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Background And Objective: Several studies were launched to investigate the potential function of ACE I/D polymorphism in gastric cancer development and prognosis, but no conclusive results have been obtained. We conducted a systematic review and meta-analysis to evaluate the association between ACE I/D polymorphism and gastric cancer.
Methods: A systemic search was performed in PubMed, Embase, China National Knowledge Infrastructure (CNKI), Wanfang and Weipu databases (until October 15,2013) to identify all published records on association between the ACE I/D polymorphism and gastric cancer. We adopted the odds ratio (OR) and 95% confidence interval (95%CI) as measure of effect. Meta-analysis was conducted using fixed/random-effects model in STATA 12.0.
Results: Eventually a total of seven studies with 1392 cases and 2951 controls were included in our meta-analysis. No association was detected between ACE I/D polymorphism and gastric cancer susceptibility (DI+DD vs II: OR=1.06, 95%CI=0.92-1.21, P=0.443). However, we found that the DD genotype was significantly associated with increased lymph node metastasis (DD vs DI+II: OR=3.48, CI=1.77-6.85, P<0.001), and more advanced clinical stage (DD vs DI+II: OR=2.43, CI=1.34-4.39, P=0.003) of gastric cancer.
Conclusion: Our results indicated that ACE I/D polymorphism could not be directly associated with gastric cancer susceptibility, but might play important role in gastric cancer prognosis. Future studies with larger sample size are warranted for further evaluation.
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http://dx.doi.org/10.1016/j.clinre.2014.06.015 | DOI Listing |
Int J Pharm
September 2025
Department of Veterinary Medicine, Central Animal Facility, Amrita Institute of Medical Sciences and Research Centre, AIMS Health Sciences Campus, Amrita Vishwa Vidyapeetham, Kochi, Kerala 682041, India.
The clinical use of gemcitabine (GEM), a frontline chemotherapeutic agent for pancreatic ductal adenocarcinoma (PDAC), is limited by its short half-life, rapid systemic clearance, associated dose-limiting toxicities and a faster development of resistance in pancreatic cancer. Aspirin (ASP), a repurposed NSAID, has been shown to sensitize PDAC cells to GEM through modulation of multiple oncogenic and inflammatory pathways. However, its clinical use is restricted by dose-dependent gastrointestinal toxicity.
View Article and Find Full Text PDFCell Mol Biol (Noisy-le-grand)
September 2025
Department of Biology, College of Education for Pure Sciences, University of Kerbala, Kerbala, Iraq.
Gastric cancer is one of the causes of deaths related to cancer across the globe and both genetic and environmental factors are the most prominent. Causes of its pathogenesis. This paper researches the expression of the C-FOS gene.
View Article and Find Full Text PDFInt J Mol Med
November 2025
Department of General Practice, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi 330008, P.R. China.
Mucin 6 (MUC6), primarily expressed in the gastrointestinal (GI) epithelium, is a member of the mucin family characterized by a protein backbone with extensive glycosylation, playing a crucial role in preserving epithelial barrier integrity. Accumulating evidence indicates that MUC6 glycosylation contributes significantly to cancer development, diagnosis, therapy and prognosis‑particularly in GI malignancies such as gastric, pancreatic and colorectal cancers. In the present review, current findings on the multifaceted roles of MUC6 across various cancers were comprehensively summarize.
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September 2025
Department of Pharmacology, Chungnam National University College of Medicine, Daejeon, Republic of Korea.
Genetic variations of long noncoding RNAs are potential biomarkers for gastric cancer (GC). However, reports on the association between single nucleotide polymorphisms (SNPs) in antisense noncoding RNA in the INK4 locus () and GC risk are few. This case-control study aimed to evaluate the association between SNPs in , GC risk, and subgroups in a Korean population.
View Article and Find Full Text PDFOver the past decades, acid production in the stomach has been regulated mainly by proton pump inhibitors (PPIs). However, despite their widespread use and solid evidence base for efficacy, PPIs have pharmacokinetic and pharmacodynamic limitations, such as a slow onset of action, response variability (dependent on CYP2C19 polymorphisms), and the need for activation in an acidic environment. These restrictions underscore the need for innovative molecular approaches to inhibiting acid production, which led to the development of a fundamentally different mechanism of action - potassium-competitive acid blockers (P-CABs), first introduced into clinical practice in 2015.
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