The Etiology and Pathophysiology Genesis of Benign Prostatic Hyperplasia and Prostate Cancer: A New Perspective

Phua, Teow J.

doi:10.3390/medicines8060030

Cited by 17 publications

(21 citation statements)

References 321 publications

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“… 10 New insights into their pathogenesis are related to prostate ageing degeneration, including the testosteron-vasculars-inflation-aging triad, as well as the cellular biological regulation of amyloidosis and autophagy. 10 In addition, we note that adaptive landscapes of benign hyperplasia or malignant tissue may change when resource availability or the environment changes in favor of a subpopulation that happens to be better able to adapt to these new conditions. 11 In the context of aging, the resources and environment around cells are constantly changing.…”

Section: Discussionmentioning

confidence: 99%

Investigation of Lymphocyte Subsets in Peripheral Blood of Patients with Benign Prostatic Hyperplasia

Lin

et al. 2021

IJGM

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To investigate the immune profiles in benign prostatic hyperplasia, changes in the absolute number of lymphocyte subsets and the proportion of T lymphocyte subsets were detected. Methods: Absolute value of lymphocyte subsets in peripheral blood (T, B and NK cells) and the proportion of T lymphocyte (native CD4 + T cell, memory CD4 + T cell, CD8 + CD28 + T cell, CD8 + CDDR + T cells and CD8 + CD38 + T cell) were measured by flow cytometry. Results:The absolute values of CD3 + T cell (972.55±330.31 vs 1757.99±439.38), CD4 + T cell (656.43±252.39 vs 899.30±262.10), and CD8 + T cell (301.97±147.76 vs 728.45 ±230.34) in patients with benign prostatic hyperplasia were significantly reduced (all P<0.05). There was no significant difference in NK cell (285.58±182.84 vs 528.92 ±208.17) and B cell (186.66±86.62 vs 334.17±130.46). The proportion of naive CD4 + T cell (3.75±0.50 vs 8.54±1.61) in T lymphocyte subsets in patients with BPH was significantly reduced (P<0.05). There was no significant difference in memory CD4 + T cell (87.9±6.37 vs 92.63±5.94), CD8 + CD28 + T cell (60.52±13.86 vs 64.32±12.78), CD8 + CDDR + T cell (36.58±12.87 vs 31.92±8.54) and CD8 + CD38 + T cell (2.1±1.90 vs 2.55±2.01). Conclusion:Immune dysfunction raised the risk of viral infection, inflammatory stimulation, and tumor induction in prostate cells, leading to hyperplasia, and immune non-response was potentially a key factor in the transformation of BPH into prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Investigation of Lymphocyte Subsets in Peripheral Blood of Patients with Benign Prostatic Hyperplasia

Lin

et al. 2021

IJGM

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“…In this context, prostate cancer (PCa) represents the second most frequent cancer in men, accounting for 1.4 million (7.3%) of newly diagnosed cases and being in the top five most diagnosed neoplasms [1]. As observed in other cancers, the accumulation of many somatic genetic and epigenetic changes sustains prostate tumorigenesis and progression, but the molecular basis of this disease is still unsolved [2]. The epithelial compartment is widely recognized as the site of origin for PCa, although it is not clear which is the specific cell subtype from which the tumor arises.…”

Section: Introductionmentioning

confidence: 99%

Elevated NF-κB/SHh/GLI1 Signature Denotes a Worse Prognosis and Represent a Novel Potential Therapeutic Target in Advanced Prostate Cancer

Vecchiotti

Verzella

Nolfi

et al. 2022

Cells

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Prostate cancer (PCa) is the second most frequent cancer in men worldwide. NF-κB seems to play a key role in cell survival, proliferation and invasion, sustaining the heterogeneous multifocal nature of PCa. In recent years, the Hedgehog (Hh) signaling pathway has attracted attention as a therapeutic target due to its implication in tumorigenesis and metastasis in several types of cancer, including PCa. Although it is well-known that Sonic Hedgehog (SHh) is a transcriptional target of NF-κB(p65), and that GLI1 is the effector of this crosstalk, the precise role played by this axis in PCa is still not completely clear. Here, we set out to explore the correlation between NF-κB activation and SHh pathways in PCa, investigating if the interplay between NF-κB(p65) and SHh-GLI1 in advanced PCa could be a prospective therapeutic target. Our findings demonstrate that a NF-κB-SHh-GLI1 gene signature is enriched in PCa patients featuring a higher Gleason score. Moreover, elevated levels of this signature are associated with worse prognosis, thus suggesting that this axis could provide a route to treat aggressive PCa.

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“…Benign Prostatic Hyperplasia (BPH) is a multi-factorial medical condition characterized by the putative proliferation of the stromal and epithelial cells of the prostate, which leads to the swelling of the prostate and eventual obstruction of urine exit in ageing men [1]. Various theories have been purported in a bid to explain the aetiology of BPH with none of them offering a comprehensive explanation on the mechanism of BPH development and progression [2,3,4]. Genetic theories according to De Souza et al, on the aetiology of BPH faults the occurrence of numerous polymorphisms responsible for BPH via encoding the androgenic receptors which are important for the activation of other genes and the production of the androgen hormone directly involved in the progression of BPH [1].…”

Section: Introductionmentioning

confidence: 99%

“…A high level of testosterone is converted to dihydrotestosterone (DHT) by the 5α-reductase enzyme and an increased serum level of DHT in association with estradiol triggers the growth and proliferation of the stromal and epithelial cells present in the prostate [6]. New findings have also linked BPH initiation and progression to the increasing levels of proinflammatory cytokines and oxidative stress [3]. The use of 5αreductase inhibitors including Finasteride and Dutasteride to treat BPH have always yielded the desired results but are associated with some undesirable side effects, which have necessitated the need to search for a more potent drug with less toxicity and have a low cost [4].…”

Section: Introductionmentioning

confidence: 99%

Combined ethanol extract of Hypselodelphys poggeana and Spermacoce radiata leaves ameliorate benign prostatic hyperplasia in rats via modulation of serum sex hormonal levels

Uroko¹,

Ijioma²,

OGWO³

et al. 2022

jrp

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This study evaluated the effects of a combined ethanol extract of and Hypselodelphys poggeana and Spermacoce radiata leaves (CESHL) on sex hormone levels and prostate weights of benign prostatic hyperplasia (BPH) induced rats. The combined extract was prepared from the plants and was subjected to acute toxicity (LD50) evaluation in rats. The study adopted five groups of rats (n = 6) with group 1 being the normal control without BPH induction, group 2 was the BPH control, group 3 was the finasteride control, and groups 4 and 5 were BPH induced rats treated with 250 and 500 mg/kg CESHL/day for 28 days. Induction of prostate hyperplasia in rats belonging to groups 2-5 was done via daily subcutaneous administration of testosterone propionate (5 mg/kg body weight) for 28 days in accordance with standard protocols. The result obtained in the acute toxicity evaluation indicated an LD50 value of above 5000 mg/kg body weight. In the main study, a significant increase (P<0.05) in serum testosterone, dihydrotestosterone, prostate weight, prostate index and reduced serum estradiol was observed in the BPH control when compared with the normal control. Treatment of BPH induced rats (groups 4 and 5) with CESHL significantly reduced serum concentrations of testosterone and dihydrotestosterone, and also elevated serum estradiol concentration when compared with the BPH control, comparing favourably with the values of these hormones in the finasteride-treated group. The BPH induced rats treated with CESHL also had significantly reduced prostate weight and prostate index relative to the BPH control and higher percentage inhibition of prostate weight and prostate index when compared with the finasteride control. Our findings show that CESHL may ameliorate benign prostate hyperplasia via mechanisms that lower serum testosterone and dihydrotestosterone levels and increase estradiol levels.

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The Etiology and Pathophysiology Genesis of Benign Prostatic Hyperplasia and Prostate Cancer: A New Perspective

Cited by 17 publications

References 321 publications

Investigation of Lymphocyte Subsets in Peripheral Blood of Patients with Benign Prostatic Hyperplasia

Investigation of Lymphocyte Subsets in Peripheral Blood of Patients with Benign Prostatic Hyperplasia

Elevated NF-κB/SHh/GLI1 Signature Denotes a Worse Prognosis and Represent a Novel Potential Therapeutic Target in Advanced Prostate Cancer

Combined ethanol extract of Hypselodelphys poggeana and Spermacoce radiata leaves ameliorate benign prostatic hyperplasia in rats via modulation of serum sex hormonal levels

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