Cyanidin-3-O-glucoside (C3G), the most widely distributed anthocyanin (ACN) in edible fruits, has been proposed for several bioactivities, including anti-inflammatory, neuro-protective, antimicrobial, anti-viral, anti-thrombotic and epigenetic actions. However, habitual intake of ACNs and C3G may vary widely among populations, regions, and seasons, among individuals with different education and financial status. The main point of C3G absorption occurs in the small and large bowel. Therefore, it has been supposed that the treating properties of C3G might affect inflammatory bowel diseases (IBD), such as ulcerative colitis (UC) and Crohn’s disease (CD). IBDs develop through complex inflammatory pathways and sometimes may be resistant to conventional treatment strategies. C3G presents antioxidative, anti-inflammatory, cytoprotective, and antimicrobial effects useful for IBD management. In particular, different studies have demonstrated that C3G inhibits NF-κB pathway activation. In addition, C3G activates the Nrf2 pathway. On the other hand, it modulates the expression of antioxidant enzymes and cytoprotective proteins, such as NAD(P)H, superoxide dismutase, heme-oxygenase (HO-1), thioredoxin, quinone reductase-oxide 1 (NQO1), catalase, glutathione S-transferase and glutathione peroxidase. Interferon I and II pathways are downregulated by C3G inhibiting interferon-mediating inflammatory cascades. Moreover, C3G reduces reactive species and pro-inflammatory cytokines, such as C reactive protein, interferon-γ, tumor necrosis factor-α, interleukin (IL)-5, IL-9, IL-10, IL-12p70, and IL-17A in UC and CD patients. Finally, C3G modulates gut microbiota by inducing an increase in beneficial gut bacteria and increasing microbial abundances, thus mitigating dysbiosis. Thus, C3G presents activities that may have potential therapeutic and protective actions against IBD. Still, in the future, clinical trials should be designed to investigate the bioavailability of C3G in IBD patients and the proper therapeutic doses through different sources, aiming to the standardization of the exact clinical outcome and efficacy of C3G.

Background: Malnutrition affects patients undergoing surgery for gastrointestinal cancers and contributes to poor postoperative outcomes, including increased complication rates, longer hospital stays, and higher mortality. Despite the availability of several malnutrition screening tools and prognostic scores, their effectiveness in predicting postoperative outcomes remains unclear. This study aimed to compare the predictive accuracy of Patient-Generated Subjective Global Assessment (PG-SGA), Global Leadership Initiative on Malnutrition (GLIM), Geriatric Nutritional Risk Index (GNRI), and Controlling Nutritional Status (CONUT) score for postoperative outcomes in patients undergoing surgery for colorectal, hepato-pancreato-biliary and upper gastrointestinal cancers. Methods: A cross-sectional observational study from March 2022 to October 2023 was conducted in two university surgical departments, after registration on ClinicalTrials database (NCT05795374). Patient characteristics, preoperative nutritional status and postoperative outcomes were analyzed. Results: In total, 480 patients were enrolled. CONUT and GNRI demonstrated high specificity (over 90% and 80%, respectively) for predicting overall complications, major complications, prolonged hospital stay, mortality, and advanced disease stage across all cancer types. Notably, CONUT showed a specificity over 97% and GNRI over 89.7% for colorectal and upper gastrointestinal cancer patients, respectively, despite their lower sensitivity. On the contrary, PG-SGA and GLIM presented better sensitivity (up to 50%), but slightly lower specificity (up to 86.4%). Conclusions: CONUT and GNRI are valuable for ruling out non-at-risk patients for adverse postoperative outcomes, while PG-SGA and GLIM provide better sensitivity. A step-up approach—initial screening with PG-SGA and GLIM, followed by detailed evaluation with CONUT or GNRI— should be validated in future studies across diverse clinical settings.

Background: Patients with pancreatic cancer are at increased risk of malnutrition and functional decline. This study aimed to identify preoperative nutritional and functional risk factors associated with postoperative complications. Methods: Adult patients with pancreatic cancer admitted to two university surgical departments in Athens, Greece, were included. Preoperative laboratory values, nutritional status, and functional status were assessed. Results: Among 96 patients included in this study, postoperative complications occurred in 69 (71.9%). Complication rates were significantly higher in patients with severe malnutrition (87.9% vs. 62.7%, p = 0.015), low Geriatric Nutritional Risk Index (GNRI) (90.5% vs. 66.2%, p = 0.023), low handgrip strength (91.7% vs. 61.5%, p = 0.037), and low gait speed (90.5% vs. 63.6%, p = 0.027). Major complications were linked to lower hemoglobin (Hb) (11.5 ± 1.9 vs. 12.8 ± 1.7 g/dL, p = 0.001), lower hematocrit (HCT) (34.7 ± 5.4% vs. 38.4 ± 4.7%, p = 0.001), and severe malnutrition (42.4% vs. 23.7%, p = 0.05). Lower Hb, lower HCT, malnutrition, and greater waist circumference were associated with postoperative mortality. Longer hospital stays were correlated with weaker handgrip strength and slower gait speed. Conclusion: Preoperative malnutrition and impaired functional status are significant predictors of adverse postoperative outcomes in pancreatic cancer surgery.

Background/Objectives: Chemerin, which is a multifunctional cytokine and adipokine, has been implicated in inflammatory and metabolic processes and might play a role in upper gastrointestinal (GI) malignancies, particularly gastric and esophageal cancer. The aim of this review is to explore the role of chemerin in the pathophysiology of upper GI cancers, as well as its potential as a biomarker for early detection and as a therapeutic target. Methods: A comprehensive review of recent studies about chemerin’s biochemical properties and interaction with its receptors, as well as its effects on inflammatory responses, immune regulation, and metabolic processes, was conducted. The clinical implications of chemerin for gastric and esophageal cancer were analyzed, whereas the potential therapeutic strategies targeting chemerin were discussed. Results: Elevated chemerin levels are associated with poor prognosis in gastric cancer and promote invasiveness and metastasis in esophageal cancer. Chemerin receptor antagonists show promising results in inhibiting cancer cell migration, invasion, and progression. Conclusions: Chemerin could represent a valuable prognostic biomarker and therapeutic target for upper GI cancers. Future observational studies should validate its clinical applications and investigate the efficacy of chemerin inhibitors as potential therapeutic targets.

Background: Gastric and esophageal cancers are among the most lethal malignancies worldwide, necessitating improved biomarkers and therapeutic targets to improve patient outcomes. Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), is a metabolic enzyme and adipokine with emerging significance in cancer progression. It has been implicated in tumor cell proliferation, angiogenesis, immune modulation, and chemotherapy resistance, yet its clinical relevance in upper gastrointestinal (GI) cancers remains unclear. This review aims to explore visfatin’s biochemical properties, its role in the pathogenesis of upper GI cancers, and its implications for potential therapeutic interventions. Methods: A comprehensive review of the literature was conducted to evaluate the role of visfatin in gastric and esophageal cancer. We analyzed studies investigating visfatin expression in tumor tissues, blood, and adipose tissue, its prognostic significance, and its potential as a therapeutic target. Preclinical and clinical studies evaluating visfatin inhibitors were also reviewed. Results: Visfatin promotes tumor progression through the activation of key oncogenic pathways leading to increased angiogenesis, epithelial–mesenchymal transition (EMT), and immune suppression. Elevated visfatin levels are associated with advanced tumor stage, reduced response to chemotherapy, and poor prognosis in both gastric and esophageal cancers. Therapeutic agents targeting visfatin, such as the inhibitor FK866, have shown promising results in reducing tumor proliferation by >50%, improving chemoresistance, and restoring antitumor immunity in preclinical studies. However, clinical translation remains limited due to toxicity concerns and the need for more targeted therapies. Conclusions: Visfatin is a promising biomarker and potential therapeutic target in gastric and esophageal cancer. However, its precise role and mechanisms require further investigation. The standardization of measurement techniques and large-scale clinical studies is needed to validate its prognostic and predictive value. Future research should focus on optimizing visfatin-targeted therapies, particularly in the context of obesity-associated malignancies and chemoresistant tumors.