Objective: To investigate the clinical application of sandwich bridging technique for constructing vascularized patches to repair large abdominal wall defects (LAWD) following abdominal wall tumor resection.

Methods: A retrospective analysis was conducted on patients who underwent bridging repair after extensive abdominal wall tumor resection. All procedures were performed by the same surgical team from Huadong Hospital Affiliated to Fudan University and Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine between January 2016 and December 2023.

Results: A total of 29 patients with LAWD after abdominal wall tumor resection were repaired using the sandwich bridging technique. Among them, 23 patients (75.9%) had type Ⅱ abdominal wall defects, and 6 patients (24.1%) had type Ⅲ abdominal wall defects. The mean tumor area was (132.1±56.3) cm², and the mean defect area was (404.5±158.6) cm². The average operation time was (250.2±99.6) min, with intraoperative blood loss of (381.0±399.2) mL. The mean follow-up period was (50.9±24.5) months. The incidence of abdominal wall hernia or bulge was 6.9%, and the incidence of incision-related complications was 17.2%.

Conclusion: The sandwich bridging technique for constructing vascularized patches is feasible for repairing LAWD caused by abdominal wall tumors.

Objective: Investigating the influence of the nucleoprotein UHRF1 (ubiquitin-like with PHD and ring finger domains 1) on radiation radioresistance in cervical squamous cell carcinoma, and to explore its potential mechanisms.

Methods: The expression level of ubiquitin-like with PHD and ring finger domains 1 (UHRF1) mRNA and protein in cervical squamous carcinoma parental cells (SiHa and CaSki) and radioresistant cells (SiHa-R and CaSki-R) were detected by real-time fluorescent quantitative PCR and Western blotting, respectively. The glycolytic activity of parental SiHa and CaSki cells and and analyzed cells SiHa-R and CaSki-R were analyzed through extracellular acidification rate (ECAR), glucose consumption, and lactate production assay. The specific shRNA targeting the UHRF1 gene (shUHRF1) was employed to establish UHRF1-silenced SiHa-R and CaSki-R cells by Lentivirus. Lentivirus-mediated. The effects of silencing UHRF1 expression on the radiosensitivity of SiHa-R and CaSki-R cells were evaluated using CCK-8 assays and colony formation assays. The impact on glycolytic activity in SiHa-R and CaSki-R cells was analyzed through ECAR, glucose consumption, and lactate production assays. The expression level of glycolysis-related proteins glucose transporter protein 1 (GLUT1), hexokinase 2 (HK2), and pyruvate kinase isozyme type M2 (PKM2) were examined by Western blotting. Furthermore, a xenograft mouse model was established using UHRF1-silenced SiHa-R cells, followed by ¹⁸F-FDG PET/CT imaging to evaluate tumor glucose metabolism and tumor volume after irradiation.

Results: The expression level of UHRF1 mRNA and protein were significantly upregulated in SiHa-R and CaSki-R cells compared with their parental counterparts (both P<0.01). The ECAR value, glucose uptake, and lactate production of SiHa-R and CaSki-R cells were significantly higher than those of their parental cells (all P<0.001). Silencing UHRF1 expression markedly reduced cell proliferation capacity and colony-forming capacity after irradiation (both P<0.01). Glycolytic activity was significantly suppressed, as indicated by decreased ECAR value, glucose uptake, and lactate production (all P<0.001). Consistently, the protein levels of GLUT1, HK2, and PKM2 were downregulated in UHRF1-silenced cells (all P<0.001). The ¹⁸F-FDG uptake and tumor volume in nude mice transplanted with shUHRF1 group tumors were significantly lower than those in the negative control group (shNC) (both P<0.001), tumor suppression rate was 30%.

Conclusion: UHRF1 is highly expressed in radioresistant cervical squamous cell carcinoma cells and enhances radioresistance by promoting glycolysis through upregulation of key glycolytic enzymes. Silencing UHRF1 expression significantly inhibits glucose metabolism in cervical squamous cell carcinoma cells and enhances their sensitivity to radiotherapy, suggesting that UHRF1 holds promise as a potential molecular target for improving the efficacy of radiotherapy in cervical squamous cell carcinoma.

Objective: To report the first successful case of using toripalimab in combination with chemotherapy, significantly prolonging the survival of a patient with stage Ⅳ choriocarcinoma (PPC), and to summarize the diagnostic and therapeutic strategies for PPC.

Methods: A case of a 64-year-old male PPC patient who progressed after receiving six cycles of concurrent chemoradiotherapy was reported. Subsequently, the patient was treated with an immune checkpoint inhibitor (ICI) in combination with the previous therapy. The efficacy was evaluated by β‌-human chorionic gonadotropin (β‌-HCG) monitoring and CT, alongside a literature review to analyze the treatment patterns.

Results: After the combination of ICI treatment, the patient’s β-HCG levels returned to normal, and the right supraclavicular lymph node metastasis was completely resolved while the hilar lung lesions remained stable, thereby extending the patient’s survival period.

Conclusion: PPC is extremely rare, with surgery and chemotherapy being the primary treatment modalities. The combination of ICIs with chemotherapy can significantly prolong the survival of patients with stage Ⅳ PPC, particularly offering new options for those who are resistant to chemotherapy.

Soft tissue sarcoma (STS) is a rare malignant tumor originating from mesenchymal tissues, with over 50 histological subtypes and significant clinical heterogeneity, making treatment particularly challenging. Although comprehensive treatment primarily focusing on surgical resection plays an important role in local control, the prognosis for patients with advanced or metastatic disease remains poor, and the benefits of traditional chemotherapy are limited. In recent years, with advances in molecular biology and genomics, targeted therapy has emerged as a new treatment strategy for STS, enabling effective modulation of tumor biological behavior through precise identification of driver genes and abnormal signaling pathways. Currently, anti-angiogenic agents, multi-target tyrosine kinase inhibitors (TKIs), mammalian target of rapamycin (mTOR) and cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors, as well as novel agents targeting neurotrophic tyrosine receptor kinase (NTRK) fusions and enhancer of zeste homolog 2 (EZH2) epigenetic regulation, have all demonstrated clinical benefits in various STS subtypes. This review summarizes recent progress in molecular targeted therapy for STS, including combination treatment strategies and resistance mechanisms, and discusses its clinical application prospects and existing challenges, aiming to provide a reference for clinical practice. In the future, continuous exploration of new molecular targets, optimization of combination regimens, and overcoming drug resistance will be essential to advance STS treatment towards precision and personalization, ultimately bringing longer survival and improved quality of life for patients.

Objective: To explore the relationship between clinicopathological characteristics and prognosis of patients with gallbladder cancer, providing references for individualized treatment decision-making.

Methods: This study employed a retrospective study design, collecting clinical management data and follow-up information from gallbladder cancer patients who underwent radical resection at Renji Hospital, Shanghai Jiao Tong University School of Medicine, between July 1, 2018, and November 30, 2023. The Kaplan-Meier method was used to plot the overall survival curve for all patients. The log-rank test was applied to compare the correlation between various clinicopathological characteristics and survival prognosis of patients with gallbladder cancer. Variables showing statistical significance (P<0.05) in the univariate analysis were further incorporated into a multivariate COX regression model to identify independent risk factors affecting the survival prognosis of patients with gallbladder cancer.

Results: This study enrolled 238 patients with gallbladder cancer. The median overall survival of them was 43.4 months (95% CI: 27.36-61.38 months), and the 1-, 3-, and 5-year overall survival rates were 79.1%, 55.1%, and 48.4%, respectively. Univariate analysis results indicated that the overall survival of gallbladder cancer patients was significantly associated with preoperative serum levels of alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), carbohydrate antigen 125 (CA125), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP) and bilirubin levels, as well as perineural invasion, surgical margin status, liver invasion, extrahepatic bile duct invasion, vascular invasion, tumor size > 3 cm, differentiation degree, gallstones, tumor location, pathological classification and pTNM stage (all P < 0.05). Multivariate COX regression analysis further identified that elevated preoperative serum CA19-9 and CA125 levels, the presence of extrahepatic bile duct invasion, and pN2 stage were independent risk factors affecting the overall survival of gallbladder cancer patients (all P < 0.05).

Conclusion: Elevated preoperative serum CA19-9 and CA125 levels, extrahepatic bile duct invasion, and pN2 stage lymph node metastasis are significantly associated with a poor prognosis in gallbladder cancer patients, and may serve as critical indicators for assessing the survival prognosis of these patients.

Objective: To investigate the value of dynamic changes in peripheral blood T lymphocyte subsets in predicting the efficacy and prognosis of PD-1 inhibitor combined with SOX regimen (oxaliplatin + temozolomide) in the treatment of advanced gastric cancer, and to provide a reference basis for clinical treatment effect evaluation.

Methods: A prospective study was conducted on 100 patients with advanced gastric cancer who received PD-1 inhibitor combined with SOX regimen treatment in Fudan University Pudong Medical Center and Renji Hospital, Shanghai Jiao Tong University School of Medicine from January 2021 to December 2024. Before treatment, during the second and fourth cycles, flow cytometry was used to detect the absolute number and proportion (%) of peripheral blood lymphocyte subsets (CD3⁺T, CD4⁺T, CD8⁺T, B cells, natural killer cells), as well as the CD4⁺/CD8⁺ ratio. Enzyme-linked immunosorbent assay was used to detect the levels of serum immunosuppressive factors (soluble PD-L1, transforming growth factor-β, interleukin-6). The efficacy was evaluated according to the Response Evaluation Criteria in Solid Tumors version 1.1. The relationship between the dynamic changes of T cell subsets and efficacy as well as progression-free survival was analyzed.

Results: The objective response rate was 32.0% and the disease control rate was 73.0% in the entire group. There were no significant differences in baseline T-cell subsets between the two groups. Repeated measures analysis of variance showed significant time effects on the absolute count of CD8⁺ T cells and the CD4⁺/CD8⁺ ratio (P<0.001). The change in CD8⁺T cells was significantly negatively correlated with the change in soluble PD-L1 (r=-0.580, P<0.001). Survival analysis indicated that the progression-free survival time was significantly better in the high CD8⁺ T cell increase group (n=18) compared to the low increase group (n=82) (P=0.004). Multivariate COX regression confirmed that CD8⁺T cell increase was an independent prognostic factor (HR=4.588, 95% CI: 1.626-12.944, P=0.004).

Conclusion: The dynamic expansion of early CD8⁺T cells is correlated with the decrease in serum soluble PD-L1 levels, and can independently predict the efficacy and survival benefit of PD-1 inhibitors combined with chemotherapy, serving as a potential biomarker for efficacy monitoring.

Src, which is a non-receptor tyrosine kinases (NRTKs), is a member of the Src-family of protein kinases (SFKs). Studies have shown that high expression of Src protein kinase in tumor patients is associated with poor prognosis and reduced survival. This suggests that inhibiting Src expression may be a promising therapeutic strategy for cancer treatment. Currently, several Src inhibitors have been approved for clinical use in the treatment of malignant tumors, and studies on the delivery of Src inhibitors using nanotechnology have also achieved certain progress in basic research. This review summarizes the latest research progress on the delivery of Src inhibitors using nanoparticles, aiming to provide a theoretical basis for the development and application of novel cancer therapeutics based on nanomaterial carriers.

Objectives: To investigate the relationship between postoperative frailty and nutritional status in elderly patients with gastrointestinal tumors.

Methods: Elderly patients with gastrointestinal tumors who underwent elective surgery at Renji Hospital, Shanghai Jiao Tong University School of Medicine from December 2022 to April 2023 were enrolled as the study objects. Clinical Frailty Scale (CFS) was used to assess postoperative frailty, and geriatric nutritional risk index (GNRI) was used to assess preoperative and postoperative nutritional risk. Demographic data and nutrition-related laboratory indicators were collected to analyze the risk factors for postoperative frailty in elderly patients with gastrointestinal tumors.

Results: A total of 242 patients were included, among whom 54 (22.31%) developed postoperative frailty. Multivariate binary logistic regression analysis showed that advanced age, higher preoperative serum albumin level, lower preoperative GNRI and postoperative serum albumin level were independent risk factors for postoperative frailty in elderly patients with gastrointestinal tumors (P<0.05). The receiver operating characteristic (ROC) curve analysis demonstrated that preoperative serum albumin level, preoperative GNRI, and postoperative serum albumin level all had certain predictive value for postoperative frailty. Their areas under the curve (AUC) were 0.652 [95% confidence interval (CI): 0.565-0.738], 0.724 (95% CI: 0.645-0.803) and 0.914 (95% CI: 0.873-0.955), respectively. Postoperative serum albumin level showed the best predictive performance, with an accuracy rate as high as 91.4%.

Conclusion: In this study, the incidence of postoperative frailty in elderly patients with gastrointestinal tumors was 22.31%. Age, preoperative serum albumin level, preoperative GNRI and postoperative serum albumin level were independent factors of postoperative frailty in elderly patients with gastrointestinal tumors. Among these, postoperative serum albumin level was the best predictor of postoperative frailty in elderly patients with gastrointestinal tumors.

Colorectal cancer is one of the malignant tumors with high incidence and mortality rates worldwide. Its diagnostic and therapeutic strategies are continuously updated with the development of molecular biology and precision medicine. Based on the important updates from three international authoritative guidelines in 2024: the European Society for Medical Oncology (ESMO), the National Comprehensive Cancer Network (NCCN), and the Chinese Society of Clinical Oncology (CSCO), this article systematically compares and interprets the latest advancements of colorectal cancer in molecular detection, targeted therapy, immunotherapy, chemotherapy and local therapy. Through an in-depth comparison and analysis of the three guidelines, this article aims to provide clinicians with the latest diagnostic and therapeutic references, and to promote the standardization and precision of colorectal cancer treatment in China.

Lung cancer is the deadliest malignancies worldwide. Among its subtypes, non-small cell lung cancer (NSCLC) is the most common pathological phenotype, and its treatment primarily relies on surgery, chemoradiotherapy, targeted therapy, and immunotherapy. In recent years, immunotherapy has shown unique advantages in controlling NSCLC progression, but its efficacy is heavily restricted by T-cell exhaustion within the tumor microenvironment. The T-cell exhaustion involves multidimensional mechanisms including continuous antigen stimulation, imbalanced cytokines, transcriptional regulation abnormalities, epigenetic modifications, and chromosomal structural remodeling, which has become a focal point in tumor immunology research. Studies targeting T-cell exhaustion mechanisms are considered to hold potential for overcoming current immunotherapy limitations. This review systematically summarizes the recent clinical and fundamental research advances on T-cell exhaustion in NSCLC, aiming to provide insights for further understanding the immune evasion mechanisms of NSCLC and to inform the development of novel immunotherapy strategies.

Objective: To investigate the expression pattern and clinical significance of myosin heavy chain 9 (MYH9) in pancreatic cancer, and its potential mechanism in regulating the sensitivity to FOLFIRINOX regimen.

Methods: Based on the public databases including TCGA (The Cancer Genome Atlas), GTEx (Genotype-Tissue Expression) and GEO (Gene Expression Omnibus), we analyzed the expression pattern of MYH9 gene in pancreatic cancer patients and its relationship with patient prognosis using the online platforms GEPIA (Gene Expression Profiling Interactive Analysis) and UALCAN (The University of Alabama at Birmingham Cancer Data Analysis Portal). The changes of the sensitivity of pancreatic cancer cells to FOLFIRINOX regimen were evaluated by interfering the expression of MYH9 gene in vitro. Further, we investigated the potential mechanism of MYH9 regulating the sensitivity of pancreatic cancer cells to FOLFIRINOX regimen using immunofluorescence and Gene Set Enrichment Analysis (GSEA).

Results: The expression of MYH9 gene was significantly upregulated in pancreatic cancer tissues, and its high expression was closely associated with poor prognosis in pancreatic cancer patients. Plate colony formation assay demonstrated that MYH9 knockdown enhanced the sensitivity of pancreatic cancer cells to FOLFIRINOX regimen. Immunofluorescence staining results suggested that alterations in DNA damage levels may be a critical mechanism through which MYH9 influences the sensitivity of pancreatic cancer cells to FOLFIRINOX regimen. GSEA and correlation analysis further revealed that abnormal activation of the NOTCH signaling pathway may be a potential mechanism by which MYH9 affects DNA damage in pancreatic cancer cells.

Conclusion: MYH9 is abnormally highly expressed in pancreatic cancer tissues and is closely related to poor prognosis in pancreatic cancer patients. MYH9 may regulate the activation of NOTCH signaling pathway to influence the DNA damage level in pancreatic cancer cells, thereby regulating the sensitivity of pancreatic cancer cells to FOLFIRINOX regimen.