Background: DNA CpG island hypermethylation causes gene silencing and is a common event in prostate carcinogenesis and progression. We investigated its role as a possible prognostic marker in patients with PCA Gleason score ≤7.
Patients And Methods: We used a quantitative, methylation-specific PCR to analyze methylation patterns at five gene loci (APC, GSTP1, PTGS2, RARbeta and TIG1) in 84 prostate cancer (PCA) tissues (Gleason Score ≤7). Methylation was correlated with established clinico-pathological parameters (preoperative PSA, pathological Gleason score, extraprostatic extension, seminal vesicle penetration, lymph node involvement, surgical margins and age) and PSA recurrence.
Results: DNA hypermethylation was frequently detected at APC (95.2%), GSTP1 (84.5%), PTGS2 (100%), RAR-beta (81.0%) and TIG1 (95.2%). DNA hypermethylation was correlated with Gleason Score (p=0.027; PTGS2) and lymph node involvement (p=0.024; RARbeta). High methylation levels at RARbeta (p=0.023) was a significant predictor of PSA recurrence following radical prostatectomy.
Conclusion: The analysis of DNA hypermethylation provides prognostic information in prognosis of low- and intermediate-grade PCA.
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Gene
January 2025
School of Life Sciences, Fudan University, Shanghai 200433, China; MOE Engineering Research Center of Gene Technology, School of Life Sciences, Obstetrics and Gynecology Hospital, Fudan University, Shanghai 200433, China. Electronic address:
Bisphenol A (BPA) is a widely used industrial compound commonly found in various everyday plastic products. Known for its endocrine-disrupting properties, BPA can enter the human body through multiple pathways. Prenatal exposure to BPA not only disrupts placental structure and function but also interferes with normal steroid metabolism.
View Article and Find Full Text PDFMol Oncol
January 2025
Department of Medicine, Clinic III - Hematology, Oncology, Palliative Medicine, Rostock University Medical Center, Germany.
Hypermethylation of tumor suppressor genes is a hallmark of leukemia. The hypomethylating agent decitabine covalently binds, and degrades DNA (cytosine-5)-methyltransferase 1 (DNMT1). Structural similarities within DNA-binding domains of DNMT1, and the leukemic driver histone-lysine N-methyltransferase 2A (KMT2A) suggest that decitabine might also affect the latter.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Yale University, New Haven, CT, USA.
Background: Alcohol Use Disorder (AUD) affects over 15 million individuals in the United States, contributing to oxidative stress, neuroinflammation, and elevating the risk of neurodegeneration. Despite this, the connection between AUD and aging conditions, particularly Alzheimer's disease (AD), remains unclear. AD, with a heritability of 60-80%, is genetically linked, necessitating an exploration of the molecular implications of AUD and genetic susceptibility to AD.
View Article and Find Full Text PDFBackground: Epigenetic mechanisms as a potential underlying pathogenic mechanism of neurodegenerative diseases have been the scope of several studies performed so far. However, there is a gap in analyzing different forms of early-onset dementia to minimize the effect of aging and the use of Lymphoblastoid cell lines (LCLs) as a possible disease model for earlier clinical phases.
Method: We performed a genome-wide DNA methylation analysis in 64 samples (from prefrontal cortex and lymphoblastoid cell lines) from Alzheimer's Disease (AD) and Frontotemporal dementia (FTD) using the Illumina Infinium MethylationEPIC V2.
Oncol Rep
February 2025
Department of Otolaryngology Head & Neck Surgery, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Laryngeal squamous cell carcinoma (LSCC), which represents a significant proportion of head and neck squamous cell carcinoma cases, is often diagnosed at advanced stages, underscoring the urgent need for effective biomarkers and therapeutic targets. Junctional adhesion molecule 3 () is implicated in various types of cancer; however, its role in LSCC remains unclear. Therefore, the present study aimed to investigate the epigenetic regulation and tumor‑suppressive functions and mechanisms of in LSCC.
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