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.

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 4/6 (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.

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: 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 (21.1%) 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%). There were 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 whether aurora kinase A (AURKA) in hepatocellular carcinoma (HCC) cells drives M2 polarization of macrophages via exosomes, and to clarify its underlying molecular mechanism.

Methods: The correlations between AURKA expression level in HCC tissues and M2 macrophage infiltration as well as prognosis of HCC patients were analyzed using the GEPIA (Gene Expression Profiling Interactive Analysis) and TIMER (Tumor Immune Estimation Resource) public databases. Based on the human HCC cell line MHCC-97H, AURKA stably overexpressed (97H-AKAOE) and knockdown (97H-AKAKD) cells were constructed. Exosomes were isolated by ultracentrifugation and characterized by transmission electron microscopy, nanoparticle tracking analysis and Western blotting. Exosomes derived from 97H-AKAOE and 97H-AKAKD cells were co-cultured with M0 macrophages, and the expression levels of M2 macrophage marker proteins CD163 and Arg-1 were assessed by real-time quantitative reverse transcription PCR (RT-qPCR) and Western blotting to evaluate the effect of AURKA on M2 polarization of macrophages. Liquid chromatography-mass spectrometry (LC-MS) was used to identify key differentially expressed proteins regulated by AURKA in exosomes, and functional rescue experiments were performed to validate their roles on M2 polarization of macrophages.

Results: AURKA was highly expressed in HCC tissues, and its expression level positively correlated with poor prognosis of HCC patients and M2 macrophage infiltration abundance (both P < 0.05). AURKA overexpression significantly enhanced the exosome-induced M2 polarization of macrophages, as evidenced by the upregulated CD163 and Arg-1, whereas AURKA knockdown suppressed this effect. Proteomic analysis revealed that lectin galactoside-binding soluble 3-binding protein (LGALS3BP) was significantly enriched in exosomes from AURKA-overexpressing HCC cells. Knockdown of LGALS3BP partially reversed the AURKA-mediated M2 polarization of macrophages.

Conclusion: AURKA in HCC cells drives M2 polarization of macrophages by upregulating exosomal LGALS3BP expression, thereby promoting the formation of an immunosuppressive tumor microenvironment in HCC. Elucidation of this mechanism provides a potential novel target for HCC immunotherapy.

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. The potential value of HIPEC in reducing postoperative recurrence of soft tissue sarcomas and improving patient prognosis was explored. 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: To construct a nano delivery system based on sonodynamic therapy to overcome cisplatin resistance of ovarian cancer by inducing pyroptosis.

Methods: A human cisplatin-resistant ovarian cancer cell line (SKOV-3/DDP) was successfully induced using a stepwise concentration gradient induction method. A composite nanoparticles (BTO/ZIF) with a core of barium titanate (BaTiO₃, BTO) and a shell of zeolitic imidazolate framework-8 (ZIF-8) was constructed. The surface of BTO/ZIF was further coated with DSPE-PEG₁₀₀₀-Pt (Ⅳ) and DSPE-PEG₁₀₀₀-AF to prepare the targeted nanoparticle BTO/ZIF@AF/Pt. The morphology, size, structure, hydrodynamic diameter, and colloidal stability (Zeta potential) of BTO/ZIF@AF/Pt nanoparticles were characterized using transmission electron microscopy, scanning electron microscopy, and Malvern particle size analyzer. The reactive oxygen species (ROS) generation capability of BTO/ZIF composite nanoparticles was assessed by ultraviolet-visible (UV) spectrophotometry and DCFH-DA probe assay. Cellular uptake of BTO/ZIF@AF/Pt nanoparticles by SKOV-3/DDP cells was verified using confocal laser scanning microscopy. Under ultrasound irradiation, the effects of BTO/ZIF@AF/Pt nanoparticles on the expression of pyroptosis-related proteins and sensitivity to cisplatin chemotherapy were examined by Western blotting.

Results: In this study, a human cisplatin-resistant ovarian cancer cell line (SKOV-3/DDP) was successfully induced, and a targeted delivery nanoparticle using BTO and metal-organic framework (MOF) composite materials as the carrier for cisplatin was also successfully constructed. Under ultrasound stimulation, BTO/ZIF@AF/Pt nanoparticles effectively generated ROS and induced pyroptosis in ovarian cancer SKOV-3/DDP cells.

Conclusion: Ultrasound-triggered ROS generation from BTO/ZIF@AF/Pt nanoparticles, combined with Zn^2＋ release, synergistically promotes ROS-induced pyroptosis in ovarian cancer SKOV-3/DDP cells, thereby effectively overcoming cisplatin resistance.

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.

Pancreatic cancer, a highly malignant tumor of digestive system, is characterized by challenges in early detection and limited therapeutic efficacy. Currently, artificial intelligence (AI) technologies—such as machine learning, deep learning, and natural language processing (NLP)—are providing innovative strategies to address key bottlenecks in the diagnosis and treatment of pancreatic cancer. Based on databases such as PubMed, Web of Science, and CNKI, this study conducted literature retrieval and screening, initially obtaining 128 articles related to AI-powered pancreatic cancer diagnosis and treatment. After in-depth review, 38 journal papers and research reports were ultimately included, covering key aspects such as AI-based disease risk prediction models, intelligent screening of medical imaging and pathological assistance diagnosis, personalized treatment strategy recommendations, efficacy monitoring, and recurrence prediction. The study systematically reviews the integration and application of AI technologies throughout the entire process of pancreatic cancer diagnosis and treatment. By conducting a meta-analysis of current practices and evidence regardin AI in pancreatic cancer diagnosis and treatment, this paper aims to provide academic references for promoting the effective translation of AI technologies into clinical practice for pancreatic cancer.

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 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 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 SC were retrospectively reviewed, with comprehensive analysis of histopathological features and immunohistochemical characteristics in all cases.

Results: In this study, SC predominantly affected elderly female patients, with a median age of 65 years. 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 Ki-67.

Conclusion: 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: 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: LAWD after abdominal wall tumor resection in 29 patients was 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 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.

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.

Lung cancer is one of the most common and deadly malignant tumors worldwide, with its significant tumor heterogeneity and drug resistance being major obstacles to achieving precision medicine. Patient-derived tumor organoids, which can faithfully recapitulate the genetic and pathological features of the original tumor, serve as a bridge linking basic research and clinical practice, and show great promise in advancing precision therapy for lung cancer. This paper systematically reviews the construction strategies and technical advantages of lung cancer organoid models, and points out that the key to future development lies in establishing standardized culture systems, conducting multicenter clinical validation, and deepening the integration of multi-omics data, with the aim of promoting the application of lung cancer organoids in drug development and individualized precision therapy.

Objective: To construct a unmethylated CpG (cytosine-phosphate-guanine) nano delivery system based on the cationic polymer carrier polyethylenimine (PEI), termed CpG-PEI, and to evaluate its efficiency in promoting intracellular delivery of CpG, tis ability to enhance anti-tumor immunotherapy, and its biosafety.

Methods: CpG-PEI nanoparticles were prepared through the electrostatic self-assembly method. The synthesis morphology, particle size, and zeta potential of CpG-PEI nanoparticles were characterized by agarose gel electrophoresis, field emission scanning electron microscopy, and dynamic light scattering (DLS); The uptake efficiency of CpG-PEI nanoparticles by RAW264.7 macrophages was assessed using flow cytometry and laser scanning confocal microscopy. The impact CpG-PEI nanoparticles on macrophage polarization was evaluated by detecting M1/M2 phenotypic markers on the surface of RAW264.7 macrophages via flow cytometry. The cytotoxicity and apoptosis-inducing effects of CpG-PEI nanoparticles were evaluated using the CCK-8 assay and Annexin V-FITC/PI double staining method to verify its biosafety.

Results: CpG-PEI nanoparticles with a particle size of 200−400 nm were successfully prepared, its electronegativity gradually changes towards a positive charge direction as the proportion of PEI in the synthesis system increases; CpG-PEI nanoparticles significantly enhanced the intracellular uptake of CpG by RAW264.7 macrophages and effectively induced macrophage polarization towards anti-tumor M1 phenotype. By adjusting the proportion of PEI in the CpG-PEI synthesis system, the cytotoxicity of the nanoparticles could be significantly reduced while maintaining efficient delivery and immune activation.

Conclusion: This study successfully developed a safe and effective CpG-PEI nanodelivery system, which enables efficient intracellular delivery of CpG in immune cells and induces polarization of RAW264.7 macrophages towards the anti-tumor M1 phenotype, providing a new delivery strategy for nucleic acid adjuvant-based tumor immunotherapy.

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: 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.

Objective: To investigate the effect of overexpression of exogenous ETS translocation variant 2 (ETV2) gene on the tube-forming ability of human umbilical vein endothelial cells (HUVECs) and to construct an endothelial cell-tumor organoid co-culture model capable of adapting to tumor growth.

Methods: A doxycycline-inducible Tet-On plasmid system was used to regulate the expression level of ETV2 gene, which was transfected into HUVECs via a lentiviral vector to establish a stable transfection HUVEC cell line (named ETV2-EC) with ETV2 expression modulated by doxycycline concentration. The tube-forming ability of ETV2-EC cells induced with different concentrations of doxycycline was assessed through tube formation assay. Subsequently, ETV2-EC cells were co-cultured with breast cancer organoids, and the optimal co-culture medium for the co-culture model was determined via Calcein-AM staining and CCK-8 assay. The viability of endothelial cells and their interactions with tumor organoids in the co-culture model were observed under an optical microscope. Finally, the effect of ETV2 overexpression on the transcriptome profile of HUVECs was analyzed by RNA-seq.

Results: Induction with 10 μmol/L doxycycline significantly enhanced the tube-forming ability and tubular structure stability of ETV2-EC cells. Both endothelial cells and tumor organoids could stably survive in the breast cancer organoid culture medium containing fibroblast growth factor 2 (FGF2) and heparin. Compared with control HUVECs, ETV2-EC cells induced with 10 μmol/L doxycycline showed longer survival time, larger tubular structure area, and greater stability when co-cultured with tumor organoids. RNA-seq analysis revealed that overexpression of ETV2 gene markedly altered the transcriptomic profile of HUVECs, and the differentially expressed genes in ETV2-EC cells were mainly associated with endothelial cell proliferation, migration, and adaptation to the tumor microenvironment.

Conclusion: Overexpression of ETV2 gene in mature endothelial cells may endow them with enhanced tube-forming ability by reactivating the suppressed genes associated with lumen formation and angiogenesis. Moreover, under co-culture conditions with tumor organoids, overexpression of ETV2 gene significantly improves the survival ability of endothelial cells and their adaptation to the tumor microenvironment.

Primary pulmonary lymphoma (PPL) is relatively rare malignancy in clinical practice, whose imaging and pathological phenotypes lack specificity. Traditional diagnosis primarily relies on clinicians' personal experience, which can easily lead to misdiagnosis and missed diagnoses. Machine learning (ML), as a core technology of artificial intelligence (AI), provides a new approach to improving the diagnostic efficacy of PPL. This article reviews the latest advances in ML applications for PPL diagnosis. In the field of radiomics, ML facilitates the extraction of high-throughput texture features from CT and positron emission tomography (PET) imaging to construct quantitative models, thereby significantly improving the diagnostic accuracy for differentiating PPL from lung cancer, organizing pneumonia, and other diseases. In the field of pathomics, deep learning techniques have enabled automated classification of lymphoma subtypes and objective immunohistochemical analysis. Additionally, genomics intergrated with ML helps elucidate the molecular characteristics of PPL to support its precise classification. Although the application of ML in PPL diagnosis still face challenges such as limited sample sizes, insufficient standardization and poor model interpretability, advancements in multimodal data integration, federated learning and interpretable AI are expected to propel the diagnosis and treatment of PPL toward intelligent and precise development.

Objective: To investigate the role and potential regulatory mechanisms of iron death-related genes, such as glutathione peroxidase 2 (GPX2) and arachidonic acid 5-lipoxygenase (ALOX5), in the progression of nasopharyngeal carcinoma (NPC), and to analyse their association with immune cell infiltration.

Methods: Gene expression profiles of the GSE102349 dataset, which includes 113 NPC tissues and 154 normal nasopharyngeal tissues, were obtained from the Gene Expression Omnibus (GEO) database. Additionally, iron death-related gene information was obtained from the Ferroptosis database (FerrDb). The limma package in R software was used to identify differentially expressed genes (DEGs) in NPC tissues, followed by gene function annotation and pathway enrichment analysis based on the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases using the clusterProfiler package. Ferroptosis-related genes were obtained from the Ferroptosis Database (FerrDb) and intersected with the DEGs to identify ferroptosis-related differentially expressed genes (Ferr-DEGs). A protein-protein interaction (PPI) network of Ferr-DEGs was constructed using the STRING database and visualized with Cytoscape software. Key modules within the PPI network were identified using the Molecular Complex Detection (MCODE) plugin in Cytoscape, and hub genes within these modules were screened using the cytoHubba plugin. Subsequently, gene set enrichment analysis (GSEA) was performed on the hub genes. Finally, the CIBERSORT and single-sample gene set enrichment analysis (ssGSEA) algorithms were employed to evaluate differences in immune cell infiltration between NPC tissues and normal nasopharyngeal tissues within the GSE102349 dataset.

Results: A total of 817 upregulated and 538 downregulated genes were identified in NPC tissues. These DEGs were primarily enriched in biological processes related to immune response, apoptosis, lipid metabolism, and ferroptosis. By intersecting the DEGs with ferroptosis-related genes, a total of 26 Ferr-DEGs were obtained, including significantly downregulated GPX2 and significantly upregulated ALOX5. These Ferr-DEGs were significantly enriched in oxidative stress response, the ferroptosis pathway, the HIF-1 signaling pathway, and immune-related processes (e.g., defense response and myeloid leukocyte activation). PPI network analysis identified the top 5 hub genes: GPX2, ALOX5, heme oxygenase 1 (HMOX1), cytochrome b-245 beta chain (CYBB), and src proto-oncogene (SRC), and GPX2 and ALOX5 occupy central positions in the key modules of the PPI network. Results of GSEA pathway enrichment analysis revealed that these hub genes were significantly enriched in pathways such as the hematopoietic cell lineage, lysosome, and Fc gamma receptor-mediated phagocytosis. Results of immune infiltration analysis indicated significantly higher proportions of memory B cells, follicular helper T cells, monocytes, M0 macrophages, and activated mast cells in NPC tissues, and the infiltration levels of these cells were positively correlated with the expression levels of most hub genes (except GPX2).

Conclusion: GPX2 and ALOX5 may participate in NPC progression by regulating ferroptosis and immune cell infiltration, and are promising new therapeutic targets for NPC treatment.

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.

Objective: To establish a predictive model of platelet transfusion efficacy in patients with myelodysplastic syndrome (MDS) based on machine learning algorithms, and to validate its predictive performance and clinical utility in a patient cohort.

Methods: A total of 160 MDS patients in Yuncheng Central Hospital Affiliated to Shanxi Medical University from January 2021 to December 2024 were enrolled as the training set and divided into an ineffective group and an effective group according to platelet transfusion efficacy. Characteristic variables for constructing the prediction model of platelet transfusion efficacy in MDS patients were sequentially screened using least absolute shrinkage and selection operator (LASSO) regression analysis and logistic regression analysis. Four machine learning algorithms, namely extreme gradient boosting (XGBoost), decision tree, random forest and logistic regression, were respectively employed to construct the prediction models. Predictive performance of each model was evaluated using sensitivity, specificity, the area under the curve （AUC） of receiver operating characteristic (ROC) and Youden index. The decision curve analysis was further used to evaluate the clinical practicability of the optimal model. In addition, 73 patients with MDS in Yuncheng Central Hospital Affiliated to Shanxi Medical University and the Second Hospital of Shanxi Medical University from January to May 2025 were selected as the time validation set to evaluate the clinical generalizability of the optimal model.

Results: Among the 160 patients with MDS in the training set, the rate of platelet transfusion inefficiency was 34.38% (55/160). The proportions of fever, splenomegaly, platelet antibody positive and platelet transfusion times ≥5 times, as well as the levels of serum interleukin (IL)-1β and IL-8 in the ineffective group were higher than those in the effective group (all P < 0.05). Logistic regression analysis showed that splenomegaly, platelet antibody positive, platelet transfusion times and the levels of serum IL-1β and IL-8 were independent risk factors for ineffective platelet transfusion in MDS patients (all P < 0.05). The AUC values of XGBoost model were 0.946 [95% confidence interval (CI): 0.899-0.975] in the training set and 0.947 (95% CI: 0.868-0.986) in the validation set, which were both significantly higher than those of the random forest model [0.871 (95% CI: 0.809-0.919) and 0.830 (95% CI: 0.723-0.907)], decision tree model [0.856 (95% CI: 0.792-0.907) and 0.814 (95% CI: 0.705-0.895)] and logistic regression model [0.849 (95% CI: 0.784-0.901) and 0.804 (95% CI: 0.695-0.888)] (all P < 0.05). Additionally, in both the training and validation sets, the XGBoost model demonstrated the sensitivities of 90.91% and 91.67%, and the specificities of 89.52% and 91.84%, which were both significantly higher than those of the other three predictive models (both P < 0.05). The XGBoost model ranked the factors that increase the risk of ineffective platelet transfusion in MDS patients in order of importance, namely platelet antibody positive, platelet transfusion frequency, serum IL-8 level， serum IL-1β level and splenomegaly. The decision curve showed that when the threshold probability ranged from 0.01 to 0.99, applying the XGBoost model to predict the efficacy of platelet transfusion in MDS patients consistently demonstrates that the clinical benefits derived from correct interventions outweigh the losses caused by misjudgments, which has good clinical practical value.

Conclusion: The efficacy of platelet transfusion therapy for MDS patients is not ideal. The XGBoost model, constructed based on five clinical indicators including platelet antibody positivity, platelet transfusion frequency, serum IL-8 level, serum IL-1β level and splenomegaly, has the best comprehensive predictive performance for the platelet transfusion effect in MDS patients and has good clinical practical value. It can provide references for clinical adjustment, optimization of treatment plans and improvement of platelet transfusion efficiency.

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 investigate the correlation between the expression levels of specific microRNAs (miRNAs) in macrophage-derived exosomes and the platinum-based chemotherapy efficacy and prognosis of non-small cell lung cancer (NSCLC) patients.

Methods: This study collected the clinicopathological data of all NSCLC patients who underwent radical surgery and postoperative standard first-line platinum-based chemotherapy at the Chinese People’s Liberation Army General Hospital of Northern Theater Command from January 2018 to October 2022 by reviewing the electronic medical records. All patients’ peripheral blood samples were obtained before surgery, and the exosomes were isolated from the blood samples. The expression levels of 7 miRNAs (miR-15b, miR-21, miR-27b, miR-93, miR-125a, miR-146a and miR-155) associated with macrophage phenotype differentiation were measured using quantitative polymerase chain reaction (qPCR). Based on the progression-free survival (PFS), all patients were divided into the platinum-resistant group (PFS time ≤ 6 months) and the platinum-sensitive group (PFS time > 6 months). They were also categorized into the death group and the survival group according to their survival status at the end of follow-up. Logistic regression was used to identify independent influencing factors of platinum resistance in NSCLC patients, and COX proportional hazards regression model was used to analyze independent influencing factors of poor prognosis in NSCLC patients.

Results: A total of 138 NSCLC patients were included in this study. Among them, there were 19 patients in the platinum-resistant group and 119 patients in the platinum-sensitive group. Compared with platinum-sensitive group, the proportion of patients with vascular invasion and the expression level of exosomal miR-155 in platinum-resistant group were significantly increased (both P < 0.05), while the expression level of exosomal miR-125a was significantly decreased (P < 0.05). During the follow-up period, a total of 55 patients died, and 83 patients survived until the end of the follow-up. Compared with the survival group, the proportion of patients with TNM stage Ⅲ-Ⅳ and poorly differentiated, the expression levels of serum CEA and exosomal miR-155 and miR-15b in the death group were significantly increased (all P < 0.05), while the expression levels of exosomal miR-146a, miR-21 and miR-125a were significantly decreased (all P < 0.05). The results of multiple logistic regression analysis showed that exosomal miR-125a [odds ratio(OR) = 0.647, 95% confidence interval (CI): 0.433-0.965] was an independent influencing factor for platinum resistance in NSCLC patients (P < 0.05). The results of COX proportional hazards regression analysis showed that exosomal miR-155 [hazard ratio (HR) = 1.180, 95% CI: 1.064-1.308], miR-125a (HR = 0.656, 95% CI: 0.476-0.903) and serum CEA (HR = 1.001, 95% CI: 1.000-1.002) were independent influencing factors for the poor prognosis of NSCLC patients (all P < 0.05). The area under the curve (AUC) of exosomal miR-125a for predicting platinum resistance in NSCLC patients was 0.738 (sensitivity was 53.8%, specificity was 89.5%). The combination of exosomal miR-155, miR-125a and serum CEA predicted the poor prognosis of NSCLC patients with AUC of 0.879 (sensitivity of 85.5% and specificity of 75.9%), which was superior to any single indicator.

Conclusion: The decreased expression level of miR-125a in macrophage-derived exosomes is an independent risk factor for platinum-based chemotherapy resistance in NSCLC patients. In addition, the combination of exosomal miR-155, miR-125a and serum CEA significantly enhances the predictive efficacy for poor prognosis in NSCLC patients with platinum resistance, and is expected to serve as an auxiliary reference indicator for clinical treatment decisions in NSCLC.

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.

Retroperitoneal soft tissue sarcoma (RPSTS) is a rare malignant tumor, and its diagnosis and treatment face significant challenges due to the high heterogeneity of the tumor. Currently, imaging examinations, such as CT and MRI, are key tools for diagnosing RPSTS. However, traditional methods have limitations in achieving precise evaluation. In recent years, machine learning technologies have shown considerable potential to further enhance the diagnosis and treatment of RPSTS. Machine learning has achieved remarkable results in subtype classification, grading, treatment monitoring, and prognostic prediction for RPSTS. For example, it can effectively distinguish different subtypes of RPSTS, such as well-differentiated liposarcoma and dedifferentiated liposarcoma, and predict important indicators, including tumor grade, treatment response, and the risk of distant metastasis. Although machine learning has made significant progress in image data processing and model optimization, the subjectivity of manual segmentation of regions of interest (ROI), the constraints of small sample data, and the “black-box” nature of deep learning models remain critical bottlenecks restricting its clinical implementation. In the future, through large-scale multicenter studies, the development of automated segmentation technologies, and improvements in model interpretability, machine learning is expected to gradually transform into a reliable clinical tool, which provides more accurate diagnostic and treatment to RPSTS patients and ultimately delivering real benefits to them.

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: 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.

Objective: To investigate the effect of serum bile acids, especially taurochenodeoxycholic acid (TCDCA), on gemcitabine resistance and survival prognosis in patients with gallbladder cancer.

Methods: Fresh gallbladder cancer tissues from 20 patients with gallbladder cancer were selected to construct mini patient derived xenograft (mini-PDX) models and patient-derived organoids. These patients were divided into a gemcitabine sensitive group and a gemcitabine resistant group using mini-PDX drug sensitivity testing. To detect serum bile acids in gemcitabine-sensitive and gemcitabine-resistant patients with gallbladder cancer using high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS), and compare the differences between the two groups. Using Kaplan-Meier method and COX proportional hazards model to assess the association between serum TCDCA levels and overall survival of gallbladder cancer patients, and conducting subgroup analysis of gallbladder cancer patients based on whether they received gemcitabine treatment. In the GBC-SD cell line and gallbladder cancer organoid models, the effects of TCDCA on gemcitabine resistance were assessed using CCK-8 cytotoxicity assay, colony formation assay, and organoid drug sensitivity test.

Results: Compared with gemcitabine-sensitive group, multiple conjugated bile acids were elevated in serum from gemcitabine-resistant patients, with TCDCA showing the most pronounced increase (P=3.3×10⁻⁵). In the clinical cohort, patients with high TCDCA had significantly shorter overall survival than those with low TCDCA [hazard ratio (HR)=1.75, 95% confidence interval (CI): 1.18-2.59; P=0.009]. Subgroup analysis revealed that this adverse prognostic association was confined to patients treated with gemcitabine (HR=2.07, 95% CI: 1.23-3.47; P=0.005), whereas no significant association in those not receiving gemcitabine (P=0.338). In vitro functional assays, TCDCA treatment significantly increased the IC₅₀ of gemcitabine in GBC-SD cells, and markedly enhanced the colony forming ability of GBC-SD cells under chemotherapeutic pressure. In gallbladder cancer organoids, TCDCA similarly attenuated gemcitabine-induced growth inhibition.

Conclusion: Serum TCDCA is a potential adverse prognostic biomarker for patients with gallbladder cancer receiving gemcitabine chemotherapy. TCDCA can directly induce gemcitabine resistance in GBC-SD cells and gallbladder cancer organoids, suggesting that targeting the bile acid metabolic microenvironment may provide a feasible therapeutic strategy to reverse gemcitabine chemotherapy resistance in gallbladder cancer.

Compared with injectable nucleic acid therapy, oral nucleic acid delivery has the advantages of good patient compliance and convenience, but it is still limited by various physiological barriers, such as acidic environment, enzymatic degradation, and endogenous lysosomal capture. To overcome the above physiological barriers to oral nucleic acid delivery, the ideal vector should have characteristics such as high stability, lysosomal escape, cell targeting, and good biocompatibility. Currently, polymeric nanoparticles, lipid nanoparticles, and extracellular vesicles play a key role in oral nucleic acid delivery by preventing nucleic acid degradation, avoiding capture by lysosomes, and enabling targeted delivery of nucleic acid. This review summarizes the role, barriers, delivery vectors and experimental studies of oral nucleic acid delivery, and puts forward the characteristics of ideal vectors to overcome physiological barriers, which provides a new strategy for oral nucleic acid delivery.

Objective: To investigate the clinical features, diagnostic considerations and therapeutic strategies for von Hippel-Lindau (VHL) disease with pancreatic neuroendocrine tumor (pNET), with the aim of enhancing early recognition and optimizing clinical management of this rare condition.

Methods: The clinical course and multidisciplinary management of one patient with VHL disease with pNET were reported. Relevant clinical, imaging, pathological and genetic data were collected and analyzed.

Results: A 25-year-old female patient was found to have space-occupying lesions in the pancreaticoduodenal region, left kidney and right adrenal gland on routine screening imaging. Based on the imaging findings and a positive family history, VHL disease was suspected. The patient underwent radical pancreaticoduodenectomy. Postoperative pathological examination and genetic testing confirmed the diagnosis of VHL disease with pNET. Adjuvant therapy with lanreotide plus surufatinib was administered postoperatively, and no definitive disease progression was observed during 6 months of follow-up.

Conclusion: VHL disease should be suspected in young patients presenting with pNET in conjunction with renal or adrenal lesions. Emphasis should be placed on genetic testing, a multidisciplinary team approach, and long-term organ-specific surveillance to guide optimal management.

Objective: To explore the synergistic inhibitory effect of apatinib combined with programmed cell death-1 (PD-1) monoclonal antibody on subcutaneous xenograft tumors of microsatellite stable (MSS) colon cancer in mice.

Methods: Transcriptome sequencing data and corresponding clinicopathological information of patients with colorectal cancer were retrieved from The Cancer Genome Atlas (TCGA) database. The single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm was employed to calculate angiogenesis scores, and the association of angiogenesis score with clinicopathological characteristics and patient prognosis were analyzed. Furthermore, ssGSEA and CIBERSORT algorithms were used to assess the correlation between immune cell infiltration and angiogenesis scores. A subcutaneous xenograft model was established using the mouse MSS colon cancer cell line CT26. Mice were divided into four groups: control group (DMSO), apatinib monotherapy group, PD-1 monoclonal antibody group, and combination treatment group (apatinib + PD-1 monoclonal antibody). Tumor growth of subcutaneous xenografts was compared among the groups. Flow cytometry was used to detect differences in immune cell infiltration within subcutaneous xenograft tumors across the groups. Immunohistochemical staining was employed to evaluate immune cell infiltration and angiogenesis within the tumors.

Results: Kaplan-Meier survival analysis demonstrated that patients with high angiogenesis scores had significantly shortened overall survival compared to those with low scores (P < 0.000 1) and had higher N staging. Tumor angiogenesis scores were significantly positively correlated with infiltration levels of M2 macrophages (r = 0.28, P < 0.01). In vivo experiments revealed that, compared with the control and monotherapy groups, tumor growth in the combination treatment group was markedly suppressed (all P < 0.05). Flow cytometry and immunohistochemical staining showed that CD4⁺ and CD8⁺T cell infiltration within tumors was significantly increased in the control and monotherapy groups (all P < 0.01), while M2 macrophage infiltration was significantly reduced (all P < 0.05). Multiplex immunofluorescence staining further indicated that the tumor vasculature in the combination treatment group was more organized compared with the control and monotherapy groups, and the co-localization pattern of CD31 and alpha-smooth muscle actin (α-SMA) demonstrated characteristics of vascular normalization.

Conclusion: Apatinib combined with PD-1 monoclonal antibody significantly inhibits the growth of MSS colon cancer xenografts in mice. The underlying mechanisms may involve increased T cell infiltration, reduced M2 macrophage infiltration, and promotion of intratumoral vascular normalization. This combination strategy holds promising potential as a novel therapeutic option for MSS colon cancer patients.

Colorectal cancer (CRC) is a malignant tumor with high incidence and mortality rates worldwide, influenced by multiple factors including genetics, epigenetics, and tumor microenvironment. Traditional omics research, based on mixed cell samples, can only obtain average signals from cell populations, making it difficult to resolve the high heterogeneity within tumors. The emergence of single cell sequencing technology provides a powerful tool for revealing the cellular lineages, molecular characteristics, and tumor microenvironment of CRC at single cell resolution. This article systematically reviews the development history and core principles of single cell sequencing technology, with a focus on summarizing recent advances in CRC tumor heterogeneity, tumor microenvironment, mechanisms of drug resistance and metastasis, and clinical translational applications. Furthermore, it discusses the current challenges in technology and data analysis at the single cell level, and provides future development directions for single cell sequencing in multi-omics integration and precision oncology.

Objective: To investigate the correlation between the dynamic changes in serum carbohydrate antigen 125 (CA125) levels and immune profiles as well as clinical prognosis in patients with recurrent ovarian cancer receiving bevacizumab combined with paclitaxel and carboplatin chemotherapy, with the aim of providing a basis for individualized treatment and prognostic evaluation.

Methods:A total of 90 patients with recurrent ovarian cancer admitted to the Cancer Hospital of Shantou University Medical College between June 2019 to June 2024 were enrolled in this study. Serum levels CA125, immunoglobulin A (IgA), IgG, IgM, complement component 3 (C3), and C4 were measured at the following time points: before chemotherapy (T0), at week 3 (T1), week 6 (T2), and week 9 (T3) of chemotherapy. A latent class growth model (LCGM) combined with a growth mixture model (GMM) was applied to characterize the trajectory of CA125 level changes throughout the chemotherapy course. Differences in demographic characteristics and immunological indicators across trajectory groups were compared, and generalized estimating equations (GEE) were used to examine the longitudinal associations between CA125 trajectory patterns and immunological indicators. Multivariate logistic regression was then employed to identify factors influencing CA125 level changes during chemotherapy, and COX proportional hazard regression model was conducted to assess the association between CA125 trajectory patterns and unfavorable prognosis.

Results: In 90 patients with recurrent ovarian cancer receiving bevacizumab combined with taxane-based and carboplatin chemotherapy, serum CA125 levels showed a progressive downward trend as chemotherapy advanced. The mean serum CA125 levels at T0, T1, T2, and T3 were 689.35±121.34 U/mL, 516.67±168.37 U/mL, 140.13±39.42 U/mL, and 30.12±9.27 U/mL, respectively (P < 0.05). Based on the trajectory of CA125 changes, patients were classified into three groups: the stable group (n=32, 35.56%), characterized by a gradual change in CA125 levels from T0 to T3 (β=−0.15, P<0.001); the rapid decline group (n=37, 41.11%), characterized by a sharp decrease in CA125 levels from T0 to T3 (β = − 1.54, P<0.001); and the slow decline group (n=21, 23.33%), characterized by a steady decrease in CA125 levels from T0 to T3 (β=−0.82, P<0.001). Age≥50 years, serous histological type, and unilateral ovarian involvement were identified as independent factors associated with a rapid decline in CA125 levels during chemotherapy (all P<0.05), while serous histological type and unilateral ovarian involvement were also independently associated with a slow decline in CA125 levels (both P<0.05). At each time point from T1 to T3, the levels of IgA, IgG, IgM, C3, and C4 in the stable group were significantly higher than those in both the rapid decline group and the slow decline groups (all P<0.05). GEE analysis revealed that, compared with the stable group, the CA125 levels in both the rapid decline group and the slow decline group were negatively correlated with all the aforementioned immunological indicators (all P<0.05). COX regression analysis showed that patients in the rapid decline group had a higher risk of unfavorable prognosis than those in the stable group [hazard ratio (HR)=1.624], whereas patients in the slow decline group had a lower risk of unfavorable prognosis (HR=0.447); these associations remained consistent across all subgroups (P<0.05).

Conclusion: During bevacizumab combined with paclitaxel and carboplatin chemotherapy, CA125 level changes in patients with recurrent ovarian cancer exhibit significant heterogeneity, with notable differences in immune profiles and prognostic outcomes across different CA125 trajectory groups. Compared with patients in the stable group, those in the rapid decline group demonstrate relatively weaker immune function and a higher risk of unfavorable prognosis, whereas patients in the slow decline group exhibited a relatively better immune status and a lower risk of unfavorable prognosis. Dynamic monitoring of CA125 trajectory patterns throughout chemotherapy may provide clinically valuable reference for assessing immune status and predicting prognosis in patients with recurrent ovarian cancer.

Objective: Linc01436 is a novel long chain non-coding RNA, which is related to the proliferation of tumor cells and tumor progression. However, its role in the progression of breast cancer and neoadjuvant chemotherapy has not been reported. This study aims to analyze the correlation between Linc01436 expression and neoadjuvant chemotherapy response and survival outcome in breast cancer patients, and explore the potential molecular mechanism of Linc01436 in breast cancer.

Methods: Univariate logistic regression, multivariate logistic regression, receiver operating characteristic (ROC) curve and Nomogram model were used to verify the predictive value of Linc01436 expression for pathological complete remission of breast cancer after neoadjuvant chemotherapy. Kaplan-Meier method was used to examine the impact of Linc01436 on prognosis. KEGG and GSEA analysis were used to enrich the biological processes that Linc01436 may be involved in. The CIBERSORT and EPIC algorithms were used to calculate the proportion of immune infiltrating cells in the tumor microenvironment. The immunophenotyping score (IPS) and MANTIS score were used to evaluate the predictive value of Linc01436 for immunotherapy.

Results: Multivariate analysis showed that the expression of Linc01436 in breast cancer tissues before neoadjuvant chemotherapy was an independent predictor of pathological complete remission after neoadjuvant chemotherapy (OR=0.25; 95% CI: 0.077-0.725; P=0.015,), especially in patients with negative expression of hormone receptor (OR=0.16; 95% CI: 0.029-0.700; P=0.022). Kaplan Meier analysis showed that high expression of Linc01436 was associated with poor prognosis of breast cancer patients in our cohort (HR=4.58; 95% CI: 1.51-14.50; P=0.028) and TCGA cohort (HR=1.56; 95% CI: 1.01-2.41;P=0.033). KEGG and GSEA enrichment analysis showed that Linc01436 was mainly involved in immune-related signaling pathways. Further bioinformatics analysis showed that Linc01436 expression was negatively correlated with CD8⁺ T cell infiltration and positively correlated with PD-L1 expression and immunotherapy score.

Conclusion: Linc01436 may be a reverse predictor of pathological partial remission and disease-free survival after neoadjuvant chemotherapy for breast cancer, especially in HR-negative subgroup. In addition, molecular signaling pathways involved in the progression of breast cancer provide a reference for optimizing the treatment of breast cancer.

Objective: To investigate the correlations between changes in cervical microcirculation parameters and ovarian reserve function after transumbilical single-port laparoscopic myomectomy

Methods: A total of 165 patients with uterine fibroids who underwent myomectomy at the 73rd Group Army Hospital of the Chinese People's Liberation Army from February 2022 to January 2025 were enrolled. Based on surgical approach, the patients were divided into three groups: the open abdominal group (55 cases, open abdominal myomectomy), the multiport group (55 cases, traditional multiport laparoscopic myomectomy), and the single-port group (55 cases, transumbilical single-port laparoscopic myomectomy). The perioperative indicators, Visual Analogue Scale (VAS) scores for postoperative pain, Cosmetic Scale (CS) and Body Image Scale (BIS) scores for incision aesthetic satisfaction, postoperative recovery and complications were compared among the three groups. Cervical microcirculation parameters, including microvessel diameter, blood flow perfusion, and capillary diameter, were measured before surgery and at 12, 24, and 72 hours postoperatively. Ovarian reserve function indicators, including serum follicle-stimulating hormone (FSH), anti-Müllerian hormone (AMH), luteinizing hormone (LH), peak systolic velocity (PSV) of the ovarian stromal artery, estradiol (E2), antral follicle count (AFC), and ovarian volume, were assessed before surgery and at 3 months after surgery. A difference-in-differences (DID) model was constructed to analyze the differences in ovarian reserve function before and after surgery. Repeated-measures (analysis of variance) ANOVA was used to evaluate the effects of surgical approach, postoperative time, and their interaction. Pearson correlation analysis was performed to assess the correlations between changes in cervical microcirculation parameters and changes in ovarian reserve function indicators.

Results: Compared with the open abdominal group, the single-port and multiport groups exhibited reduced drainage volume on the first postoperative day, lower BIS scores, higher CS scores, and lower rates of myoma recurrence and menstrual cycle disorders within 1 year postoperatively (all P < 0.05). The single-port group also had a significantly lower overall postoperative complication rate than the open abdominal group (P < 0.05), but no significant difference was found between the single-port and multiport groups (P > 0.05). Compared with the multiport group, the single-port group exhibited lower drainage fluid volume on the first postoperative day, lower BIS scores, and higher CS scores (all P < 0.05). The VAS scores of all three groups significantly decreased postoperatively, with the single-port group showing the lowest VAS scores at all time points (all P < 0.05). The time×group interaction effect on cervical microcirculation parameters was significant (P < 0.001), and the single-port group maintained higher levels of these parameters at all postoperative time points than the multiport and open abdominal groups (all P < 0.05). The DID full model showed that the open abdominal group had the most significant time×group interaction effect when compared with the single-port and multiport groups (both P < 0.001), while no significant difference was observed between the multiport and single-port groups (P > 0.05). Correlation analysis revealed that the correlations between changes in cervical microcirculation parameters and ovarian reserve function indicators were strongest in the single-port group (Bonferroni-corrected P < 0.008), with the correlation coefficients between Δblood flow perfusion and ΔE₂, ΔAMH, and ΔAFC being 0.56, 0.53, and 0.50, respectively.

Conclusion: Transumbilical single-port laparoscopic myomectomy is an effective treatment for uterine fibroids. Compared with traditional surgical approaches, single-port laparoscopy demonstrates more pronounced minimally invasive disadvantages and can effectively reduce the impact on ovarian reserve function by maintaining cervical microcirculation homeostasis, thus demonstrating good clinical application value.

RNA modification refers to the post-transcriptional chemical remodeling of RNA molecules, including modifications of bases, ribose, and phosphate groups. Among these, base modifications such as N6-methyladenosine (m⁶A) and pseudouridine (ψ) are the most common. Together, these modifications cooperatively construct a dynamic post-transcriptional regulatory network. Through their diversity and reversibility, RNA modifications precisely regulate RNA metabolism, including stability, degradation, translation efficiency and subcellular localization. Abnormal expression of RNA modification regulators is closely associated with various diseases, particularly malignant tumors. As a core component of epitranscriptomics, RNA modification plays a crucial role in the initiation, progression and therapeutic resistance of pancreatic cancer. Recent studies have shown that RNA modifications promote malignant phenotypes of pancreatic cancer cells, such as proliferation, invasion, metastasis, immune evasion and chemoresistance, by regulating the metabolic dynamics of tumor-related RNAs. RNA modification regulators, including methyltransferases, demethylases and RNA modification binding proteins, are decisive factors in this process, influencing multiple signaling pathways and post-transcriptional regulatory networks. Notably, targeting RNA-modifying enzymes, such as FTO inhibitors, has significantly suppressed tumor progression in preclinical models, validating the feasibility of RNA modification as a therapeutic target. This review systematically summarizes the mechanisms by which RNA modification regulators function in the development and progression of pancreatic cancer, and integrates the associated signaling pathways and regulatory networks they mediate, aiming to provide a theoretical foundation for the development of precision therapies targeting RNA modification.