase in prostate cancer development and therapy

Graham

Meeker

2017

Nat Rev Urol

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“…In the present study, treatment of rats with testosterone propionate for 28 days increased prostate weight and prostate index as well as levels of serum testosterone and PSA, indicating BPH [1]. In addition, testosterone increased levels of prostate MDA and reduced GSH, SOD, and catalase activity, suggestive of oxidative stress.…”

Section: Discussionmentioning

confidence: 50%

“…Benign prostatic hyperplasia (BPH) is the most common urological disease in elderly men, affecting well over 42% of men in their 50s and more than 80% of octogenarians [1]. BPH is a chronic, slowly progressive disease which begins as a simple micronodular hyperplasia that evolves into macroscopic nodular enlargement [2].…”

Section: Introductionmentioning

confidence: 99%

Potential of <b><i>Moringa oleifera</i></b> in the Treatment of Benign Prostate Hyperplasia: Role of Antioxidant Defence Systems

et al. 2017

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Objective: This study sought to evaluate the protective effect of ethanolic leaf extract of Moringa oleifera on testosterone-induced benign prostatic hyperplasia (BPH) in male Sprague-Dawley rats. Materials and Methods: BPH was induced in rats by the administration of testosterone propionate (3 mg/kg, s.c., in olive oil) for 4 weeks. M. oleifera (50, 100, or 200 mg/kg), celecoxib (20 mg/kg), or M. oleifera (50 mg/kg) + celecoxib (20 mg/kg) were orally administered daily 15 min before testosterone. On day 29, blood was collected to measure the levels of serum testosterone and prostate-specific antigen before the animals were sacrificed. The prostates were weighed, assayed, and histologically examined. Results: M. oleifera significantly reduced the testosterone-induced increase in prostate weight (20.16%), prostate index (65.85%), serum testosterone (72.86%), and prostate-specific antigen (48.49%). Testosterone caused a significant increase in malondialdehyde (73%) as well as a reduction in glutathione (62.5%), superoxide dismutase (50%), and catalase (64%) activities which were attenuated by M. oleifera with a peak effect obtained at 100 mg/kg. The disruption of prostate histoarchitecture by testosterone was also ameliorated by M. oleifera. Conclusion: M. oleifera prevented testosterone-induced BPH through enhancement of antioxidant defence mechanisms, and hence could be used as an adjunct in the treatment of BPH.

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“…Wang et al (21) also found cyclooxygenase 2 (COX-2) expressed in macrophages and epithelial prostate cells within significant inflammation. Under certain conditions, if high level of T-lymphocytes is reached, surrounding cells are killed by CD8+ cytotoxic T cells and prostatic tissue is replaced by fibromuscular nodules (9, 12). Local hypoxia and inflammation also promote fibroblast to myofibroblast transformation, which leads to extracellular changes forming suitable microenvironment for continuous inflammation (9, 13, 22).…”

Section: Bph and Inflammationmentioning

confidence: 99%

“…Local hypoxia and inflammation also promote fibroblast to myofibroblast transformation, which leads to extracellular changes forming suitable microenvironment for continuous inflammation (9, 13, 22). Inflammation is also continuously stimulated by androgens and changes within metabolic syndromes, but exact pathways are still mostly unknown (12, 23, 24). …”

Section: Bph and Inflammationmentioning

confidence: 99%

Inflammation in Prostatic Hyperplasia and Carcinoma—Basic Scientific Approach

et al. 2017

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Chronic inflammation is associated with both benign conditions and cancer. Likewise, inflammatory cells are quite common in benign prostatic hyperplasia (BPH) and prostatic tissue harboring cancer. Triggers that activate inflammatory pathways in the prostate remain a subject of argument and are likely to be multifactorial, some of these being bacterial antigens, different chemical irritations, and metabolic disorders. Acute and chronic inflammation in prostate leads to accumulation of immunocompetent cells, mainly T lymphocytes and macrophages, but also neutrophils, eosinophils, and mast cells, depending on the type of offending agent. Inflammatory processes activate hyperproliferative programs resulting in nodules seen in BPH, but are also important in creating suitable microenvironment for cancer growth and progression. Inflammatory cells have mostly been shown to have a protumoral effect such as tumor-associated macrophages, but some cell types such as mast cells have antitumoral effects. This review outlines the recent findings and theories supporting the role of inflammatory responses as drivers of both benign and malignant epithelial processes in the prostate gland.

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Inflammatory mediators in the development and progression of benign prostatic hyperplasia

Cited by 164 publications

References 102 publications

Telomeres and telomerase in prostate cancer development and therapy

Telomeres and telomerase in prostate cancer development and therapy

Potential of <b><i>Moringa oleifera</i></b> in the Treatment of Benign Prostate Hyperplasia: Role of Antioxidant Defence Systems

Inflammation in Prostatic Hyperplasia and Carcinoma—Basic Scientific Approach

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