As an RNA-binding protein, insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is involved in enhancing the progression of a few malignant tumors by recognizing N6-methyladenosine on targeted RNA. However, the specific effects of IGF2BP2 on gastric cancer (GC) and the underlying mechanisms remain unclear. In this study, the expression level of IGF2BP2 was evaluated by analyzing data from a public database and performing immunohistochemical staining with GC specimens. The effect of IGF2BP2 on GC cell metastasis was investigated by Transwell assays and animal studies. RNA immunoprecipitation (RIP) was performed to identify potential mRNA bound to IGF2BP2. The levels of these identified RNAs were measured by RT-PCR, while corresponding proteins were quantified via Western blot. It was revealed that IGF2BP2 expression in GC tissues was significantly upregulated, and its overexpression was significantly associated with worse survival in GC patients. The aberrant expression of IGF2BP2 was demonstrated to promote the invasion and metastasis of GC cells by both in vivo and in vitro experiments. In subsequent experiments, it was then verified that by directly interacting with HMGA1 mRNA, IGF2BP2 augmented its stability and thus increased its expression. The knocking down of IGF2BP2 could significantly decrease the migration and invasion of GC cells, which could be reversed by increasing HMGA1 expression. Additionally, both in vitro and in vivo epithelial–mesenchymal transition (EMT) of GC cells were enhanced by IGF2BP2/HMGA1 axis. In conclusion, it was proven in our study that the IGF2BP2/HMGA1/EMT axis contributed to GC metastasis, suggesting its potential as a novel predictive and therapeutic biomarker for GC.

Background: Gastric cancer (GC) is one of the most common malignancies in the human digestive tract. CD4+T cells can eliminate tumor cells directly through the mechanism of cytolysis, they can also indirectly attack tumor cells by regulating the tumor TME. A prognostic model of CD4+T cells is urgently needed to improve treatment strategies and explore the specifics of this interaction between CD4+T cells and gastric cancer cells. Methods: The detailed data of GC samples were downloaded from the Cancer Genome Atlas (TCGA), GSE66229, and GSE84437 datasets. CD4⁺ T cell-related genes were identified to construct a risk-score model by using the Cox regression method and validated with the Gene Expression Omnibus (GEO) dataset. In addition, postoperative pathological tissues of 139 gastric cancer patients were randomly selected for immunohistochemical staining, and their prognostic information were collected for external verification. Immune and molecular characteristics of these samples and their predictive efficacy in immunotherapy and chemotherapy were analysed.Results: The training set and validation set had consistent results, with GC patients of high PROC and SERPINE1 expression having poorer prognosis. In order to improve their clinical application value, we constructed a risk scoring model and established a high-precision nomogram. Low-risk patients had a better overall survival (OS) than high-risk patients, consistent with the results from the GEO cohort. Furthermore, the risk-score model can predict infiltration of immune cells in the tumor microenvironment of GC, as well as the response of immunotherapy. Correlations between the abundance of immune cells with PROC and SERPINE1 genes were shown in the prognostic model according to the training cohort. Finally, sensitive drugs were identified for patients in different risk subgroup.Conclusion: The risk model not only provides a basis for better prognosis in GC patients, but also is a potential prognostic indicator to distinguish the molecular and immune characteristics of the tumor, and its response to immune checkpoint inhibitor (ICI) therapy and chemotherapy.

Background Laparoscopic segmental resection (LSR) is a common treatment modality for endoscopically unresectable colorectal polyps. Laparoscopic endoscopic cooperative surgery (LECS) has emerged as a promising alternative, yet current evidence of its efficacy remains limited. Objectives This meta-analysis aims to compare the therapeutic outcomes of LECS versus LSR for endoscopically unresectable colorectal polyps and to provide robust evidence for clinical practice. Methods This meta-analysis was prospectively registered on the PROSPERO website. We systematically searched PubMed, Embase, Cochrane Library, Web of Science, CNKI, Wanfang Data, VIP, and CBM for randomized controlled trials (RCTs) and observational studies from database inception to May 16, 2025. Data analysis was conducted using Review Manager 5.4 and Stata 18 software. Certainty of evidence was assessed using Grading of Recommendations Assessment, Development and Evaluation (GRADE). Results A total of 13 studies involving 715 patients were included in this study. Meta-analysis results showed that the LECS group had a significantly shorter length of hospital stay (MD: −2.89 days, 95% CI: −3.43 to −2.34, 13 studies, 715 patients), shorter operation time (MD: −41.62 min, 95% CI: −56.96 to −26.28, 12 studies, 593 patients), fewer postoperative overall complications (OR: 0.29, 95% CI: 0.17 to 0.49, 9 studies, 513 patients), and lower estimated blood loss (MD: − 26.12 mL, 95% CI: −37.07 to −15.17, 8 studies, 435 patients) when compared to the LSR group. Conclusions LECS demonstrates superior short-term outcomes compared to LSR and should be considered a preeminent alternative for endoscopically unresectable colorectal polyps. However, long-term efficacy remains to be confirmed by well-designed, high-quality trials. Graphical abstract

Background: Surgical treatment has been widely controversial for gastric cancer accompanied by liver metastasis (GCLM). This paper aims to develop and validate a nomogram to predict the survival and estimate surgical benefits for GCLM patients.Methods: A total of 616 GCLM patients from the Surveillance, Epidemiology, and End Results Program (SEER) database and 74 GCLM patients receiving primary tumor resection (PTR) from the Chinese center were included in this study. Patients from the SEER database were divided into training set (with PTR) (n=493) and non-operative set (without PTR) (n=123). Patients undergoing PTR from China were included as external validation set. Independent risk factors associated with the overall survival of GCLM patients undergoing PTR were identified in the training set via log-rank test and Cox regression analysis. Afterwards, a comprehensive model and corresponding nomogram were constructed and validated by validation set.Results: The survival of patients undergoing PTR (n=493) was longer than that without PTR (n=123) (log-rank test, p<0.0001) in SEER cohort. T stage (HR=1.40, 95% CI=1.14, 1.73), differentiation grade (HR=1.47, 95% CI=1.17, 1.85), non-hepatic metastases (HR=1.69, 95% CI=1.29, 2.21), and adjuvant therapy (HR=0.34, 95% CI= 0.28, 0.42) were closely related with the survival of GCLM with PTR, and thus, a four-factor nomogram was established. However, GCLM patients receiving PTR in the high-risk subgroup (n=255) screened out by the nomogram did not have better survival outcomes compared with patients without PTR (n=123) (log-rank test, p=0.25).Conclusions: The nomogram could predict survival of GCLM patients receiving PTR with acceptable accuracy. In addition, although PTR did improve the survival of whole GCLM patients, patients in the high-risk subgroup were unable to benefit from PTR, which could assist clinicians to make decisions for the treatment of GCLM.

Background: Mucinous gastric cancer (MGC) is a rare subtype of gastric cancer (GC) characterized by distinct histological features and clinical behavior. However, the lack of specific in vitro models for MGC has hindered progress in understanding its carcinogenic mechanisms and developing effective therapeutic strategies. Methods: Patient-derived MGC organoids were established from paired primary tumor (MGC-T) and synchronous peritoneal metastatic nodule (MGC-ND) tissues obtained from a patient with MGC. To validate the generalizability of the findings, two additional independent MGC organoids (MGC2 and MGC3) and six non-MGC gastric cancer organoids were established in parallel under identical three-dimensional culture conditions. Histological and immunohistochemical analyses were performed to evaluate the fidelity of organoid recapitulation of parental tumor features. High-throughput drug sensitivity screening was conducted using a panel of 11 chemotherapeutic agents. Furthermore, organoid-based drug responses were correlated with the clinical outcomes of eight patients who received oxaliplatin-based adjuvant chemotherapy. Results: All MGC organoids faithfully maintained the histological architecture, mucus secretion capability, and biomarker profiles of the parental tumors over serial passages. High-throughput drug sensitivity screening revealed consistent resistance to 5-fluorouracil and oxaliplatin, and marked sensitivity to taxane-based agents, across the MGC panel. Preliminary clinical correlation in eight patients showed 87.5% concordance between organoid-based predictions and actual chemotherapy outcomes. Conclusion: We established and characterized patient-derived MGC organoids from three patients, demonstrating faithful histological and molecular preservation, dynamic mucus secretion, and reproducible drug sensitivity pattern. Preliminary clinical correlation in a small cohort showed promising concordance. These proof-of-concept findings establish a platform for future precision oncology research in this rare gastric cancer subtype, pending larger prospective validation.