Gastric cancer, with disproportionately higher incidence in East Asia, arises from complex host-microbiome-environment interactions beyond Helicobacter pylori (HP) infection. However, the molecular architecture linking environmental carcinogens, microbial succession and host response remains unclear.

The optimal surgical strategy for adenocarcinoma of oesophagogastric junction (AEG) remains debated, particularly regarding lymphadenectomy extent, gastrectomy type and surgical approach, with real-world prospective evidence being scarce.

Post-infection disorders of gut-brain interaction (PI-DGBI) are a subset of chronic gastrointestinal disorders triggered by acute infectious gastroenteritis. These conditions impose a significant burden on patients' quality of life.

Postoperative recurrence (POR) is a major challenge in the long-term management of Crohn's disease (CD), affecting up to 70% of patients within the first year after surgical resection. The multifactorial pathogenesis of POR complicates prevention, while evolving surgical techniques and different anastomotic configurations further hinder accurate prediction and monitoring.Current surveillance strategies, including standard ileocolonoscopy and faecal calprotectin, remain limited by suboptimal accuracy, the absence of validated scoring systems and the lack of standardised monitoring intervals. Recent advances in high-resolution endoscopic imaging, such as confocal laser endomicroscopy and endocytoscopy, enable real-time, in vivo microstructural assessment of the anastomosis, offering opportunities for earlier and more precise detection of recurrence. In parallel, developments in intestinal ultrasound and cross-sectional imaging are reshaping non-invasive monitoring by providing transmural evaluation. Beyond imaging, multiomics approaches, spanning genomics, transcriptomics, proteomics, metabolomics and metagenomics, are uncovering novel biological pathways linked to POR, providing new mechanistic insights.Artificial intelligence (AI) has the potential to integrate clinical, endoscopic, imaging and omics data into predictive multimodal models for POR, supporting individualised risk stratification, early detection and personalised treatment strategies. While promising, these innovations require prospective validation, methodological standardisation and integration into clinical workflows before translation into routine practice.This review summarises the current understanding of POR, highlights emerging diagnostic and monitoring technologies and explores how AI-enabled endoscopy and multi-omics approaches may transform future management, paving the way towards precision medicine for POR in CD.

RNA 5-methylcytosine (m5C) has emerged as a critical epigenetic regulator in cancer biology, yet its role in the tumour immune microenvironment (TME) remains incompletely understood.

Coexistence of metabolic dysfunction-associated steatotic liver disease (MASLD) increases hepatocellular carcinoma (HCC) risk after HCV cure.

Genetic studies of stool frequency (SF), an indirect proxy for gastrointestinal transit, may reveal therapeutically tractable pathways relevant to IBS and other dysmotility disorders.

The pathogenesis of liver fibrosis centres on the activation of hepatic stellate cells (HSCs). Adenosine-to-inosine RNA editing, primarily catalysed by adenosine deaminase acting on RNA1 (ADAR1), is the most prevalent post-transcriptional modification that increases transcriptome diversity.

IBD is characterised by recurrent flares, but evidence on whether modifiable dietary factors influence flare risk is limited.

Oncological principles favour en bloc R0 excision for curative endoscopic resection. In Barrett's neoplasia, endoscopically curable cancers include T1a and selected early T1b disease. Although endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD) are established treatments, optimal lesion selection remains debated.

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterised by remarkable cellular heterogeneity, which emerges early from the interplay of oncogenic KRAS signalling and inflammatory injury. However, the transcriptional, metabolic and functional properties of these pre-malignant cell states that initiate and drive PDAC progression remain elusive.

Why alcohol-associated liver disease (ALD) resolves after abstinence in most people but progresses to liver failure in others remains poorly understood. Experimental models show that increased exposure to proinflammatory cytokines exacerbates ALD, yet clinical trials targeting these cytokines have failed. The tumour necrosis factor alpha (TNFα)-inducible zinc finger protein 36 (ZFP 36) family of RNA binding proteins controls the outcomes of TNFα exposure by destabilising suites of messenger RNAs (mRNAs) that execute the pleiotropic downstream actions of TNFα.

Accumulating evidence has demonstrated that distinct tumour-promoting and tumour-restraining cancer-associated fibroblast (CAF) subtypes coexist in pancreatic ductal adenocarcinoma.

CLDN18.2 has emerged as a promising therapeutic target in gastric and gastro-oesophageal junction cancers. However, its clinical efficacy in pancreatic ductal adenocarcinoma (PDAC) has been modest, suggesting the presence of regulatory mechanisms impairing its efficacy.

Dysosmobacter welbionis is a recently discovered butyrate producer whose presence in stool correlates with improved metabolic health. Whether its abundance is reduced in individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) remains unknown. Mechanistic insight into its butyrate production from myo-inositol, a dietary compound from fruits, beans, grains and nuts with metabolic benefits, is also limited.

Over 90% pancreatic cancers harbour activating kirsten rat sarcoma viral oncogene homolog (KRAS）mutations. However, monotherapies targeting the KRAS vertical pathway, with recently developed KRAS inhibitors or rapidly accelerated fibrosarcoma (RAF)/MEK/ERK inhibitors, have demonstrated limited clinical benefit. Therefore, there is an urgent need to identify novel therapeutic targets and combination strategies with KRAS inhibition.

Immune checkpoint inhibitors (ICIs) have revolutionised cancer treatment and patients' survival. However, ICIs also cause severe immune-related adverse events, notably colitis, resulting in ICIs therapy discontinuation and tumour immunotherapy failure. This study investigates long myosin light chain kinase 1 (MLCK1), a known regulator of tight junction and gut permeability, to elucidate the mechanisms underlying ICI-mediated colitis and identify approaches to reduce this toxicity.

Inflammatory bowel disease (IBD) arises from complex interactions among diet, host and gut microbiome. Although diet influences intestinal inflammation, the microbial and metabolic pathways involved, and their differences between Crohn's disease (CD) and ulcerative colitis (UC), the two main subtypes of IBD remain unclear.

IBD is rising worldwide and is now a global disease. With the expanding armamentarium of medical therapies, including biologics and small molecules, there is a decline in hospitalisation rates and IBD-related surgeries. However, high costs, injectable therapy, risk of opportunistic infections and the lifelong nature of the disease pose significant challenges in the management of IBD. Developing countries are also constrained by a lack of trained manpower, as well as economic and infrastructural limitations. Strategies aimed at the prevention of IBD may alleviate the suffering and cost of this disease. Suggested approaches include implementation of prevention and interception trials using dietary, pharmacological and precision medicine approaches. However, these would necessitate massive funding and equitable infrastructural support for identifying the population at risk (for prevention trials) and those with preclinical disease (for interception trials). Hence, these strategies are unlikely to be globally practicable or economically viable, particularly in the Global South. It is believed that IBD, like certain non-communicable diseases (NCDs) such as metabolic syndrome and cardiovascular disorders, may be preventable by modifying the risk factors. Therefore, in this review, we advocate for an alternative approach of combining evidence-based IBD prevention strategies with the time-tested strategies of NCD prevention approaches already being implemented. We suggest a sieving strategy for selecting preventive measures through a series of sieves-interventions that have evidence to support prevention, align with NCD prevention and are economically viable.

Streptococcus anginosus has been linked with an increasing risk of gastric cancer (GC) and recognised as a signature for GC screening.