Background: The aim of the meta-analysis was to derive a more precise assessment of the association between p16 promoter methylation and thyroid cancer risk.
Materials And Methods: The PubMed, Web of Science databases and Chinese CNKI were searched for relevant articles. Ultimately, seventeen case-control studies were included with a total of 804 thyroid cancer cases and 487 controls analysis by R Software (R version 3.1.2) including meta. Crude odds ratios with 95% confidence intervals were calculated using the random-effects model which were used to assess the strength of relationship between p16 methylation and lung carcinogenesis. Funnel plots were carried out to evaluate publication bias.
Results: The meta-analysis results showed that the frequency of p16 promoter methylation in cancer tissue/blood was significantly higher than that normal tissue/ blood (OR=5.46, 95%CI 3.12-9.55, P<0.0001) by random effects model with small heterogeneity.
Conclusions: Thus, p16 promoter methylation may be associated with thyroid cancer risk.
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http://dx.doi.org/10.7314/apjcp.2015.16.16.7111 | DOI Listing |
Neoplasia
December 2024
Department of Pathology, Ajou University School of Medicine, Suwon 16499, Republic of Korea. Electronic address:
Glioblastoma, isocitrate dehydrogenase (IDH)-wildtype (GBM), is the most malignant brain tumor in adults, with limited therapeutic intervention. Previous studies have identified a few prognostic markers for GBM, including the methylation status of O-methylguanine-DNA methyltransferase (MGMT) promoter, TERT promoter mutation, EGFR amplification, and CDKN2A/2B deletion. However, the classification of GBM remains incomplete, necessitating a comprehensive analysis.
View Article and Find Full Text PDFClin Appl Thromb Hemost
December 2024
Department of Hematology and Transfusion sciences, School of Allied Medical Sciences, Tehran University of Medical sciences, Tehran, Iran.
Objective: DNA methylation, as an epigenetic alteration, plays an essential role in the development of atherosclerosis and venous thrombosis. E-cadherin, a tumor suppressor gene and adhesion molecule, has a crucial function in platelet aggregation and hemostasis. P16, a cell cycle regulator, is involved in venous thrombosis.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Biophysics of Environmental Pollution, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska Str. 141/143, 90-236 Lodz, Poland.
The aim of the present study was to investigate the concentration- and size-dependent effects of non-functionalized polystyrene nanoparticles (PS-NPs) of varying diameters (29 nm, 44 nm, and 72 nm) on specific epigenetic modifications and gene expression profiles related to carcinogenesis in human peripheral blood mononuclear cells (PBMCs) in vitro. This in vitro human-cell-based model is used to investigate the epigenetic effect of various environmental xenobiotics. PBMCs were exposed to PS-NPs at concentrations ranging from 0.
View Article and Find Full Text PDFMol Med Rep
February 2025
Biomedical Section, Hull-York Medical School, University of Hull, Hull, HU6 7RX, UK.
Tissue factor (TF) possesses additional physiological functions beyond initiating the coagulation cascade. Cellular signals initiated by cellular TF or on contact with TF‑containing microvesicles, contribute to wound healing through regulating a number of cellular properties and functions. TF regulates the cell cycle checkpoints, however the underlying signalling mechanisms have not been determined.
View Article and Find Full Text PDFMol Genet Genomics
November 2024
Department of Endocrinology, Staff Hospital of Changqing Oilfield, Xi'an, 710018, China.
Pro-differentiation and anti-senescence treatment may be potential strategies for senile osteoporosis therapy. However, the regulatory mechanism underlying osteoblast differentiation and senescence in senile osteoporosis remain to be clarified. In the present study, the preosteoblast cell line MC3T3-E1 was used to induce osteoblast differentiation.
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