With the introduction of Janus kinase inhibitors like tofacitinib, the treatment landscape for ulcerative colitis (UC) is changing quickly. Response heterogeneity is still a significant clinical challenge in spite of its quick onset and oral convenience. Extending tofacitinib induction beyond the standard eight weeks can produce significant benefits in a subset of patients without sacrificing safety, according to evidence from pivotal trials and real-world studies. We review recent real-world evidence, highlight lessons learnt from extended induction therapy, and present a practical framework to help guide tailored treatment decisions in this editorial. After 16 weeks of prolonged induction, more than half of patients with moderate-to-severe UC experienced remission, with durable persistence and favorable safety, according to a multicenter 52-week real-world study published in this issue of the World Journal of Gastroenterology. Crucially, outcomes and maintenance dosing were impacted by modifiable factors like smoking and biologic exposure. Mechanistic findings support a response-guided rather than fixed-duration induction paradigm by indicating that immune kinetics, mucosal healing rates, and previous biologic exposure may account for delayed responses. An effective, patient-centered strategy that could maximize tofacitinib's therapeutic potential and assist in guiding refractory UC patients towards long-term remission is extended induction.

Chronic hepatitis B (CHB) infection is a global public health burden, affecting over 250 million persons globally, and is associated with substantial morbidity and mortality due to cirrhosis, hepatic decompensation, and hepatocellular carcinoma. Metabolic syndrome and metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasingly common co-morbidity among patients with CHB, affecting an estimated 25%-40% of individuals. The physiologic and clinical impact of co-existing CHB and metabolic syndrome and/or MASLD [met-hepatitis B virus (HBV)] is poorly understood, although recent data suggest important associations with poorer antiviral response and clinical outcomes. This review summarizes current and emerging evidence addressing this relationship, and outline recommendations for the diagnosis, risk stratification, staging, and management of Met-HBV.

Pancreatic cancer, a highly malignant gastrointestinal tumor, has a five-year survival rate of only 10%. With the increasing aging population, its incidence is rising across East Asia, North America, and Europe. Chemotherapy remains a basic strategy of the current treatment regimen for pancreatic cancer. However, the development of multidrug resistance poses a significant challenge, drastically reducing the efficacy of chemotherapy agents. The mechanisms underlying resistance in pancreatic cancer remain incompletely understood. To overcome this obstacle, scientists are dedicated to discovering new therapeutic strategies and addressing the issue of resistance. Plant-derived chemicals played essential roles in many documented ancient cultures, such as those in ancient China, ancient Egypt, ancient India, and ancient Babylon. Many modern medications are derived from plants, including paclitaxel, a widely used and effective chemotherapy agent originally derived from the Pacific yew tree. Although the development of plant-based compounds for cancer treatment is still under development, these compounds offer several advantages, including a long history of safe use, fewer side effects, lower costs, and improved patient acceptance. Recent studies have shown that plant-derived chemicals can significantly inhibit tumor cell proliferation and reversal drug resistance. Clinical trials have demonstrated promising therapeutic effects of these compounds in cancer treatment. This review summarizes recent research on the role of plant-derived compounds in overcoming drug resistance in pancreatic cancer. It provides insights into the mechanisms of drug resistance and highlights the potential of plant-based compounds as alternative therapeutic strategies. Considering the limitations of current therapies and the growing issue of drug resistance, plant-derived compounds offer a promising direction for enhancing treatment outcomes. This review aims to inform future research and promote the development of more effective, safer, and patient-friendly treatment options for pancreatic cancer.

Liu et al recently published research suggesting that multistrain probiotics significantly relieved bismuth quadruple therapy (BQT)-associated gastrointestinal symptoms without affecting eradication success. They conducted a rigorous randomized, double-blind, placebo-controlled trial, demonstrating that a 4-week regimen of a multistrain probiotic supplement significantly reduced symptoms such as reflux, dyspepsia, and diarrhea. The reduction in side effects and enhanced patient comfort highlight the clinical utility of probiotics as a safe and well-tolerated adjunct to BQT. Our contribution was about to involve the traditional Chinese medicine treating Helicobacter pylori-related chronic gastritis. They can have similar functions in regulating gut microbiota. Future research should build on this foundation to refine probiotic formulations, explore their long-term effects, and clarify their role in achieving higher eradication rates.

Cholelithiasis represents a common clinical condition within the digestive tract and continues to pose a substantial global health challenge, largely due to its high rate of recurrence and a scarcity of effective non-surgical interventions. Although protein succinylation has been widely characterized as a post-translational modification, its implications in cholelithiasis pathogenesis had remained poorly defined. A groundbreaking study by Wang et al demonstrates that lysine acetyltransferase 2A-mediated succinylation of adenosine monophosphate-activated protein kinase suppresses cholelithiasis. This work not only provides novel mechanistic insights into cholelithiasis but also establishes succinylation as a promising therapeutic target, thereby addressing a critical knowledge gap in the field.

Pediatric inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), presents significant diagnostic challenges due to its heterogeneous clinical presentation and reliance on invasive procedures such as endoscopy. Recent studies highlight the potential of non-invasive biomarkers, particularly serum cytokines, for distinguishing pediatric IBD from non-IBD conditions. CXCL9, interleukin 8, and interleukin 22 have shown strong discriminatory ability, correlating with disease activity and aiding in the differentiation between CD and UC. These biomarkers may also inform disease progression and treatment needs, including the identification of patients likely to require biologic therapy. However, important gaps remain in translating biomarker findings into routine clinical practice, especially for predicting long-term treatment response. This editorial summarizes recent advances in non-invasive biomarkers for pediatric IBD, focusing on serum, fecal, and genetic markers, and discusses their integration with conventional diagnostic approaches. Ongoing validation in large pediatric cohorts is required to support clinical implementation and optimize biomarker-guided management strategies.

A major driver of hepatocellular carcinoma (HCC)'s aggressiveness is its ability to hijack the immune system, specifically by recruiting immunosuppressive tumor-associated macrophages. These M2-type macrophages are coerced into promoting tumor growth and metastasis. This study by Escobedo-Calvario et al reveals that the protein growth differentiation factor 11 can effectively "re-educate" these pro-tumoral macrophages by reducing classic M2 markers, rewiring cellular metabolism, and boosting production of reactive oxygen species, which ultimately switch the macrophages from a pro-tumor state toward an anti-tumor state. When applied to HCC cells, growth differentiation factor 11 also reduced the cancer cells' capacity to proliferate and migrate - key hallmarks of deadly metastasis. This two-pronged attack could represent a groundbreaking strategy to enhance current immunotherapies and control the aggressiveness of HCC, offering new hope for future treatments.