Patients with metabolic dysfunction-associated steatotic liver disease (MASLD) are at increased risk of both hepatic and extrahepatic adverse outcomes. However, the evidence regarding lean MASLD and its prognosis remains controversial.

Our previous genome-wide association study (GWAS) identified that chromosome 1p36.22 locus contributes to the risk of hepatocellular carcinoma (HCC).

For large non-pedunculated rectal polyps, en bloc resection via endoscopic submucosal dissection (ESD) is typically recommended due to presumed higher risk of submucosal invasive cancer (SMIC) compared with the colon; however, data on cancer risk by location remain controversial.

With population ageing, elderly patients account for a growing proportion of hepatic surgery recipients. Hepatic ischaemia-reperfusion injury (HIRI) is a major cause of postoperative liver dysfunction, particularly in aged livers, yet its mechanisms remain poorly understood.

The identification and characterisation of somatic cancer driver mutations in the non-coding genome remains challenging.

The burden of gastric cancer remains substantial in Asia. Gastric premalignant conditions, including chronic atrophic gastritis, intestinal metaplasia and dysplasia, are important intermediate stages in the gastric carcinogenesis cascade. The sojourn time allows endoscopic surveillance to have a pivotal role in early detection and timely intervention.

The combination of atezolizumab and bevacizumab (ATZ/BVZ) therapy has significantly advanced therapeutic approaches for hepatocellular carcinoma (HCC). However, less than 30% of patients achieve durable responses, highlighting the urgent need to understand mechanisms underlying resistance.

Acute-on-chronic liver failure (ACLF) is characterised by intense systemic inflammation and high short-term mortality, yet effective targeted therapies are lacking.

The clinical and molecular heterogeneity of IBD-both between patients and within the same individual over time-continues to pose a significant challenge to the implementation of truly personalised treatment strategies. Unlike oncology, where somatic mutation patterns define an actionable information layer, IBD lacks detectable dominant molecular drivers that can guide therapeutic choices. Although the therapeutic landscape has broadened with the advent of numerous biologics and small molecule drugs, predictive (ex ante) biomarkers for treatment response remain elusive. In this review, we assess the current progress and limitations of biomarker-guided precision therapy in IBD. We argue that traditional binary response definitions at single landmark endpoints fail to reflect the multidimensional and dynamic nature of therapeutic outcomes. We hence propose combined, and thus individualised, endpoints such as comprehensive disease control as a more holistic and responsive therapy goal in IBD. We propose to integrate the individual longitudinal dynamics of treatment response, and also continuous, objective monitoring of subclinical residual inflammation, analogous to the concept of minimal residual disease in oncology. In this concept, longitudinal assessment of patient-reported outcomes and molecular profiling in response to therapy may serve as early predictors of long-term outcomes, guide early therapeutic adjustments and reveal mechanisms that open new therapeutic avenues, such as adjunct or combination treatments. Adopting this dynamic, data-driven approach to treatment adaptation could shift management of IBD from reactive to proactive and substantially improve long-term outcomes with the vision to fully control a life-long disease.

Colorectal cancer (CRC) is one of the most common malignant cancers and its incidence is steadily rising particularly in young patients. While screening measures and the widespread availability of surgical treatment have led to an impressive improvement of prognosis within the overall CRC population, patients with metastatic CRC still face 5-year survival rates of around 10-25%. Despite continuous development of new systemic treatment strategies that include cytotoxic chemotherapy and targeted therapy, most patients with metastatic CRC eventually progress. However, a small proportion of patients with mismatch repair-deficient or microsatellite unstable CRC responds exceptionally well to treatment with immune checkpoint inhibitors, thereby proving that CRC is in principle amenable to immunotherapy and showing that long-term disease stabilisation can be achieved even in metastasised stages. However, the reasons for the lack of response to immunotherapy in the vast majority of CRC cases remain to be elucidated. Yet, recent evidence suggests that the tumour stroma, which includes non-immune cells in the colorectal tumour microenvironment, mediates immunosuppressive mechanisms that prevent effective immunotherapy. These findings open new avenues for the development of advanced immunotherapies for CRC. In this review, we summarise major developments in the systemic therapy of CRC within the last couple of decades, provide an overview of emerging and soon-to-be implemented therapeutic strategies and present concepts from clinical and preclinical research to manipulate tumour cells and the tumour stroma to sensitise microsatellite stable colorectal tumours to immunotherapy.