Objective: To investigate the expression of insulin-like growth factor 1 receptor (IGF-1R) in desmoplastic small round cell tumor (DSRCT) and evaluate the inhibitory efficacy of OSI-906, an IGF-1R selective inhibitor, on the growth of DSRCT cells.

Methods: The clinical and pathological data of 8 cases of DSRCT diagnosed at Renji Hospital, Shanghai Jiao Tong University School of Medicine from 2012 to 2024 were collected and analyzed. The expression of IGF-1R in DSRCT tissues was detected using immunohistochemistry (IHC), and its distribution features were analyzed. Alamar-Blue and CCK8 assays were performed to detect the half maximal inhibitory concentration (IC₅₀) of OSI-906 in three DSRCT cell lines, and Western blotting was used to detect the expression of key proteins in the IGF-1R kinase receptor-related signaling pathway.

Results: IGF-1R protein expression was localized at the cell membrane or cytoplasm, a moderate-to-strong positive expression rate of 75% was found in all 8 DSRCT tissue samples. Alamar-Blue and CCK8 assays revealed that the IC₅₀ of OSI-906 for JN-DSRCT-1, DSRCT-B1Z and DSRCT-B3OD cell lines were 6.942, 60.440 and 3.487 µmol/L, respectively, and OSI-906 inhibited the viability of DSRCT-B3OD cell line in a dose-dependent manner. Western blotting analysis demonstrated that the expression level of phosphorylated AMPK was significantly upregulated, while the expression level of phosphorylated mTOR was significantly downregulated.

Conclusion: IGF-1R is highly expressed in DSRCT cells. In vitro, the OSI-906 shows a certain inhibitory effect on the growth of DSRCT cells, possibly by regulating the AMPK/mTOR pathway. These findings highlight the significance of IGF-1R as a potential therapeutic target in DSRCT.

Bispecific antibody (BsAb) refers to a large class of novel immunotherapeutic drugs that can recognize two different epitopes or antigens, combining the ability to activate the patient’s immune system and target tumor target cells. Several clinical trial studies on oncology have shown that BsAb has become an important strategy for the treatment of advanced solid tumors such as advanced lung and gastric cancers. Compared to the combination of two kinds of monoclonal antibodies, BsAb has shown specific biological activity and lower resistance when applied to the treatment of advanced solid tumors. This paper provides an overview of the development history, mechanism of action, classification, and clinical applications of BsAb in advanced solid tumors, and discusses the possible biomarkers for the clinical efficacy.

Objective: This study aims to evaluate the correction effect of adaptive radiotherapy (ART) based on fan beam CT (FBCT) and image-guided radiotherapy (IGRT) using the uLinac HalosTx medical linear accelerator on the setup errors of tumor patients. It also analyzes the impact of the planning duration of ART on body position stability, with the intention of providing a reference for clinical optimization of ART procedures.

Methods: Using a retrospective cohort analysis, 27 patients with malignant tumors (5 patients with esophageal cancer, 13 patients with cervical cancer, and 9 patients with prostate cancer) admitted to Renji Hospital, Shanghai Jiao Tong University School of Medicine from September 2024 to March 2025 were included. Through FBCT three-dimensional registration technology, the setup errors in the X (Lat), Y (Lng), and Z (Vrt) directions were measured before and after the ART plan was formulated, and the impact of different durations of ART planning (0-20 min, >20-25 min, >25 min) on the setup errors was analyzed.

Results: The setup errors in the X (Lat), Y (Lng), and Z (Vrt) directions in patients with esophageal cancer decreased from 0.190±0.131 cm, 0.197±0.152 cm and 0.267±0.208 cm, respectively, to 0.098±0.062 cm, 0.094±0.092 cm and 0.074±0.057 cm (P<0.001); the setup errors in patients with cervical cancer decreased from 0.185±0.131 cm, 0.331±0.270 cm and 0.244±0.209 cm, respectively, to 0.066±0.085 cm, 0.133±0.096 cm and 0.087±0.073 cm (P<0.001); the setup errors in the patients with prostate cancer decreased from 0.169±0.137 cm, 0.294±0.221 cm and 0.279±0.177 cm, respectively, to 0.052±0.067 cm, 0.132±0.125 cm and 0.084±0.079 cm (P<0.001). The relationship between the duration of ART planning and setup errors showed that there were no significant differences in the setup errors in the X (Lat), Y (Lng) and Z (Vrt) directions in patients with esophageal cancer among different duration groups (P>0.05); however, there were significant differences in the setup errors in patients with pelvic malignancies among different duration groups (P<0.05), with increase in the setup errors in the three-dimensional directions as the duration of planning increased.

Conclusion: ART can effectively improve setup accuracy and significantly reduce the setup errors in patients with esophageal, cervical or prostate cancer. However, for patients with pelvic malignancies, it is recommended to strictly control the duration of ART planning to avoid the accumulation of setup errors caused by prolonged time.

Objective: To explore an effective chemotherapy regimen for advanced primary colonic sclerosing epithelioid fibrosarcoma.

Methods: The diagnosis and treatment process of a patient with primary left colon sclerosing epithelioid fibrosarcoma with metastasis were reported.

Results: One patient with primary sclerosing epithelioid fibrosarcoma of the left colon underwent radical surgery for left colon cancer. Two months after surgery, multiple pelvic and abdominal metastases occurred, and the patient received first-line chemotherapy with FOLFIRI regimen. The progression-free survival was 17 months. Afterwards, due to significant progression of abdominal and pelvic metastases, a second tumor reduction surgery was performed. Three weeks after surgery, CT scan showed multiple metastases in the abdominal and pelvic cavity, and second-line chemotherapy with epirubicin was given for two cycles; CT evaluation showed a significant increase in tumor size, and after 2 cycles of chemotherapy with the third line GT regimen (gemcitabine+docetaxel), the CT evaluation showed partial remission. Therefore, a total of 7 cycles of GT regimen chemotherapy were completed, and regular follow-up showed partial remission. The progression-free survival time has exceeded 19 months.

Conclusion: Sclerosing epithelioid fibrosarcoma is a highly malignant tumor with strong invasiveness and poor prognosis. The GT regimen chemotherapy achieved significant efficacy in this case of advanced primary colonic sclerosing epithelioid fibrosarcoma, which can provide reference for the systematic treatment of this disease in the future.

Objective: To establish normal or specific gene-deficient gallbladder epithelial organoids and gallbladder cancer organoids for investigating the molecular mechanisms driving gallbladder cancer progression.

Methods: Gallbladder and gallbladder cancer tissues were enzymatically digested with collagenase Ⅳ, followed by neutralization, filtration, and centrifugation to isolate epithelial cell pellets. The isolated epithelial cells were embedded in Matrigel and cultured in a three-dimensional system. Gene editing technologies, including the Cre-loxP transgenic mouse and CRISPR-Cas9 system, were employed to generate gallbladder epithelial organoids with specific gene knock-outs or mutations. The gene editing efficiency was verified using flow cytometry, puromycin selection, and Sanger sequencing. The growth behavior and functional features of the organoids under different culture conditions were observed, and the effects of small pharmaceutical molecules (such as Wnt agonists and inhibitors) on the growth of the organoids were further assessed.

Results: Murine gallbladder epithelial organoids and human gallbladder cancer organoids were successfully generated and stably propagated in the long term under optimized organoid culture conditions. A gallbladder epithelial organoid model with specific gene knock-outs was successfully established, providing a robust platform for molecular mechanism research in gallbladder cancer. Further research demonstrated that the Wnt signaling pathway was highly activated in gallbladder cancer organoids, with growth dynamics significantly modulated by Wnt agonists or inhibitors.

Conclusion: Normal murine gallbladder epithelial organoids and human gallbladder cancer organoids, combined with advanced gene-editing technologies, serve as powerful tools for deciphering the molecular mechanism and developing targeted therapeutic strategies through building disease models with high efficiency and accuracy. Wnt signaling is one of the critical regulatory signaling pathways in gallbladder progression, highlighting its potential as a therapeutic target.

Objective: To investigate the impact of different radiotherapy doses on the concurrent chemoradiotherapy efficacy and prognosis in patients with stage Ⅱ-Ⅳa esophageal squamous cell carcinoma (ESCC) receiving S-1 (Tegafur-gimeracil-oteracil potassium) chemotherapy.

Methods: Based on inclusion and exclusion criteria, 154 eligible patients with ESCC were selected from those treated at the Department of Radiation Oncology of the First Affiliated Hospital of Bengbu Medical University between January 2019 and January 2023. According to prescribed radiation dose, these patients were divided into a standard-dose radiotherapy (SD-RT) group (n = 75, total radiation dose: 50-54 Gy) and a high-dose radiotherapy (HD-RT) group (n = 79, total radiation dose: 60 Gy). Since a relatively high proportion of the enrolled patients were elderly (age > 75 years, accounting for > 70%) with poor physical condition, and some patients declined standard intravenous chemotherapy due to personal reasons, all enrolled patients received oral S-1 concurrent chemotherapy during radiotherapy. Follow-up evaluations were conducted 1 - 3 months after concurrent chemoradiotherapy. The short-term clinical efficacy and the incidence of acute radiotherapy-related adverse reactions were evaluated for both the SD-RT and HD-RT groups according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. Long-term survival was analyzed using Kaplan-Meier curves. Log-rank test and multivariate COX regression analysis were used to identify independent prognostic factors affecting progression-free survival (PFS) and overall survival (OS) of ESCC patients.

Results: Among the 154 ESCC patients, the objective response rate (ORR) and disease control rate (DCR) were 88.0% and 97.3% in the SD-RT group, respectively, while those of the HD-RT group were 93.7% and 100%. There was no statistically significant difference in the short-term clinical efficacy between the two groups (P=0.516, χ²=2.369), but significant differences were observed in both PFS and OS (PFS^{SD-RT vs HD-RT}: 20.0 months vs 26.0 months, P=0.009; OS^{SD-RT vs HD-RT}: 26.0 months vs 34.0 months, P=0.047). Subgroup analysis based on clinical stage demonstrated that HD-RT can improve the long-term survival in patients with stage Ⅲ-Ⅳa ESCC (PFS^{SD-RT vs HD-RT}: 15.0 months vs 20.0 months, P=0.002; OS^{SD-RT vs HD-RT}: 17.0 months vs 22.0 months, P=0.006), but did not significantly benefit patients with stage Ⅱ ESCC. Additionally, the subgroup analysis according to median gross tumor volume (GTV) showed that ESCC patients with smaller tumor volumes (≤43.39 cm^⊃3;) exhibited greater sensitivity to HD-RT compared to those with larger tumors (>43.39 cm³) (PFS^{SD-RT vs HD-RT}: 18.0 months vs 26.0 months, P = 0.028; OS^{SD-RT vs HD-RT}: 22.0 months vs 32.0 months, P = 0.025). In terms of radiation-related toxicity, there were no significant statistical differences between the SD-RT and HD-RT groups in the incidence of myelosuppression (P = 0.539), radiation esophagitis (P = 0.882), or radiation pneumonitis (P=0.636). Log-rank test and multivariate COX regression analysis identified radiation dose, T stage, and clinical stage as independent prognostic factors for PFS of ESCC patients (all P < 0.05), while radiation dose and clinical stage were independent prognostic factors for OS of ESCC patients (both P < 0.05).

Conclusion: For ESCC patients treated with S-1-based concurrent chemoradiotherapy, increasing the total radiation dose to 60 Gy can improve their long-term survival outcomes without increasing the risk of radiation-related adverse events. This survival benefit was particularly pronounced in ESCC patients with advanced-stage disease (Ⅲ-Ⅳa) and smaller tumor volumes (≤43.39 cm³).

Primary bone lymphoma (PBL) is a rare malignancy characterized by lymphoma cells primarily invading bone tissue. Unlike other lymphoma subtypes, PBL usually remains confined to bone at diagnosis without involving lymph nodes or other organs. It affects individuals of all ages, generally showing a better prognosis than secondary bone lymphoma. However, the low incidence of PBL has led to limited large-scale studies, with most researches relying on case reports or small retrospective analyses, causing challenges in diagnosis and delays in treatment. This review summarizes the clinical manifestations, diagnostic methods, treatment strategies, and prognostic outcomes of PBL to enhance understanding of its management and improve patients’ outcomes and quality of life.

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.

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.

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.

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: Retroperitoneal liposarcoma is a rare malignant tumor derived from fat cells, and its clinicopathological characteristics remain unclear. This study aims to explore the clinicopathological characteristics of retroperitoneal liposarcoma in the Chinese population based on nearly 20 years of diagnosis and treatment experience in a single center.

Methods: We retrospectively collected the clinical and pathological data of patients with retroperitoneal liposarcoma who were diagnosed and treated at Renji Hospital, Shanghai Jiao Tong University School of Medicine from 2004 to 2023. Recurrence and prognosis information of the patients was obtained through outpatient follow-up or telephone follow-up.

Results: Over the past 20 years, Renji Hospital has diagnosed and treated a total of 172 patients with retroperitoneal liposarcoma, including 96 males and 76 females. These patients have undergone 297 hospitalizations and 228 surgeries at Renji Hospital. The overall survival rates at 3, 5, and 10 years were 73.3%, 60.0%, and 36.8%, respectively. The pathological subtype transformation rate of retroperitoneal liposarcoma was 32.2%. On average, each patient underwent 2.3 surgeries, with the maximum number of surgeries being 12. In addition to the tumor, 52.8% of patients had surrounding organs resected, with the kidney (21.0%) being the most commonly resected organ. The perioperative mortality rate was 2.2%, and the incidence of unplanned reoperations was 1.8%. The overall complication rate was 15.4%, with small bowel obstruction being the most common complication (21.2%). 13.1% of patients received adjuvant therapy other than surgery. However, only one patient received systematic adjuvant therapy according to the guidelines at that time.

Conclusion: Retroperitoneal liposarcoma is a rare malignant disease with favorable prognosis. Surgery is the main method to treat retroperitoneal liposarcoma, and postoperative recurrence is the biggest obstacle to its therapeutic effect. Currently, standardized adjuvant therapy for retroperitoneal liposarcoma still needs to be strengthened, and the development of effective drugs is also a direction that requires significant attention in the future.

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: To investigate the clinicopathological characteristics of sebaceous carcinoma (SC) and enhance the diagnostic accuracy and differential diagnosis capabilities among pathologists for this malignancy.

Methods: Clinical data from seven patients with sebaceous carcinoma (SC) were retrospectively reviewed, with comprehensive analysis of histopathological features and immunohistochemical characteristics in all cases.

Results: In this study, sebaceous carcinoma (SC) predominantly affected elderly female patients, with a median age of 65 years (male-to-female ratio = 1：2). The majority of cases (6/7) represented periocular SC, with the left upper eyelid being the most frequently involved anatomical site（5/7）. Histopathological examination revealed that all seven SC cases exhibited predominantly nested or lobulated growth patterns, intraepidermal infiltrative growth was observed in 4 cases. Variable sebaceous differentiation with additional morphological characteristics were noted. Including tumor necrosis (n=5)、ductal differentiation (n=2)、keratinization(n=2)、perifollicular growth pattern (n=2) and cystic degeneration (n=1). Immunohistochemistry showed that tumor cells were positive for epithelial membrane antigen (EMA) and androgen receptor (AR), negative for carcinoembryonic antigen (CEA), and highly expressed for nuclear associated antigen Ki-67 (Ki-67).

Conclusion: Sebaceous carcinoma (SC) represents a rare cutaneous malignancy characterized by histologically evident sebaceous differentiation. While classical SC exhibits distinctive morphological features, significant histological heterogeneity may occur. Therefore, accurate diagnosis requires comprehensive evaluation incorporating both architectural features and immunohistochemical profiling to reliably distinguish SC from its histological mimics.

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 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.

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.

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.

Retroperitoneal liposarcoma poses significant therapeutic challenges due to its unique anatomical location and biological characteristics. Recent advancements in surgical techniques, the optimization of radiotherapy strategies, and the development of novel pharmacological agents have greatly transformed the treatment landscape. Surgical management has shifted from solely focusing on radical resection to strategies that balance complete tumor removal and organ function preservation. Multidisciplinary team approaches have demonstrated significant improvements in patient prognosis by integrating expertise across surgery, radiology, pathology, and oncology. Radiotherapy, supported by precision techniques, serves as a complementary treatment for local tumor control. However, its efficacy remains constrained by factors such as tumor histology and radiation dosage limitations. In pharmacotherapy, traditional cytotoxic chemotherapy is increasingly being supplanted by targeted therapies and immunotherapy combinations, while breakthroughs in molecular subtyping and liquid biopsies are paving the way for personalized treatment approaches. Looking ahead, the integration of radiomics, artificial intelligence-supported treatment strategies, and multimodal combination therapies is expected to advance retroperitoneal liposarcoma management. This evolution is anticipated to achieve a better balance between radical surgical intervention and quality-of-life preservation, thus delivering substantial survival benefits and improved outcomes for patients.

Retroperitoneal sarcoma (RPS) is a kind of highly heterogeneous soft tissue tumor. Radical surgery remains the mainstay of treatment. However, the high postoperative local recurrence rate significantly impacts long-term survival. The efficacy of traditional systemic chemotherapy in RPS is limited, necessitating the exploration of more effective adjuvant treatment strategies to reduce the local recurrence rate. This paper summarizes the current status of hyperthermic intraperitoneal chemotherapy (HIPEC) in the treatment of RPS, along with recent advances in basic and clinical research. We explore the potential value of HIPEC in reducing postoperative recurrence of soft tissue sarcomas and improving patient prognosis. The combination of cytoreductive surgery (CRS) and HIPEC has been shown to prolong both disease-free survival and overall survival in RPS patients, with particular benefits observed in specific pathological subtypes such as leiomyosarcoma and dedifferentiated liposarcoma. However, large-scale prospective studies on the efficacy of HIPEC in preventing postoperative recurrence of RPS are still lacking. Future research should focus on conducting multi-center, large-scale prospective studies to further validate the efficacy of HIPEC in RPS and to define the patient populations that may benefit the most from this approach.

Objective: Explore the efficacy of compound zaofan pills in treating chemotherapy-induced bone marrow suppression in patients with non-small cell lung cancer (NSCLC), and identify patient subtypes with different clinical characteristics based on principal component analysis and cluster analysis, and compare the differences in efficacy between different subtypes of patients.

Methods: The clinical data of chemotherapy-induced bone marrow suppression NSCLC patients who received treatment with compound zaofan pills at the First Affiliated Hospital of Kunming Medical University from January 2022 to December 2022 were collected. Principal component analysis was used to reduce the dimensionality of multidimensional clinical indicator data, extract key features, and perform Gaussian clustering analysis on this basis to classify patient subtypes. After all patients received treatment with compound zaofan pills, Kaplan Meier method and log-rank test were used to compare the differences in survival prognosis among different subtypes of patients, and analyze their improvement in clinical indicators related to bone marrow suppression.

Results: This study included 80 patients with NSCLC and chemotherapy-induced bone marrow suppression, who were ultimately classified into three categories through principal component analysis and cluster analysis. Characteristics of class I patients: TNM stage Ⅰ-Ⅱ, good drug compliance, high degree of bone marrow suppression, mainly treated with gemcitabine combined with platinum based chemotherapy, and the best prognosis; characteristics of class Ⅱ patients: TNM stage Ⅲ-Ⅳ, moderate medication adherence, moderate to low degree of bone marrow suppression, mainly treated with paclitaxel combined with platinum based chemotherapy, and relatively poor prognosis; characteristics of class Ⅲ patients: TNM stage Ⅲ-Ⅳ, poor drug compliance, lowest degree of bone marrow suppression, mainly treated with docetaxel combined with platinum based chemotherapy, and the worst prognosis.

Conclusion: In the treatment of chemotherapy-induced bone marrow suppression in NSCLC, patient compliance is one of the key factors affecting treatment efficacy and prognosis. The use of principal component analysis and cluster analysis methods can help to gain a deeper understanding of the factors that affect patient treatment compliance, identify subgroups of patients with different treatment responses to compound zaofan pills, and develop more targeted treatment plans to achieve better treatment outcomes and prognosis.

The small intestine is an organ with irreplaceable function in the digestive system, and the incidence rate of its primary malignant tumors is less than 2% of gastrointestinal tumors. However, in recent years, the incidence rate of small intestinal malignancies has increased significantly, making its diagnosis and treatment increasingly important in the field of digestive tract diseases. The discovery of new blood biomarkers and advances in endoscopic and imaging technologies have jointly promoted the early and accurate diagnosis of small intestinal malignancies. With the development of genetic technology, there are more precise targeted treatment options for the treatment of small intestinal malignancies. The latest diagnosis and treatment guidelines for small intestinal adenocarcinoma released by the American Joint Committee on Cancer (AJCC) in 2024 provide standards for the diagnosis and treatment of this disease worldwide. At present, primary malignant tumors of the small intestine are still an area that needs further exploration.

Objective: To report the first successful case of using toripalimab in combination with chemotherapy, significantly prolonging the survival of a patient with stage Ⅳ primary pulmonary 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.

Retroperitoneal sarcoma (RPS) is a rare malignant tumor originating from the retroperitoneal mesenchymal tissue. While surgical resection remains the cornerstone of curative treatment, a significant challenge is the high rate of local recurrence, underscoring the critical need for effective multimodality approaches. Radiotherapy, as an important means of local treatment, has been demonstrated to play a corresponding role in neoadjuvant, intraoperative, and adjuvant settings. Notably, preoperative radiotherapy is recommended as an effective treatment approach due to its capacity to enhance the rate of local control. Furthermore, with the continuous advancement of radiotherapy technology, proton and heavy ion therapies have shown significant advantages. Compared to traditional photon radiation therapy, they can enhance the radiosensitivity of RPS and provide better protection for organs at risk. This comprehensive review synthesizes recent evidence from landmark studies to delineate current practice patterns, analyze ongoing controversies, and highlight technological innovations shaping the radiotherapeutic management paradigm for RPS.

Objective: To investigate the effect of A disintegrin and metalloproteinase 6 (ADAMTS6) on the proliferation, migration, and ferroptosis of thyroid carcinoma (THCA) cells and its potential underlying mechanisms.

Methods: By searching bioinformatics websites and databases, the difference in the expression of ADAMTS6 gene between tumor tissues and normal thyroid tissues in the THCA dataset from The Cancer Genome Atlas (TCGA) database was analyzed, and the correlation between ADAMTS6 expression and prognosis of THCA patients as well as the correlation with the prognosis and clinicopathological characteristics of THCA patients were further analyzed. Real-time fluorescence quantitative PCR and Western blotting were used to detect the expression of ADAMTS6 in THCA and normal thyroid tissues. Western blotting was also used to evaluate the expression of ADAMTS6 in normal thyroid cells and THCA cells. TPC-1 and BCPAP cells with ADAMTS6 knockdown were constructed using siRNA technology, followed by CCK-8 assay, colony formation assay, and EdU assay to detect the effects of ADAMTS6 knockdown on the proliferation of BCPAP and TPC-1 cells, respectively, and Transwell assay to detect the effects on the migration of BCPAP and TPC-1 cells. BCPAP cells with ADAMTS6 knockdown were treated with the ferroptosis inducer RSL-3, and then CCK-8 assay was used to detect the effect on cell viability, flow cytometry was used to detect the effect on cellular lipid peroxidation, and Western blotting was used to detect the effects on the expression levels of ferroptosis-related proteins solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), and β‌-catenin protein in the Wnt/β-catenin signaling pathway. BCPAP cells with ADAMTS6 knockdown and RSL-3 treatment were further treated with the Wnt/β‌-catenin signaling pathway activator CHIR-99021, and then flow cytometry was then used to assess the effect on cellular lipid peroxidation, while Western blotting was used to detect the effects on the expression of ferroptosis-related proteins SLC7A11 and GPX-4, and β-catenin protein in the Wnt/β-catenin signaling pathway.

Results: Database analysis and Western blotting results indicated that ADAMTS6 expression was upregulated in THCA (P < 0.05). High ADAMTS6 expression was negatively correlated with overall survival (P < 0.05) and positively correlated with tumor stage and lymph node metastasis in THCA patients (all P<0.05). After ADAMTS6 knockdown, the expression levels of ADAMTS6 mRNA and protein in BCPAP and TPC-1 cells were significantly decreased (all P<0.05), and their proliferative and migratory abilities were markedly reduced (all P<0.05). Treatment of ADAMTS6-knockdown BCPAP cells with RSL-3 further reduced the ferroptosis resistance of BCPAP cells to and promoted cellular lipid peroxidation (all P<0.05). Western blotting results showed that, compared with control cells, the expression levels of SLC7A11, GPX4, and β‌-catenin proteins in BCPAP cells were significantly decreased after ADAMTS6 knockdown (all P<0.05). The Wnt activator CHIR-99021 upregulated the expression levels of GPX4, SLC7A11, and β‌-catenin proteins in ADAMTS6-knockdown BCPAP cells treated with RSL-3 (all P<0.05), while lipid peroxidation decreased (all P<0.05).

Conclusion: ADAMTS6 is highly expressed in THCA tissues and its high expression is associated with poor prognosis in patients. Knockdown of ADAMTS6 inhibits the proliferation, migration, and ferroptosis resistance of THCA cells, and the underlying mechanism may be related to the downregulation of Wnt/β‌-catenin signaling pathway activity.

Objective: To investigate the effects of astragalus polysaccharide (APS) on tumor growth in mice with colorectal cancer (CRC) xenografts through in vivo experiments, and to further explore the impact of APS on macrophage polarization within the tumor microenvironment and its potential mechanism of action.

Methods: A mouse xenograft model was established using murine-derived CRC CT-26 cells. The mice were treated for three weeks via intraperitoneal injection with APS, the STING inhibitor (C-176), or APS combined with C-176. A control group received an equal volume of 0.9% sodium chloride solution via intraperitoneal injection. Changes in body weight and tumor volume were monitored. After euthanasia, the tumor inhibition rate was calculated. Pathological changes in tumor tissues were assessed by HE staining, and apoptotic cells within tumors were detected by TUNEL staining. The serum levels of M2 macrophage-related factors, interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) were measured by ELISA. Immunofluorescence was employed to determine the localization and expression of IL-10 and TGF-β in tumor tissues, as well as the polarization status of M1 macrophages (CD68^⁺CD11c^⁺) and M2 macrophages (CD68^⁺CD163^⁺). The mRNA and protein expression levels of colony-stimulating factor 1 receptor (CSF1R), stimulator of interferon genes (STING), and TANK-binding kinase 1 (TBK1) in tumor tissues were detected by quantitative real-time PCR and Western blotting, respectively.

Results: The CT-26 cell xenograft mouse model was successfully established. APS inhibited the growth of mouse xenografts, with a tumor inhibition rate of 27.91%. APS promoted apoptosis of tumor cells within the tumor tissue, with an apoptosis rate of 31.6%. APS downregulated the expression levels of the M2 macrophage-related factors IL-10 and TGF-β in both mouse peripheral serum and tumor interstitium (all P<0.001). Immunofluorescence results indicated that APS induced macrophage polarization towards the M1 phenotype while suppressing the polarization tendency towards the M2 phenotype. Results from quantitative real-time PCR and Western blotting suggested that APS downregulated the expression of CSF1 mRNA and protein while activating the STING-TBK1 pathway, thereby reshaping the phenotype of tumor-associated macrophages.

Conclusion: APS inhibits M2 macrophage polarization in tumor tissues of CRC-bearing mice by regulating the CSF1/STING-TBK1 signaling pathway, thereby exerting an anti-tumor effect.

Objective: To investigate the effects of tripartite motif containing 21 (TRIM21) on the proliferation, invasion and migration of pancreatic cancer cells.

Methods: Based on the Gene Expression Profiling Interactive Analysis (GEPIA) online platform, this study integrated transcriptome sequencing data and clinical prognostic data from the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases to analyze the expression differences of the TRIM21 gene in pancreatic cancer tissues and adjacent normal tissues, as well as the correlation between TRIM21 expression levels and the prognosis of patients with pancreatic cancer. Stable pancreatic cancer cell lines (human-derived PANC-1 and mouse-derived Panc02) with TRIM21 knockdown or overexpression were constructed using siRNA interference and plasmid transfection techniques. The efficiency of TRIM21 knockdown and overexpression was verified by Western blotting. Its effects on proliferation of PANC-1 and PANC-02 cells were detected by colony formation assay, and the effects on migration and invasion of PANC-1 and PANC-02 cells were detected by wound healing assay and Transwell migration and invasion assays, respectively.

Results: The expression level of TRIM21 gene in pancreatic cancer tissues was significantly higher than that in adjacent normal tissues (P < 0.05). High expression of TRIM21 was significantly associated with poor prognosis of patients with pancreatic cancer (P < 0.05). TRIM21 knockdown can significantly inhibit the proliferation, invasion and migration of PANC-1 and PANC-02 cells (all P < 0.05). Conversely, TRIM21 overexpression can significantly promote the proliferation, invasion and migration of PANC-1 and PANC-02 cells (all P < 0.05).

Conclusion: TRIM21 plays a tumor-promoting role in pancreatic cancer, promotes the proliferation, invasion and migration of pancreatic cancer cells, and is significantly related to the poor prognosis of patients with pancreatic cancer. The TRIM21 gene shows promise as a potential therapeutic target for pancreatic cancer.

Objective: To investigate the expression characteristics of folate receptor alpha (FOLR1) in hepatic stellate cells (HSCs) and its potential role in liver diseases, as well as to construct a mouse model with HSC-specific knockout of the FOLR1 gene.

Methods: In this study, single-cell RNA sequencing and TCGA data were used to analyze the expression patterns of FOLR1 in liver cancer tissues and HSCs. Lrat-Cre and FOLR1 flox mice constructed by CRISPR-Cas9 gene editing technology were used to generate HSC-specific FOLR1 knockout mice, and the phenotype was verified in diethylnitrosamine (DEN)+CCl₄-induced HCC model. Real-time fluorescence quantitative PCR, enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry were used to evaluate the expression level of FOLR1 mRNA and protein in each group of mice.

Results: FOLR1 was significantly upregulated in activated HSCs and was associated with poor prognosis in HCC patients. The HSC-specific FOLR1 knockout mouse model was successfully established, with good knockout efficiency validated by PCR and sequencing. Real-time fluorescence quantitative PCR results indicated that, compared to FOLR1^fl/fl mice, the FOLR1^ΔHSC mice exhibited a 60.31% downregulation of FOLR1 mRNA expression in liver tissues induced by DEN and CCl₄ (P < 0.05). ELISA results showed a 38.32% decrease in serum FOLR1 protein concentration (P < 0.01), and immunofluorescence staining results revealed a 67.96% reduction in the area of positive FOLR1 protein staining in liver tissues (P < 0.01).

Conclusion: The HSC-specific FOLR1 knockout mouse model was successfully constructed, which provides a unique animal model platform for further exploring the possible mechanism of FOLR1 in HSCs.

Objective: To explore the influencing factors of acute radiation dermatitis (ARD) in patients with breast cancer who received radiotherapy after breast conserving surgery, so as to identify the patients who need close monitoring.

Methods: This study included 281 patients with breast cancer who received radiotherapy in the Department of Radiotherapy of the Tenth People’s Hospital Affiliated to Tongji University from January 1, 2020 to December 31, 2023 after breast conserving surgery. Clinical records were collected, and platelet counts and cytokines including IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-17A, TNF-a, IL-12p70, IFN-α and IFN-γ in peripheral blood were measured. The relationship between clinical pathological features, radiotherapy methods, laboratory examination indicators, and ARD was evaluated.

Results: Among 281 patients receiving radiotherapy after breast conserving surgery for breast cancer, 39 patients (13.9%) developed grade 2 ARD or higher. The results of univariate analysis showed that lymph node staging, hospitalization during radiotherapy, radiotherapy segmentation method, regional lymph node irradiation, affected breast volume, platelet count, and IL-5 level were associated with grade 2 ARD or higher. The results of multivariate logistic analysis showed that hospitalization during radiotherapy, radiotherapy segmentation method, and platelet count were independent risk factors for the occurrence of grade 2 ARD or higher (P＜0.05).

Conclusion: For patients undergoing radiotherapy in outpatient clinics, using conventional fractionation methods for radiotherapy, and having high platelet counts before radiotherapy, special attention should be paid to skin management in the irradiation area to reduce the occurrence of ARD.

Objective: To investigate the structural characteristics of invadopodia in pancreatic cancer cells.

Methods: The formation of invadopodia in low invasive pancreatic cancer PANC1 cells and high invasive pancreatic cancer BXPC3 cells was observed under laser confocal microscope after immunofluorescence staining, and the relationship between the formation of invadopodia and proteolytic function was studied through gelatin matrix degradation experiment. Transforming growth factor-β (TGF-β) was used to treat pancreatic cancer BXPC3 cells, and gelatin matrix degradation test and immunofluorescence test were used to detect the effect of TGF-β on the formation of invadopodia of BXPC3 cells; The real-time fluorescence quantitative PCR was used to detect the effect of TGF-β on the mRNA expression of matrix metalloproteinases (MMP)-1 and MMP-9 in BXPC3 cells. Finally, a higher resolution structured illumination microscope (SIM) was used to reconstruct the three-dimensional structure of the invadopodia of BXPC3 cells, further exploring its spatial structural characteristics.

Results: Through immunofluorescence experiment, it was found that in high invasive pancreatic cancer BXPC3 cells, scattered single dot like invadopodia could be formed, and special rosette ring structure could also be formed. However, in low invasive pancreatic cancer PANC1 cells, there was no such obvious invadopodia feature. The invadopodia formed in BXPC3 cells were related to the function of matrix degradation, and the number of invadopodia was increased after stimulation by TGF-β, and the expression level of MMP-9 mRNA was up-regulated (P<0.000 1), thus increasing the proteolytic activity of cells. The three-dimensional structure of invadopodia in BXPC3 cells was further reconstructed using SIM.

Conclusion: Based on laser confocal microscopy and SIM, the structural characteristics of invadopodia in pancreatic cancer cells were preliminarily observed and described, and the effects of TGF-β on the formation and function of invadopodia in pancreatic cancer cells were explored.

Objective: To develop a tannic acid (TA) and silk fibroin (SF)-based hydrogel for paclitaxel (PTX) delivery, and to evaluate its drug-loading capacity, release performance, and inhibitory effects on breast cancer cells.

Methods: First, SF-TA hydrogel drug carriers were prepared through the interaction between TA and SF. The microstructure of the hydrogel was observed using scanning electron microscopy, while the formation mechanism of the SF-TA hydrogel was analyzed via Fourier transform infrared spectroscopy. A rheometer was employed to characterize the viscoelastic properties of the hydrogel, and the weight loss method was used to evaluate its swelling rate and water retention capacity. Subsequently, the biocompatibility of the SF-TA hydrogel with mouse skin fibroblasts L-929 cells and mouse blood cells was evaluated using the CCK-8 assay and hemolysis assay, respectively. The effect on the activity against Staphylococcus aureus and methicillin-resistant S. aureus (MRSA) was detected by the plate coating counting method. The in vitro degradation rate of SF-TA hydrogel was measured by the weighing method, while in vivo degradation characteristics were monitored via mouse live imaging. In vivo biosafety evaluation (including body weight monitoring, blood biochemistry testing, and blood cell counting) assessed the biocompatibility of SF-TA hydrogel. PTX-loaded SF-TA@PTX hydrogels was prepared and their PTX drug loading capacity and release characteristics were analyzed via high-performance liquid chromatography (HPLC); finally, the CCK-8 assay was employed to evaluate the SF-TA@PTX hydrogel’s effects on the survival rates of mouse mammary carcinoma 4T1 cells, human breast cancer MDA-MB-231 cells, and mammary epithelial HC11cells. The bromoindole dihydrochloride double staining method was used to assess the SF-TA@PTX hydrogel’s impact on the viability of 4T1 cells. Calcein acetoxymethyl ester (Calcein-AM)/propidium iodide (PI) double staining was employed to assess the SF-TA@PTX hydrogel’s impact on 4T1 cell activity.

Results: The SF-TA hydrogel was successfully prepared, exhibiting a loose porous structure with viscoelastic properties similar to those of human tissue. The swelling rate was found to be (34.4%±4.2%), and the hydrogel demonstrated excellent biocompatibility. It showed significant antibacterial activity, inhibiting the growth of over 90% of S. aureus and MRSA. The hydrogel exhibited excellent degradability, with rapid degradation within 6 days, and demonstrated good in vivo biosafety. The drug loading capacity for PTX was remarkable, with an encapsulation efficiency of (94.7±1.7)% and a drug loading content of (1.4±0.1)%, showing sustained and steady drug release over time, with a cumulative release of (91.2±9.6)% over 108 hours. In cell experiments, the SF-TA@PTX hydrogel significantly inhibited the proliferation of 4T1 and MDA-MB-231 breast cancer cells, effectively killing over 50% of the tumor cells.

Conclusion: The SF-TA hydrogel, as a drug delivery system for paclitaxel, exhibits high drug loading capacity, stable drug release characteristics, and significant anti-tumor cell effects, demonstrating its potential for breast cancer treatment.

Histone deacetylase 7 (HDAC7), as a key molecule in epigenetic regulation, plays a crucial role in the initiation and progression of various tumors. Recent studies have revealed that HDAC7 not only participates in tumor cell proliferation, invasion and metastasis, but also potentially suppresses the antigen recognition capacity of immune cells by regulating the survival, maturation, differentiation and subcellular functions of immune cells such as CD4^＋ T cells, macrophages and dendritic cells. It also modulates tumor immune escape and the tumor microenvironment by suppressing immune cell activation and immune response effects through regulating the proliferation, differentiation and infiltration of immune effector cells such as CD8^＋ T cells, B lymphocytes and natural killer cells. Therefore, this review will summarize the role and related mechanism of HDAC7 in tumor immunity, and further discuss the current status of HDAC7 inhibitor applications in tumor therapy and future research directions.

Objective: This study aims to evaluate the correction effect of online adaptive radiation therapy (ART) on the setup error of patients with pelvic malignancies, analyze the impact of bladder filling status changes on setup accuracy before and after the development of ART plans, and analyze the factors related to positional changes.

Methods: A retrospective analysis was conducted on the clinical medical records of 21 patients with pelvic malignancies (including 15 cases of cervical cancer and 6 cases of prostate cancer) from September 2024 to June 2025. Using fan-beam CT three-dimensional registration technology, the setup errors in the L (Lat), X (Lng), and Y (Vrt) directions were measured before and after the ART plan was formulated. The treatment target and organs at risk (OAR) were automatically delineated by the radiotherapy planning system, and then manually modified to obtain quantitative data on bladder volume changes and target volume changes. The patients were divided into three groups: low bladder deviation change group (<40%), medium bladder deviation change group (40%-80%), and high bladder deviation change group (>80%). The influence of various factors on positional changes was analyzed.

Results: Before and after the ART plan was formulated, the setup errors in the L (Lat), X (Lng), and Y (Vrt) directions were significantly reduced from -0.62 to 0.70 cm, -1.13 to 1.36 cm, and -0.66 to 0.83 cm before the ART plan was formulated, respectively, to -0.34 to 0.17 cm, -0.22 to 0.43 cm, and -0.31 to 0.35 cm after the ART plan was formulated. The relationship between bladder filling status and setup error during the ART plan formulation period showed that as the bladder volume changes increased, the error in the abdominal-back direction would significantly increase in a short period of time, while the bladder filling status and lesion volume changes during the ART implementation were positively correlated with the patient’s positional changes.

Conclusion: ART can significantly improve the repeatability accuracy of body position and effectively reduce the inter-fraction setup error in patients with cervical cancer and prostate cancer. For patients with pelvic malignancies, highly repeatable bladder capacity (deviation <40%) is a key factor in achieving excellent body position consistency. At the same time, in the ART process, it is necessary to prioritize the assessment of bladder filling status and lesion volume changes to avoid the risks of insufficient target dose coverage and excessive OAR exposure dose caused by anatomical displacement.

DNA damage repair is a protective mechanism initiated by cells in response to genetic damage caused by endogenous or exogenous factors, playing a crucial role in maintaining genomic stability and cellular homeostasis. Factors such as ultraviolet radiation, chemicals, and ionizing radiation can induce various types of DNA damage, including single-strand breaks (SSBs), double-strand breaks (DSBs), base modifications, and intermolecular crosslinks. To ensure genetic integrity, cells have evolved a sophisticated and highly coordinated DNA damage repair system encompassing multiple repair pathways and intricate regulatory networks. In recent years, fidgetin-like protein 1 (FIGNL1) has emerged as a novel regulatory factor whose role in DNA damage repair has garnered increasing attention. Previous studies indicate that FIGNL1 plays a crucial role in homologous recombination repair, contributing to the maintenance of genomic stability. Concurrently, its abnormal expression may influence tumor cell sensitivity to chemotherapeutic agents and radiotherapy, participating in the development of treatment resistance. This review summarizes recent research on FIGNL1 in DNA damage repair and explores its potential significance in maintaining genomic homeostasis and contributing to tumor treatment resistance.

Objective: To investigate the influencing factors of radiation-induced pneumonia in patients with advanced wild-type non-small cell lung cancer (NSCLC) after receiving radiotherapy with Cyberknife, and to analyze the relationship between the expression of tissue infiltrating memory B cells (MBCs) and radiation-induced pneumonia.

Methods: Wild-type advanced NSCLC patients who received radiotherapy with Cyberknife from January 2020 to January 2022 were selected as the study subjects. A total of 128 patients with and without radiation pneumonitis were included, and their clinical medical records were collected. The number of infiltrations of tissue infiltrating MBCs were calculated, and the patients were divided into MBCs high-expression group and MBCs low-expression group according to a median expression level of 23%. The clinical characteristics of patients with and without radiation-induced pneumonia were compared. A hierarchical regression model was used to analyze the relationship between different clinical characteristics and MBCs expression. Logistic regression was used to analyze the relationship between MBCs expression and radiation-induced pneumonia. Multiple regression equations were used to analyze the relationship between MBCs expression and lung function indicators. A restrictive cubic spline model (combining spline functions with logistic regression) was used to analyze the dose-response relationship between MBCs expression and the risk of radiation-induced pneumonia, and a survival curve was constructed to analyze the impact of MBCs expression on survival.

Results: There were significant differences in age, hypertension history, diabetes history and comprehensive care between the radiation-induced pneumonia group and the no radiation-induced pneumonia group (P＜0.05). The differences in tumor location, underlying lung disease, Karnofsky performance status (KPS) score, forced expiratory volume in one second/forced vital capacity (FEV1/FVC), planned target volume (PTV), mean lung dose (MLD), volume percentage receiving 5 Gy radiation dose (V5), volume percentage receiving 10 Gy radiation dose (V10), volume percentage receiving 20 Gy radiation dose (V20), and MBCs expression were all statistically significant (P＜0.01). The results of stratified regression analysis showed that age, underlying lung diseases, and FEV1/FVC had significant negative effects on MBCs expression (P＜0.05). After excluding confounding factors with collinearity, MBC expression remained independently correlated with the occurrence of radiation pneumonitis (P＜0.05). Multiple linear regression analysis showed that the expression of MBCs was positively correlated with lung function indicators (P＜0.05). The one-year survival rates of the patients in MBCs high-expression group and low-expression group were 77.78% and 50.01%, respectively, and the two-year survival rates were 62.22% and 43.37%, respectively, both with statistically significant differences (P＜0.05).

Conclusion: There is an independent correlation between MBCs expression and radiation-induced pneumonitis. For patients with radiation-induced pneumonitis, the patients with high expression of MBCs have a higher survival rate than those with low expression of MBCs.

In recent years, malignant tumors have become a major global public health issue, with mortality rate ranking second among all diseases, only after cardiovascular diseases. Tumor development is associated with multiple factors. Among them, the calcium-dependent membrane-binding protein (Copine) family, as a novel calcium-sensing protein, exhibits differential expression in various malignant solid tumors and plays a critical regulatory role in tumorigenesis and progression. Copine-7 (also known as CPNE7), a member of the Copine protein family, is significantly overexpressed in gastrointestinal tumors such as gastric and colorectal cancers, and its expression level is positively correlated with TNM stage (P < 0.01). Furthermore, high expression of CPNE7 has been confirmed to be closely associated with poor prognosis, including shortened overall survival. Further analysis reveals that CPNE7 promotes tumor cell proliferation by activating the MAPK/PI3K-AKT signaling pathway and enhances tumor cell metastatic ability by regulating the epithelial-mesenchymal transition (EMT) process. This review focuses on the latest research progress regarding CPNE7 in various malignant solid tumors, systematically summarizes the mechanisms of CPNE7 in tumor development, and aims to provide new insights and evidence for precise diagnosis and targeted therapy of tumors.

Objective: To establish risk predictive models for female breast cancer using synthetic minority oversampling technique (SMOTE) algorithm to deal with unbalanced screening data, and compare the performance of established models based on original data and processed data.

Methods: This analysis was based on the data derived from a breast cancer screening program conducted in 2008-2015 among 15 046 women aged 35-74 years in Shanghai. The dataset was randomly divided into a training set and a testing set by a ratio of 7:3. Logistic regression was used to identify risk factors and establish predictive models based on original data and processed data using SMOTE algorithm. Area under the curve (AUC), sensitivity, specificity, Brier score and F1 value were used to compare the performance of two established models.

Results: Age, menarche age, age at first delivery, daily intake of vegetables and fruits, previous fibroadenoma of breast, and family history of breast cancer were identified as risk factors for breast cancer. The AUC and 95% confident interval of the established model based on original data was 0.621 (0.531-0.711) in the testing set, while that of the model based on processed data was 0.659 (0.546-0.772).

Conclusion: The prediction model based on processed data using SMOTE algorithm performs better than the model based on original data. Our results suggest that SMOTE algorithm may help to solve the problem of data imbalance in medical data.

Colorectal cancer (CRC) has shown an increasing disease burden in recent years, with a trend of younger onset age. Due to the low cancer screening rate among young people, most CRC patients are diagnosed at an advanced stage. Therefore, it is necessary to further explore the risk factors related to CRC occurrence and the novel interventional targets emerging during CRC development, in order to reduce the risk of CRC occurrence and improve the prognosis of CRC patients. Abnormal lipid metabolism plays a crucial role in the occurrence and development of CRC. The dysregulation of lipid parameters can lead to an increased risk of CRC, and the lipid metabolism reprogramming that occurs during CRC development can further promote the proliferation and invasion of CRC. This paper aims to elucidate the mechanism by which abnormal lipid metabolism promotes the occurrence and development of tumor cells, and to review the research progress of CRC prevention and treatment strategies based on lipid metabolism. A deeper understanding of the relationship between abnormal lipid metabolism and CRC occurrence and development is of great significance for developing CRC prevention and treatment strategies.

Objective: To investigate the regulatory role of calmodulin-binding transcriptional activator 1 (CAMTA1) on the proliferation of colorectal cancer cells and its correlation with tumor immune infiltration.

Methods: Based on the transcriptomic sequencing data of colorectal cancer from The Cancer Genome Atlas (TCGA) database, the expression level of CAMTA1 mRNA in colorectal tumor tissues were analyzed, and its correlation with patient prognosis was evaluated. The expression levels of CAMTA1 mRNA in human normal colorectal mucosal epithelial cell line FHC and colorectal cancer cell lines (DLD1, HT29, and HCT116) were detected by quantitative PCR (qPCR). Meanwhile, the differential expression of CAMTA1 mRNA and protein in clinically matched fresh primary colorectal cancer tissues and their adjacent normal tissues were detected using qPCR and immunohistochemistry. Overexpression plasmids carrying the CAMTA1 gene were transiently transfected into HT29 cells and mouse colorectal cancer cell line MC38, and CAMTA1 siRNA (siCAMTA1) was introduced into HT29 cells via lentiviral infection. The CCK-8 assay was used to assess the effects of CAMTA1 silencing or overexpression on the proliferation of HT29 and MC38 cells. In addition, a subcutaneous xenograft model was established in C57BL/6 mice using MC38 cells with stable CAMTA1 overexpression to monitor tumor growth in vivo. Finally, the relationship between CAMTA1 expression level and the extent of immune cell infiltration in colorectal cancer were analyzed using the TIMER database and single-sample gene set enrichment analysis (ssGSEA).

Results: The analysis results based on the TCGA dataset showed that CAMTA1 mRNA expression was significantly down-regulated in colorectal cancer tissues (P < 0.01), and its low expression was associated with shorter recurrence-free survival in patients. In clinical fresh colorectal cancer tissues, both CAMTA1 mRNA and protein expression levels were significantly down-regulated (both P < 0.05), and CAMTA1 mRNA expression was also significantly reduced in colorectal cancer cell lines in vitro (all P < 0.05). The results of functional assays in vitro demonstrated that CAMTA1 overexpression inhibited the proliferation of HT29 and MC38 cells, while CAMTA1 silencing promoted the proliferation of HT29 cells. The results of functional experiments in vivo further showed that CAMTA1 overexpression suppressed the growth of MC38 cell-derived xenografts in mice and reduced the infiltration of CD8⁺ T cells in tumor tissues. ssGSEA analysis revealed that CAMTA1 expression levels were significantly positively correlated with the infiltration levels of certain T helper cells [such as Type 2 Th (Th2) cells and T gamma delta (Tgd) cells] (R = 0.208, P < 0.05), while negatively correlated with the infiltration levels of macrophages, neutrophils, CD8⁺ T cells, and activated dendritic cells (aDCs).

Conclusion: The expression level of CAMTA1 is downregulated in colorectal cancer and is closely associated with poor prognosis of patients. CAMTA1 exerts tumor-suppressive effects by inhibiting the proliferation of colorectal cancer cells and modulating tumor-associated immune cell infiltration, and is expected to become a potential prognostic biomarker and therapeutic target for colorectal cancer.