Background: Barrett’s esophagus (BE) is described by the transformation of the normal squamous epithelium into metaplastic columnar epithelium, driven by chronic gastroesophageal reflux disease (GERD). BE is a recognized premalignant condition and the main precursor to esophageal adenocarcinoma (EAC). Understanding the molecular mechanisms underlying BE carcinogenesis is crucial for improving prevention, surveillance, and treatment strategies. Methods: This narrative review examines the molecular abnormalities associated with the progression of BE to EAC. Results: This study highlights inflammatory, genetic, epigenetic, and chromosomal alterations, emphasizing key pathways and biomarkers. BE progression follows a multistep process involving dysplasia and genetic alterations such as TP53 and CDKN2A (p16) mutations, chromosomal instability, and dysregulation of pathways like PI3K/AKT/mTOR. Epigenetic alterations, including aberrant microRNA expression or DNA methylation, further contribute to this progression. These molecular changes are stage-specific, with some alterations occurring early in BE during the transition to high-grade dysplasia or EAC. Innovations in chemoprevention, such as combining proton pump inhibitors and aspirin, and the potential of antireflux surgery to halt disease progression are promising. Incorporating molecular biomarkers into surveillance strategies and advancing precision medicine may enable earlier detection and personalized treatments. Conclusions: BE is the primary preneoplastic condition for EAC. A deeper understanding of its molecular transformation can enhance surveillance protocols, optimize the management of gastroesophageal reflux inflammation, and refine prevention and therapeutic strategies, ultimately contributing to a reduction in the global burden of EAC.

Purpose: Familial adenomatous polyposis is a hereditary condition that predisposes individuals to colorectal cancer. This study aimed to evaluate the efficacy and safety of pharmacological therapies for reducing polyp number, burden, and size in individuals with familial adenomatous polyposis.Methods: A systematic search was conducted in PubMed, Embase, Web of Science, and Cochrane. Randomized trials assessing the effects of pharmacological interventions on polyp number, polyp burden, and polyp size were included, and adverse events were also analyzed.Results: Sixteen studies (n=985) met the inclusion criteria. The mean participant age was 38±8.3 years, with a mean follow-up of 14.6±15.8 months. Of these studies, 62.5% focused on colorectal polyps, 18.8% on rectal polyps, 18.8% on duodenal polyps, and 12.5% addressed both colorectal and duodenal polyps. Pharmacological interventions were associated with a modest but statistically significant reduction in the number of polyps (Hedges g, −0.57; 95% confidence interval [CI], −1.08 to −0.05) and in average polyp size (Hedges g, −0.26; 95% CI, −0.49 to −0.04). However, no significant reduction in overall polyp burden was observed (Hedges g, −1.07; 95% CI, −2.21 to 0.06). In subgroup analyses, nonselective cyclooxygenase inhibitors produced a large reduction in polyp burden (Hedges g, −2.72; 95% CI, −3.28 to −2.16), while metformin also demonstrated benefit in a single study (Hedges g, −1.06; 95% CI, −1.86 to −0.27). Adverse events were generally infrequent and comparable to placebo. Conclusion: Chemopreventive interventions may reduce polyp number, burden, and size, and they appear to have a favorable safety profile.

The impact of Helicobacter pylori (HP) on postoperative outcomes after sleeve gastrectomy (SG) is still controversial. A systematic review and meta-analysis were performed to compare the incidence of early complications after SG between HP-positive and HP-negative patients. Eight retrospective comparative studies were included, comprising 4,877 individuals. The prevalence of HP infection in gastric resected specimens ranged from 7.77 to 43.20%. There were no statistically significant differences between groups for overall complications (OR 1.46; 95%CI 0.95–2.23; p=0.08), bleeding (OR 1.35; 95%CI 0.70–2.60; p=0.38), and leak (OR 1.74; 95%CI 0.80–3.81; p=0.17) rates. The need for routine screening and treatment of HP infection before SG remains ambiguous.