Pancreatic ductal adenocarcinoma (PDAC) is characterised by a dismal prognosis and insensitivity to immune checkpoint blockers (ICBs); however, the underlying mechanism remains elusive.

Gastric cancer (GC) is one of the most common malignancies worldwide and it is the third leading cause of cancer-related death in China. While Helicobacter pylori is a known GC pathogen, its abundance declines in tumours and the role of other bacteria in GC metastasis remains unclear.

Liver metastasis is a common and fatal event for patients with pancreatic ductal adenocarcinoma (PDAC). Dysregulated mitochondrial dynamics reshape biological processes, including metabolism reprogramming, which disrupts immune cell function and promotes metastatic progression.

Plasmablast-derived HBV surface antigen (HBsAg)-specific monoclonal antibody (mAb) and structural basis for binding to native HBsAg are poorly known.

Chronic visceral pain in IBS with diarrhoea (IBS-D) is a profound therapeutic challenge. While aberrant central processing is implicated, the key brain regions driving this visceral pain and their suitability as neuromodulatory targets remain undefined.

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.

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.

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.

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.

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.

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.

Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality with limited therapeutic options. Despite promising immunotherapy, response rates remain suboptimal. Tumour-associated macrophages (TAMs) constitute a pivotal component of the immunosuppressive HCC microenvironment, yet TAM heterogeneity and contributions to tumour progression and immunotherapy resistance remain poorly defined.

The efficacy of pharmacological glycogen synthase kinase-3β (GSK3β) inhibition is currently being investigated in unselected cohorts of metastatic pancreatic ductal adenocarcinoma (PDAC). Here, we sought to determine the clinical significance of nuclear GSK3β accumulation in patients with resectable PDAC.

Perianal fistulising disease (PFD) is a complication that affects about 20% of patients with Crohn's disease (CD) whose aetiology remains unknown.