WTAP stabilizes MMP12 expression to promote the malignant phenotypes of esophageal cancer cells.

Microbiota and esophageal cancer: From dysbiosis to carcinogenesis.

Assessment of proton versus photon therapy in the reduction of lymphopaenia in thoracic cancers: A scoping review.

Proton beam therapy versus photon therapy for multiple malignancies: An umbrella systematic review and meta-analysis.

Assessment of stapled vs handsewn anastomoses in video-assisted thoracoscopic and laparoscopic McKeown esophagectomy for esophageal cancer.

A PINN-driven Fokker-Planck dynamical modeling and control framework for EGFR signaling pathways in esophageal cancer

Real-world insights into young-onset gastroesophageal adenocarcinoma: an all-Ireland population-based cancer registry analysis.

The intensification of radiotherapy is an effective way to improve the therapeutic efficacy of radiation-sensitive malignancies such as esophageal cancer (EC). Esophageal squamous cell carcinoma (ESCC) accounts for 85% of all EC cases worldwide, with a relatively higher incidence and mortality in East Asia. In this study, we explored the functions and mechanisms of programmed cell death 10 (PDCD10) in the malignancy and radiotherapy sensitivity of ESCC cells. We observed that PDCD10 is highly expressed in ESCC tissues and is correlated with a poor prognosis in patients with ESCC. PDCD10 downregulation suppressed ESCC cell proliferation, migration, and invasion but promoted apoptosis. In addition, it enhanced ionizing radiation (IR)-induced ESCC cell damage, whereas PDCD10 overexpression had the opposite effect. Mechanistically, PDCD10 increased the phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) in ESCC cell lines. The administration of LY294002, a PI3K inhibitor, significantly inhibited the oncogenic functions of PDCD10, leading to an increase in IR-induced cell damage. These findings establish PDCD10 as a critical intrinsic regulator of the sensitivity of ESCC cells to IR through the modulation of the PI3K/AKT pathway.

Noteworthy in Cardiothoracic Surgery 2025 highlights several of the most influential trials and emerging trends shaping cardiothoracic surgical practice. In structural heart disease, new randomized data have expanded consideration of transcatheter aortic valve replacement to asymptomatic patients while reinforcing the importance of longer-term durability and lifetime valve management in lower-risk populations. In heart transplantation, advances in minimally invasive and robotic techniques, alongside growing international experience with donation after circulatory death, underscore both the promise of innovation and the need for disciplined management of ischemic and preservation times. Endovascular management of complex thoracic aortic disease continues to evolve with broader use of branched devices. In thoracic oncology, practice changing trials support a shift towards perioperative chemotherapy and immunotherapy for resectable esophageal, gastroesophageal junction, and lung cancers, redefining surgical timing, coordination, and multidisciplinary care. Finally, continued adoption of minimally invasive and robotic approaches reflects a broader trend toward reducing surgical morbidity while maintaining oncologic and transplant outcomes.

Alcohol consumption is a modifiable, dose‑dependent risk factor that accelerates cancer initiation, progression, and therapy resistance across breast, liver, colorectal, esophageal, and melanoma cancers. Alcohol metabolism generates acetaldehyde, a genotoxic metabolite that induce DNA damage and impairs repair; drives oxidative stress, hormonal imbalance and promoting a tumor‑supportive microenvironment. These effects are amplified by obesity and insulin resistance, which heighten aggressiveness and blunt treatment response. Alcohol reshapes the tumor immune microenvironment (TIME) and undermines therapies, including immunotherapy. It impairs dendritic cell antigen presentation and co‑stimulation, limits CD4⁺/CD8⁺ priming, and expands immunosuppressive MDSCs and M2‑like TAMs that inhibit cytotoxic T cells and express checkpoint ligands. Concurrent cytokine shifts (TNFα, IL‑6), persistent ROS-NF‑κB signaling, and stromal/vascular remodeling promote immune exclusion and weaken responses to checkpoint blockade, targeted agents, and chemotherapy. Alcohol‑related gut dysbiosis is linked to ICB responsiveness-dampens antitumor immunity. Alcohol increases exosome biogenesis; circulating vesicles enriched in hepatocyte and inflammatory miRNAs (e.g., miR‑122, miR‑192) reprogram immune signaling and metastasis, forming a vesicular axis linking exposure to TIME dysfunction and resistance. Risk is synergistic with tobacco and worsens with aging as detoxification and DNA repair decline. Sex‑specific pharmacokinetics and composition confer vulnerability in women, while socioeconomic barriers delay diagnosis and care. Personalized prevention strategies that incorporate alcohol reduction, smoking cessation, and nutritional support, with emerging biomarkers such as exosomal miRNAs and alcohol‑related metabolites for early detection and risk stratification, are needed to mitigate alcohol‑related carcinogenesis, given the lack of definitive human evidence on alcohol's independent effects on immunotherapy and chemotherapy efficacy.

Patterns of sex differences in cancer mortality in Colombia: a population-based analysis, 1980-2023.

The Krüppel-like family (KLF) are important transcriptional regulators that have important, context-specific roles in gastrointestinal (GI) malignancies. Their roles are very heterogeneous; each of the KLF members may play tumor-suppressive or tumor-promoting roles, depending on the type of tumor, clinical stage and the cellular microenvironment, which fine-tunes the core biological processes of tumor cell proliferation, apoptosis, epithelial-mesenchymal transition and metabolism. This is a context-dependent functional heterogeneity that poses a big challenge in the translation of KLF family transcription factors from basic research into clinical applications. In addition to these classical regulatory functions, KLFs have a key role in the restructuring of the tumor immune microenvironment (TIME). KLFs have the potential to affect the effectiveness of cancer immunotherapy by modulating immune cell infiltration, immune cell functions and immune evasion by tumors. The present review is a systematic review that summarizes the molecular regulatory mechanisms of KLFs in the major GI malignancies, such as colorectal, gastric, liver, esophageal and pancreatic cancer. The present review points to their control of major signaling pathways, including Wnt/β-catenin and PI3K/AKT, and their new roles in the remodeling of TIME. Moreover, the present review assesses their translational utility as diagnostic and prognostic biomarkers and therapeutic targets, and confronts the clinical issues involved in targeting transcription factors, thus giving a theoretical basis for oncology approaches in different types of GI cancer.

Employment disruption and missed workdays after neoadjuvant therapy receipt for high-risk gastrointestinal cancer.

Chronic pancreatitis (CP) is driven by smoking, excessive alcohol use, and chronic inflammation - all known contributors to carcinogenesis. However, its association with malignancies beyond the pancreas remains underexplored. This study aimed to assess the frequency and spectrum of cancers in patients with CP. A retrospective cohort study was conducted at Nottingham University Hospitals of patients diagnosed with CP between 1 January 2006 and 31 December 2014, identified through a multisource case ascertainment strategy. Cancer frequencies were assessed in patients residing within Greater Nottingham. Age-adjusted standardised incidence ratios (SIRs) were calculated using national cancer incidence data from England as the reference population. Statistical analyses were performed using R (version 4.3.3). Of the 1003 CP patients identified, 678 resided in Greater Nottingham (median age at diagnosis 68 years (IQR 53-79); 66% male; 92% Caucasians. The median follow-up period was 7.3 years (IQR 2.8-11.6). Compared to the general population, patients with CP demonstrated significantly higher SIRs for upper respiratory tract (12.4; 95%CI 6.6-21.1; p < 0.0001), pancreatic (10.8; 95%CI 6.2-17.6; p < 0.0001), liver (8.8; 95%CI 2.4-22.6; p < 0.0001), lung (5.6; 95%CI 4.0-7.7; p < 0.0001), renal tract (4.8; 95%CI 2.7-7.9; p < 0.0001) oesophageal (4.8; 95%CI 1.8-10.4; p = 0.0001) and colorectal (2.5; 95%CI 1.4-4.2; p = 0.0009) cancers. CP confers a markedly elevated risk of both pancreatic and extra-pancreatic cancers. These findings hypothesise that CP might be a high-risk state for malignancy that could warrant proactive, risk-based cancer surveillance in this vulnerable population.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are increasingly prescribed for type 2 diabetes and obesity, conditions frequently encountered in gastroenterological practice. Their pleiotropic effects along the gut-pancreas-liver axis have raised both therapeutic interest and safety concerns, particularly regarding hepatic outcomes, gastrointestinal cancers, peri-endoscopic management, and gastrointestinal adverse events. This position paper, endorsed by the Italian Society of Gastroenterology (SIGE), was developed according to the GRADE framework and provides evidence-based recommendations for the safe and effective management of GLP-1RAs in gastroenterology, highlighting their favorable benefit-risk profile while identifying key knowledge gaps requiring future prospective studies. GLP-1RAs may be safely used in patients with diabetes or obesity and metabolic dysfunction-associated steatotic liver disease. In cirrhotic patients with diabetes or obesity, GLP-1RAs appear safe and are associated with reduced hepatic decompensation. Available evidence does not support an increased risk of esophageal, gastric, colorectal, or pancreatic cancer, while a potential reduction in hepatocellular carcinoma incidence is suggested. Routine discontinuation of GLP-1RAs before upper gastrointestinal endoscopy is not recommended. GLP-1RAs increase the risk of mild, transient gastrointestinal adverse events and cholelithiasis but are not associated with severe gastrointestinal complications or acute pancreatitis.

Predictive impact of systemic inflammation and tertiary lymphoid structures on pathological complete response in neoadjuvant-treated advanced esophageal squamous carcinoma patients.

ASO Visual Abstract: Association of Adjuvant Immunotherapy with Improved Survival for Stage II-III Esophageal Cancer: Four-Year National Perspective.

Endoscopic submucosal dissection using the water pressure method for superficial esophageal cancer within a cervical pseudodiverticulum.

Immune checkpoint inhibitor-induced myocarditis with atrioventricular conduction abnormalities: a case report.

Advancing Particle Therapy to Improve Cancer Care: Report on "2nd World Forum on Particle Therapy".