Chronic colonic inflammation can lead to colitis-associated cancer (CAC) in ulcerative colitis (UC) patients. The host-microbiome interface plays a critical role in CAC development. Quorum-sensing molecules (QSMs) are bacterial products that regulate bacterial processes. We investigated whether QSMs are related to risk factors for CAC in UC patients and drive CAC development in mouse models.

Primary biliary cholangitis (PBC) is a chronic, progressive autoimmune disease characterized by the destruction of intrahepatic biliary epithelial cells, progressive fibrosis, and the expression of anti-mitochondrial antibodies. Although ursodeoxycholic acid (UDCA) can significantly improve liver biochemical parameters and delay disease progression as a first-line treatment, 40% of patients still have a poor response to UDCA treatment. Inflammation involving different regions of the hepatic lobule may be related to the therapeutic effect of UDCA. The aim of this study is to investigate the relationship between liver inflammation zones and UDCA treatment response in PBC patients, and to further analyze the predictive value of liver lobular zones for treatment response.

Precise staging is essential for treatment options and patient benefits in individuals with unresectable pancreatic ductal adenocarcinoma (PDAC). Laparoscopic biopsy is a minimally invasive procedure used to identify radiographically occult metastases and accurately stage unresectable PDAC. The cancer antigen 125 (CA125) levels change rule after laparoscopic biopsy and its correlation with overall survival (OS) in patients with unresectable PDAC remains unclear.

The underlying mechanisms of incomplete response to ursodeoxycholic acid (UDCA) therapy in patients with primary biliary cholangitis (PBC) remain unclear. This study aimed to investigate the clinicopathological characteristics and potential mechanisms of hepatobiliary (HB) cells in PBC patients with an incomplete response to UDCA.

Peptic ulcer disease (PUD) remains a cause of gastrointestinal mortality despite advances in Helicobacter pylori eradication and gastroprotection.

Severe acute pancreatitis (SAP) is a critical gastrointestinal disorder associated with high mortality. Dysregulated ferroptosis, an iron-dependent form of cell death, is recognized as a pivotal mechanism driving SAP progression. Although Homoplantaginin (Homo) exhibits notable anti-inflammatory and antioxidant properties, its specific role in modulating ferroptosis during SAP remains unclear.

Total bilirubin (TB) has been regarded as a key prognostic factor for patients with primary biliary cholangitis (PBC), yet the prognostic significance of direct bilirubin (DB) is unclear. This study aimed to investigate the role of DB in predicting outcomes in patients with PBC.

Esophageal squamous cell carcinoma (ESCA) represents a prevalent, highly aggressive malignancy of the digestive tract. Notably, both its proliferation and metastatic dissemination are facilitated by the tumor microenvironment (TME). One intriguing option for non-invasive biomarkers has been found to be miRNA. MicroRNA-21-5P is an essential regulator of biological processes such as the growth, migration, invasion, and metastasis of some malignancies. The prediction software successfully identified CNTFR as the putative target gene for miR-21-5P. To confirm this interaction, a luciferase reporter gene test was conducted to assess the binding of miR-21-5P to CNTFR. By using quantitative polymerase chain reaction (RT-qPCR), in comparison to normally adjacent tissues, the tumor tissues of patients with ESCA exhibited elevated relative expression amounts of miR-21-5P and decreased relative expression amounts of CNTFR. Furthermore, miR-21-5P mimics were able to drastically lower the CNTFR gene level, as demonstrated by RT-qPCR and western blot. On the other hand, esophageal cancer cells' expression of CNTFR can be markedly elevated by miR-21-5P inhibitors. Within the context of this research, the association between miR-21-5p and CNTFR was established through bioinformatics, luciferase reporter gene, CCK-8, EdU, transwell, flow cytometry, qRT-PCR, and WB analysis. In summary, our work identifies the miR-21-5p suppresses CNTFR expression to promote ESCA cell proliferation, invasion, and migration; these findings highlight the miR-21-5p/CNTFR axis as a promising candidate for non-invasive diagnostic biomarker development and targeted therapeutic strategy optimization in ESCA.

Sulfotransferase family 1E member 1 (SULT1E1) is a key estrogen-metabolizing enzyme whose dysregulation has been implicated in several hormone-related malignancies. However, its expression pattern, biological function, and clinical significance in hepatocellular carcinoma (HCC) remain poorly understood.

Cisplatin plus 5-fluorouracil (CF) remains a cornerstone of treatment for locally-advanced esophageal cancer (EC). However, resistance to CF-based neoadjuvant chemotherapy (NAC) remains a major clinical challenge. Clarifying whether resistance-associated molecular features are induced by treatment or already present before therapy is crucial for improving patient stratification.

Triglyceride-glucose (TyG) index and its composite parameters have been proposed as surrogate indicators of insulin resistance. However, their association with metabolic dysfunction–associated fatty liver disease (MAFLD) among older adults living at moderate altitude remains insufficiently examined. The present study aims to investigate the association between TyG-related indices and MAFLD in this population and to identify the optimal screening indicator.

Multimodal profiling of inflammatory bowel disease (IBD) patient tissue and blood samples has revealed the disease spectrum in unprecedented detail, and cellular and molecular correlates of disease severity and outcome in IBD have been elaborated. Incorporating these in the clinical setting would offer a unique opportunity to increase the granularity of current clinical measures and to better assess treatment response. Remission and healing at a cellular/molecular level are also likely to have predictive value for long-term outcomes. Here, we outline a path forward to implementing the most promising molecular disease descriptors as future clinical treatment targets in IBD. We focus on the concept of cellular/molecular measures of inflammation, remission, healing, response to therapy, and target pathway engagement. Monitoring mode-of-action-specific pharmacodynamic modules in the context of disease-related resolution pathways will guide assessment of novel and existing therapies. Artificial intelligence-assisted tools will be key to enabling this development, improving reproducibility, limiting costs, and delivering fast detection.

Genetic susceptibility to inflammatory bowel disease (IBD) has been widely studied, whereas the genetic contribution to disease progression remains relatively underinvestigated. In a Danish nationwide cohort, we aimed to explore if genetic susceptibility to IBD associated with disease severity.

Angiofibroma of soft tissue (AFST) is a rare benign mesenchymal tumor, typically occurring in the deep soft tissues of the extremities. Histologically, it is characterized by bland spindle cells and an abundant branching vasculature. Owing to the absence of specific markers, this lesion is frequently misdiagnosed as other spindle cell neoplasms, leading to inappropriate clinical management. Primary AFST arising in the small intestine has not been formally reported to date. This report presents a case of primary small intestinal AFST manifesting initially as intussusception and intestinal obstruction.