Background/aims: We previously reported that aberrant methylation of p16 and/or E-cadherin genes in serum DNA could serve together as a tumor marker in gastric cancer. We presently investigated whether sensitivity could be increased by consideration of a third gene, which encodes retinoic acid receptor-1 (RARbeta).
Methodology: We performed a methylation-specific polymerase chain reaction (MSP) in serum DNA to detect aberrant methylation of RARbeta from 109 preoperative gastric cancer patients, in which the first two genes had been characterized. We also examined all three genes in sera from 10 outpatients during postgastrectomy follow-up.
Results: Aberrant methylation of RARbeta was demonstrated in 26 preoperative patients (24%). Considering this with previous results, 52 patients (48%) of the 109 preoperative showed hypermethylation of at least one gene (p16, E-cadherin, and/or RARbeta). No aberrant methylation was detected in control sera. In the follow-up group, aberrant methylation was demonstrated in 2 of the 3 patients who had definite radiologic evidence of recurrences. One of the patients showing promoter hypermethylation without definite findings of recurrence at the time of analysis developed peritoneal recurrence 6 months later.
Conclusions: Including the MSP assay in conventional follow-up could facilitate early detection of recurrent disease in gastric cancer patients.
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Biol Sex Differ
January 2025
Department of Laboratory Medicine and Pathology, School of Medicine, University of Washington, Seattle, WA, 98195, USA.
Background: X chromosome inactivation (XCI) is a female-specific process in which one X chromosome is silenced to balance X-linked gene expression between the sexes. XCI is initiated in early development by upregulation of the lncRNA Xist on the future inactive X (Xi). A subset of X-linked genes escape silencing and thus have higher expression in females, suggesting female-specific functions.
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January 2025
Jiangxi Key Laboratory of Molecular Medicine, Jiangxi Medical College, The Second Affiliated Hospital of Nanchang University, Nanchang University, Nanchang, 330006, China.
SMAD3, a protein-coding gene, assumes a pivotal role within the transforming growth factor-beta (TGF-β) signaling pathway. Notably, aberrant SMAD3 expression has been linked to various malignancies. Nevertheless, an extensive examination of the comprehensive pan-cancer impact on SMAD3's diagnostic, prognostic, and immunological predictive utility has yet to be undertaken.
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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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December 2024
Functional and Molecular Neuroimaging Unit, Bellaria Hospital, Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
Objectives: The aim of the present study was to analyze the methylation status in patients who presented with an Oral Squamous Cell Carcinoma (OSCC) concomitantly with multifocal Proliferative Verrucous Leukoplakia (PVL)(PVL-OSCC).
Methods: Nine patients with OSCC and concomitant PVL lesions were selected. Two brushing samples were collected simultaneously from OSCC and PVL lesions in contralateral mucosa from each patient.
Mol Nutr Food Res
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Laboratory of Experimental Immunology, Department of Immunology, The "Stephan Аngeloff" Institute of Microbiology, Bulgarian Academy of Sciences, Sofia, 1113, Bulgaria.
Systemic lupus erythematosus (SLE) is a complex autoimmune disease with a number of immunological aberrations in the mechanisms of innate and adaptive immune responses. Spontaneous and induced mouse models of the disease have contributed significantly to the advancement in lupus treatments. The involvement of humanized models, engrafted with lupus patients' immune cells, represented the possibility to study the development of SLE.
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