In the past 5 years, clinical trials on immune checkpoint inhibitors (ICIs) for the treatment of locally advanced rectal cancer (LARC) have flourished globally, and China has become one of the leading regions in this field. In response to the breakthrough progress and accumulation of evidence from key clinical trials, the Chinese Society of Colorectal Surgery has recognised the need for updated consensus guidance on the development of perioperative and organ-preserving treatment strategies for LARC. This expert consensus guidance provided unified standards for the indications, medication regimens, efficacy evaluations and follow-up of ICIs in this population, with a focus mainly on perioperative management and organ-sparing strategies. The diagnostic part of this consensus guidance is based on the internationally recognised definition of mismatch repair/microsatellite instability detection and emphasises the importance of multidisciplinary teams in treatment decision-making. In terms of treatment, based on the results of key trials that have changed clinical practice in the past 5 years, this expert consensus provides graded recommendations for the duration of preoperative immunotherapy and the necessity of postoperative adjuvant therapy, local resection and organ preservation strategies. Moreover, we refined the management process for the safety of perioperative immunotherapy. This document aims to provide a reference for surgeons; internal medicine, radiation therapy, pathology and imaging physicians; patients and nursing staff involved in the treatment of LARC, as well as health policy makers.

Gut microbiota dysbiosis is linked to autism spectrum disorder (ASD) in children. However, the role of bacterial genomic structural variations (SVs) in ASD remains largely unexplored.

Metabolic dysfunction associated steatotic liver disease (MASLD), the most common chronic liver disease globally, may originate early in life. While maternal obesity is linked to offspring MASLD, the roles of paternal obesity and mediation by childhood adiposity remain unclear.

Hypertriglyceridaemia-induced acute pancreatitis (HTG-AP) is frequently complicated by acute lung injury (ALI), which worsens prognosis. Oleic acid (OA), a major circulating free fatty acid, may play a key role, but the underlying mechanism remains unclear.

CDH1 is commonly mutated in sporadic diffuse gastric cancer (DGC) and germline CDH1 mutations underlie most cases of the cancer syndrome hereditary DGC.

Barrett's oesophagus (BE) continues to rise in prevalence alongside oesophageal adenocarcinoma; understanding and identifying early neoplastic changes is critical. Crypt dysplasia (CD) in BE is an emerging concept characterised by dysplasia confined to the crypt base without surface involvement. Recent studies suggest that CD shares molecular alterations with low-grade and high-grade dysplasia, such as TP53 mutations and chromosomal instability, and may represent an early phase of neoplasia. Grading of CD remains inconsistent, with limited correlation to clinical outcomes, although classifying CD into low-grade and high-grade categories provides a practical diagnostic framework. High-grade crypt atypia typically warrants a diagnosis of CD, whereas low-grade crypt atypia poses greater diagnostic challenges and requires careful differentiation from reactive changes. This framework also incorporates exclusionary criteria, such as inflammation, ulceration and erosion. This review encompasses key features of CD, the diagnostic pitfalls encountered in clinical practice and the underlying biology driving crypt dysplasia. Future studies focusing on the natural history of CD, its molecular underpinnings and interobserver reproducibility will be pivotal in refining diagnostic criteria and improving patient outcomes in BE.

Inflammatory bowel disease (IBD) is typically diagnosed after the onset of symptoms in the context of established, characteristic patterns of intestinal inflammation. However, there is now substantial evidence pointing to a prolonged, biologically active preclinical phase of disease. Analysis of archived biological samples from large-scale longitudinal cohort studies of healthy individuals, some of whom develop incident IBD, has identified different molecular features that can be detected many years before clinical presentation. These include increased titres of antimicrobial and autoreactive antibodies and perturbations in a complex network of circulating, immunologically active proteins. As well as affording 'diagnostic' opportunities to identify individuals destined to develop IBD, an integrated view of these multiple different molecular features enables speculation of potential proximal drivers of preclinical IBD. Consistently recognised associations include dysregulated mononuclear phagocyte-lymphocyte interactions, augmented chemotaxis, frequently relating to interferon-γ-driven chemokine programmes and evidence of early tissue injury, such as increased circulating extracellular matrix components and metalloproteinases. Increased levels of circulating antibacterial and antiviral antibody responses hint towards disordered host-microbe interactions as potential prime triggers for the transition between health and early disease, although it is possible that these serological responses are an epiphenomenon linked to early mucosal damage and microbial translocation. There is now a timely opportunity to develop these different molecular features into scalable and clinically tractable biomarker panels to detect preclinical disease and enable strategies to proactively intercept IBD before it even develops.

Capillarisation of liver sinusoidal endothelial cells (LSECs) constitutes an early pathological event that promotes hepatic stellate cell activation and initiates liver fibrogenesis. Previous studies suggest that Ras-associated protein 1A (RAP1A) might be involved in liver fibrosis. However, the role of RAP1A in LSEC capillarisation remains unclear.

As it is a tumour-associated antigen in epithelial cells, research on claudin18.2 (CLDN18.2) has focused on its role as a therapeutic target in pancreatic cancers and its part in maintaining tight junctions.

The gut microbiota plays a crucial role in regulating host immunity, metabolism and inflammation, with accumulating evidence linking its composition and function to the development and progression of cancers in the reproductive tract. Patients with ovarian, endometrial and cervical cancers exhibit distinct alterations in their gut microbiota, characterised by reduced microbial diversity and shifts towards taxa associated with dysbiosis and chronic inflammation. Mechanistically, gut-derived metabolites and microbial translocation appear to influence systemic immune responses and oestrogen metabolism, thereby fostering a tumour microenvironment conducive to cancer growth. Beyond its role in tumourigenesis, the gut microbiota also affects treatment outcomes. Dysbiosis can reduce sensitivity to chemotherapy and alter immunotherapy responses, while antibiotic use during cancer treatment has been linked to poorer prognosis. Clinically, these insights highlight emerging applications of microbiome modulation as biomarkers for patient stratification and as adjuvant approaches to enhance therapeutic efficacy in gynaecological oncology, underscoring the therapeutic potential of targeting the microbiota-through dietary interventions, probiotics or faecal microbiota transplantation-to improve cancer treatment outcomes. However, most of these applications remain investigational, and current evidence is limited by heterogeneity across study designs, patient cohorts and cancer subtypes. This review summarises current understanding of gut microbiota profiles in reproductive tract cancers, examines potential mechanisms by which the microbiota influences malignancy, discusses its impact on therapy response and explores its emerging role in precision oncology.

Cancer-associated fibroblasts (CAFs) are key stromal components of the tumour microenvironment (TME) that profoundly influence tumour progression. However, CAFs exhibit pronounced phenotypic and functional heterogeneity, and whether conserved CAF subtypes with shared functional hallmarks exist across different cancer types remains unclear.