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Principales causes connues qui font l'objet de recherches
­ 
L'âge en prenant en compte depuis quelques années du rajeunissement de la population atteinte
L'obésité
Les régimes hyper-insuliniques
Le manque d'activité physique, la sédentarité
L’alimentation pro-inflammatoire avec trop de produits laitiers animaux et viandes rouges et charcuteries et/ou de phytohormones avec le soja
Les anabolisants du dopage sportif et de la puissance sexuelle
Les infections prostatiques = prostatites à répétition
L'intoxication tabagique et autres addictions respiratoires
Les pesticides et perturbateurs endocriniens
La génétique
Le papillomavirus et les infections sexuellement transmissibles
Le stress de la vie moderne


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BUFFALO, NY — February 19, 2025 — A new #research paper was #published by Aging (Aging-US) on January 6, 2025, in Volume 17, Issue 1, titled “The profile of oxidative stress markers (arachidonic and linoleic acid derivatives) in patients with benign prostatic hyperplasia in relation to metabolic syndrome.”

A team of researchers, led by first author Weronika Ratajczak and corresponding author Olimpia Sipak from Pomeranian Medical University, examined how inflammation and metabolic health contribute to benign prostatic hyperplasia (BPH), a common condition that causes prostate enlargement in aging men, leading to urinary problems. Their findings suggest that inflammatory-related molecules in the blood may play a key role in BPH development, especially in men with metabolic syndrome—a group of conditions including obesity, high blood sugar, and high cholesterol.

BPH affects millions of men as they age, making urination more difficult and sometimes painful. While age and hormonal changes are known factors, the precise causes of prostate enlargement remain unclear. This study provides new evidence that inflammation, especially lipid-derived inflammatory markers, may be a driving factor behind BPH, particularly in those with poor metabolic health.

The research team analyzed blood samples from 219 men, including 144 with BPH and 75 without, measuring markers related to inflammation and oxidative stress. The results showed that men with BPH had significantly higher levels of pro-inflammatory molecules such as 12S-HETE and 5-HETE while having lower levels of anti-inflammatory substances like lipoxin A4. The imbalance was even more pronounced in men with both BPH and metabolic syndrome, indicating a possible link between poor metabolic health and worsening prostate conditions​.

“Furthermore, there is mounting evidence that links the onset of inflammation with the development of prostate diseases, including benign prostatic hyperplasia and prostate cancer.”

Metabolic dysfunction and chronic inflammation may not only contribute to BPH development but also exacerbate its severity. Monitoring metabolic health could play a role in reducing the risk of prostate enlargement.

Future research is needed and may focus on whether anti-inflammatory treatments or lifestyle changes—such as improved diet, weight management, and exercise—could help slow the progression of BPH or reduce its symptoms​.

DOI - https://doi.org/10.18632/aging.206187

Corresponding author - Olimpia Sipak - olimpiasipak-szmigiel@wp.pl

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Keywords - aging, benign prostatic hyperplasia (BPH), metabolic syndrome (MetS), lipid markers, inflammation, fatty acids derivatives

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

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"Prostate cancer in Black men carries higher incidence and mortality rates, emphasizing early screening, symptom awareness, and understanding risks to address disparities and improve outcomes."

Shield Black Men from Prostate Cancer's Alarming Threat

BUFFALO, NY - June 4, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on May 20, 2025, titled “Targeting PCNA/AR interaction inhibits AR-mediated signaling in castration resistant prostate cancer cells."

In this study, authors Shan Lu and Zhongyun Dong from the University of Cincinnati College of Medicine investigated how interfering with a protein interaction could reduce prostate cancer growth. Their study based on prostate cancer cells shows that blocking the link between PCNA, a protein important for DNA repair, and the androgen receptor (AR), which drives prostate cancer growth, can slow down cancer cell multiplication. This discovery could lead to a new treatment for patients with advanced prostate cancer, particularly those no longer responding to hormone therapy.

Prostate cancer is one of the most common cancers in men. Many patients eventually become resistant to hormone treatment. In this advanced stage, called castration-resistant prostate cancer (CRPC), tumors continue to grow by using either the full-length androgen receptor (AR-FL) or altered versions called AR variants (AR-Vs). This study shows that the interaction between AR and PCNA helps both AR-FL and AR-Vs remain active, supporting cancer cell survival and growth.

The researchers identified a new region in the AR that binds to PCNA. They developed a small peptide, R9-AR-PIP, to mimic this region and block the AR-PCNA connection. They found that this peptide reduced AR’s ability to bind DNA and lowered the levels of key genes involved in cancer cell growth. Importantly, the peptide was effective against both types of AR, including the variant forms that are especially challenging in CRPC.

“We identified a second PIP-box (PIP-box592) in the DNA binding domain of AR and found that dihydrotestosterone enhances the binding of full-length AR (AR-FL) but not a constitutively active variant (AR-V7) to PCNA.”

They also tested a small molecule, PCNA-I1S, which interferes with PCNA’s ability to move to the cell nucleus and interact with AR. This molecule showed similar effects as the peptide, reducing AR activity and stopping cancer cell growth. Together, these findings suggest that targeting PCNA/AR interactions could be a promising strategy to fight CRPC, especially in patients with limited treatment options.

One key result was that both the peptide and the small molecule reduced the levels of cyclin A2, a protein that helps cells divide and is often overexpressed in CRPC. Since this protein is linked to patients' poor outcomes, its reduction could be especially beneficial.

This study improves our understanding of how prostate cancer continues to grow even after hormone treatments fail. By blocking a crucial helper of the androgen receptor, researchers have uncovered a new way to potentially slow or stop the disease. Further studies in animal models are needed, but this approach could lead to more effective treatments for men with advanced prostate cancer.

DOI - https://doi.org/10.18632/oncotarget.28722

Correspondence to - Zhongyun Dong - dongzu@ucmail.uc.edu

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Keywords - cancer, PCNA, androgen receptor, PCNA inhibitors, AR splicing variants, CRPC

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Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

Cancer and aging are two sides of age-related tumorigenesis.

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

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