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Background: Few studies have examined prostate cancer incidence and aggressiveness in urban-rural Appalachian populations. We examined these rates in urban-rural Appalachia and non-Appalachia Pennsylvania (PA), and the association between these areas and more aggressive prostate cancer at diagnosis.
Methods: Men, ages ≥ 40 years with a primary prostate cancer diagnosis, were identified from the 2004-2014 Pennsylvania Cancer Registry. Age-adjusted incidence rates for prostate cancer and more aggressive prostate cancer at diagnosis were calculated by urban-rural Appalachia status. Multivariable Poisson regressions were conducted. Multiple logistic regressions were used to examine the association between the geographic areas and more aggressive prostate cancer, after adjusting for confounders.
Results: There were 94,274 cases, ages 40-105 years, included. Urban non-Appalachia had the highest 2004-2014 age-adjusted incidence rates of prostate cancer and more aggressive prostate cancer (293.56 and 96.39 per 100,000 men, respectively) and rural Appalachia had the lowest rates (256.48 and 80.18 per 100,000 men, respectively). Among the cases, urban Appalachia were more likely [OR = 1.12; 95% confidence interval (CI) = 1.08-1.17] and rural Appalachia were less likely (OR = 0.92; 95% CI = 0.87-0.97) to have more aggressive prostate cancer at diagnosis compared with urban non-Appalachia.
Conclusions: Lower incidence rates and the proportion of aggressive disease in rural Appalachia may be due to lower prostate cancer screening rates. More aggressive prostate cancer at diagnosis among the cases in urban Appalachia may be due to exposures that are prevalent in the region.
Impact: Identifying geographic prostate cancer disparities will provide information to design programs aimed at reducing risk and closing the disparity gap.
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http://dx.doi.org/10.1158/1055-9965.EPI-19-1232 | DOI Listing |
JAMA
September 2025
Division of Surgery and Interventional Science, UCL, London, United Kingdom.
Importance: Multiparametric magnetic resonance imaging (MRI), with or without prostate biopsy, has become the standard of care for diagnosing clinically significant prostate cancer. Resource capacity limits widespread adoption. Biparametric MRI, which omits the gadolinium contrast sequence, is a shorter and cheaper alternative offering time-saving capacity gains for health systems globally.
View Article and Find Full Text PDFInt J Surg
September 2025
Department of Radiology, Sichuan Provincial People's Hospital East Sichuan Hospital&Dazhou First People's Hospital, Dazhou, China.
Ann Nucl Med
September 2025
Department of Nuclear Medicine, Marmara University School of Medicine, Istanbul, Turkey.
Objective: This study aims to systematically evaluate the inter- and intra-observer agreement regarding lesions with uncertain malignancy potential in Ga-68 PSMA PET/CT imaging of prostate cancer patients, utilizing the PSMA-RADS 2.0 classification system, and to emphasize the malignancy evidence associated with these lesions.
Methods: We retrospectively reviewed Ga-68 PSMA PET/CT images of patients diagnosed with prostate cancer via histopathology between December 2016 and November 2023.
Cancer Causes Control
September 2025
Department of Population Health Sciences, Weill Cornell Medicine, New York, NY, USA.
Purpose: The U.S. Preventive Services Task Force recommends that men aged 55-69 years undergo shared decision-making (SDM) regarding prostate cancer (PCa) screening, and routine screening is not recommended for older men or those with limited life expectancy.
View Article and Find Full Text PDFMed Oncol
September 2025
Department of Biotechnology, Institute of Engineering and Management, University of Engineering and Management, Kolkata, Kolkata, India.
Oligomeric proanthocyanidins (OPCs), condensed tannins found plentiful in grape seeds and berries, have higher bioavailability and therapeutic benefits due to their low degree of polymerization. Recent evidence places OPCs as effective modulators of cancer stem cell (CSC) plasticity and tumor growth. Mechanistically, OPCs orchestrate multi-pathway inhibition by destabilizing Wnt/β-catenin, Notch, PI3K/Akt/mTOR, JAK/STAT3, and Hedgehog pathways, triggering β-catenin degradation, silencing stemness regulators (OCT4, NANOG, SOX2), and stimulating tumor-suppressive microRNAs (miR-200, miR-34a).
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