Oncolytic virus is a unique anti-tumor immunotherapy that can specifically infect and lyse tumor cells, while inducing and activating the body's own anti-tumor immune response to attack tumors. So far, three oncolytic viruses have been approved for marketing. In 2005, China first approved recombinant human adenovirus type 5 (H101/Oncorine) combined with chemotherapy for the treatment of advanced nasopharyngeal cancer patients. In 2015, the US Food and Drug Administration (FDA) approved herpes simplex virus type I (T-VEC) for the treatment of recurrent melanoma after primary surgery, T-VEC was subsequently approved in Europe. In 2021, Japan's Ministry of Health, Labour and Welfare approved third-generation recombinant herpes simplex virus type I (Delytact/G47Δ) for the treatment of malignant glioma. Although the approval of H101 in China marks a breakthrough in the development of oncolytic viruses, compared to T-VEC and Delytact, H101 has not significantly impacted the treatment of patients with advanced nasopharyngeal carcinoma. This may be due to its inability to provide a complete tumor response as a monotherapy, and the fact that most nasopharyngeal carcinoma patients in China undergo radiotherapy, making it difficult for them to benefit from chemotherapy combined with H101. Therefore, this treatment regimen still needs improvement. In recent years, with the maturity of genetic engineering technology, oncolytic viruses have been continuously improved and refined. This review summarizes the clinical research progress of oncolytic viruses and discusses their characteristics and development prospects.

Pancreatic cancer is a malignant tumor with extremely poor prognosis, and its biological behavior is closely related to its genetic characteristics. Traditional preclinical research models struggle to accurately simulate the complex genetic heterogeneity and histological characteristics of pancreatic cancer. In recent years, the development of organoid models and CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) technology has provided new tools for pancreatic cancer research. Organoids can simulate the genetic and histological features of primary tumors, while CRISPR technology enables precise genetic manipulation in organoids. CRISPR Gene-Editing Organoids can model the occurrence and evolution of pancreatic cancer, conduct gene function analysis, and perform drug screening. This review discusses the recent advancements in the application of organoid models combined with CRISPR technology in pancreatic cancer research, which are expanding our understanding of pancreatic cancer.

In January 2024, professor Shen Baiyong's team at the Pancreas Center-Shanghai Key Laboratory of Translational Research in Pancreatic Tumor, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, published a research paper in Nature Medicine titled “Prospective observational study on biomarkers of response in pancreatic ductal adenocarcinoma”. The team conducted a prospective observational study that included a total of 1 171 pancreatic cancer patients who underwent radical resection. First, paired samples of tumors from 191 pancreatic ductal adenocarcinoma (PDAC) patients were obtained by microdissection and subjected to proteomic analysis, which revealed unique protein modules of pancreatic tumors, particularly those related to chemotherapeutic drug sensitivity. Further, the research team established a prognostic risk model for pancreatic cancer at the proteomic level and validated the validity and reliability of this prognostic model with an external cohort. Using multicenter and large sample data, the study constructed and validated the generalizability of two protein markers in predicting the efficacy of chemotherapy in pancreatic tumors.

Glioma is the most common primary malignant neoplasm of the central nervous system, of which with the poor prognosis for its refractory to all kind of therapy, and new methods are urgently need for clinical glioma treatment. Immunotherapy is a new milestone in tumor treatment, which showed effective results in a variety of solid tumors. At present, the basic research and clinical trials of immunotherapy in glioma are also become hot topics. This article reviews the current status and progress of glioma immunotherapy for better understand the efficacy and limitations of these therapeutic methods, aims to provide new immunotherapy strategies for glioma.

Pancreatic cancer has an insidious onset and a high degree of malignancy, and due to the limited efficacy of traditional treatments such as surgery and chemotherapy, this tumor has been one of the malignant tumors with the highest morbidity and mortality rates. In recent years, cell therapy, which utilizes and modifies the patient's own immune cells to target and kill tumor cells, is gradually becoming one of the potential alternatives to traditional treatment of tumors, and has achieved positive results in hematologic tumors. However, cell therapy in solid tumors, such as pancreatic cancer, is still in the research stage, and although it has achieved some efficacy, it is still full of challenges. In this review, the mechanism of chimeric antigen receptor-T cells (CAR-T), T cell receptor-T cells (TCR-T), and tumor infiltrating lymphocytes (TILs) in cell therapy and the efficacy in the treatment of pancreatic cancer were thoroughly discussed. Meanwhile, the main reasons for the poor effect of cell therapy in pancreatic cancer and the current research progress in improving the effect of cell therapy are preliminarily analyzed.

Objective: This study aimed to investigate the correlation between the use of glucose-lowering drugs and the risk of pancreatic cancer through propensity score matching (PSM), which provides a scientific basis for clinical decision-making.

Methods: This study retrospectively analyzed the clinical data of patients diagnosed with type 2 diabetes mellitus (T2DM) and treated with glucose-lowering drugs in Nanjing Drum Tower Hospital between 2000 and 2023. The patients were divided into two groups: those with T2DM alone and those with T2DM combined with pancreatic cancer. PSM was employed to align the baseline characteristics of patients across groups, minimizing the impact of confounding factors. According to the use of glucose-lowering drugs, the correlation between the use of various types of glucose-lowering drugs and the occurrence of pancreatic cancer was explored by logistic regression analysis, and the drug influencing factors that might potentially affect the occurrence of pancreatic cancer were screened out. Additionally, the relationship between the use of glucose-lowering medications, both as monotherapy and in combination, and the occurrence of pancreatic cancer was further analyzed.

Results: The logistic regression analyses showed that previous use of sulfonylureas was significantly associated with pancreatic cancer in patients with T2DM, and previous use of dipeptidyl peptidase-4 (DPP-4) inhibitors was weakly associated with pancreatic cancer, and sulfonylureas [odds ratio (OR)=0.631，95% CI: 0.415-0.961，P=0.032] and dipeptidyl peptidase-4 (DPP-4) inhibitors (OR=0.639，95% CI: 0.388-1.052，P=0.078) may be associated with a reduced risk of pancreatic cancer in T2DM patients. Other drugs, including insulin, metformin, α-glucosidase inhibitors, and sodium-glucose transporter-2 (SGLT-2) inhibitors, were not significantly associated with pancreatic cancer development. In a further analysis of glucose-lowering treatment regimens, it was shown that metformin in combination with other oral glucose-lowering agents was associated with pancreatic cancer [adjustment OR (aOR)=0.463， 95% CI：0.224-0.959， P=0.038] and may be a protective factor for pancreatic carcinogenesis.

Conclusion: The use of sulfonylureas and DPP-4 inhibitors in T2DM patients is related to the reduction of pancreatic cancer, and compared with the use of drugs alone, the use of drugs combined with oral hypoglycemic drugs can further reduce the incidence of pancreatic cancer.

As an important metal element in human body, copper can be involved in many important biological processes such as cell metabolism, anti-oxidation, detoxification, iron absorption and so on. Copper in the human body is mainly ingested through diet, combined with transport proteins in the digestive tract into the blood, and then transported to all tissues of the body through carrier proteins. It is strictly regulated by copper ion chaperone protein and carrier protein, and its intake and excretion are in a dynamic balance. Copper plays an important role in tumor cell growth, migration and angiogenesis, so when copper homeostasis is out of balance, it can affect tumor cell growth and lead to apoptosis. Recent studies have found that copper can induce a new type of cell death - Cuprotosis, which is different from the classical cell death forms such as necrosis, pyrodeath, autophagy and necrotic apoptosis, and is closely related to the regulation of copper metabolism. Therefore, the novel cell death mechanism induced by copper has triggered extensive research. In the breast cancer related research, it was found that the genes and proteins related to copper death play an important role in the progression of breast cancer disease, immune cell infiltration, drug resistance, combination therapy and disease prognosis assessment, etc. Therefore, the cuprotosis mechanism should be further studied and applied in clinical anti-tumor therapy. It is expected to provide new treatment options for breast cancer patients.

The incidence of cachexia in pancreatic cancer is high, which seriously affects the therapeutic effect and survival rate of patients. There is currently no effective intervention for tumor cachexia, so studying its regulatory mechanism has important clinical significance. In 2024, Professor Li Min's team from the Health Science Center of the University of Oklahoma published a research report on Cancer Cell entitled "The crosstalk between macroscopic and cancer cells potentials pancreatic cancer cachexia", which first revealed the relationship between the immune microenvironment (macrophages) of pancreatic cancer and the body's macro environment cachexia (muscle atrophy), opening up a new direction and new intervention ideas for the study of pancreatic cancer cachexia.

Pancreatic cancer is a highly malignant digestive system tumor with poor prognosis. Its incidence is closely related to the level of regional development. Epidemiology shows that with the progress of urbanization, the proportion of obese people in the world is increasing over the years. Meanwhile, obesity has also been found to be one of the risk factors for pancreatic cancer. However, the mechanism of obesity regulating pancreatic cancer is still unclear at present. Researches show that obese people with pancreatic cancers have different tumor pathological mechanisms and higher risk of surgical complications. Therefore, this article will review the potential transformation mechanism between microscopic pathological changes and clinical manifestations of obesity related pancreatic cancer.

Craniopharyngioma is a rare benign intracranial tumor, and surgical removal is the primary treatment modality. However, due to the deep location of the tumor, its close relationship with the optic nerve, hypothalamic-pituitary axis and essential tissue and vascular structures, and its local invasiveness, treatment still poses numerous challenges. In recent years, there have been advancements in treating craniopharyngioma, including improvements in surgical techniques, equipment, and strategies such as neuroendoscopy, the introduction of novel treatment modalities such as targeted therapies, etc. This paper provides a comprehensive review of these developments.

Objective: To explore whether anlotinib or bevacizumab has better efficacy in patients with recurrent glioblastoma.

Methods: The clinical characteristics and treatment data of patients with recurrent glioblastoma admitted to Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, were collected retrospectively. All patients received maximal resection of the tumor combined with postoperative adjuvant radiotherapy and chemotherapy, and the recurrence was detected by head contrast-enhanced MRI. According to the choice of anti-vascular therapy, the patients were divided into anlotinib group and bevacizumab group. Survival curves were drawn to compare the overall survival time of the two groups of patients, and subgroup analysis was performed according to the basic information of the patients and whether they received temozolomide chemotherapy or radiotherapy after recurrence.

Results: A total of 37 patients were enrolled in the study, 19 in the anlotinib group and 18 in the bevacizumab group. The median overall survival time was 16.3 months, with 19.6 months in the anlotinib group and 12.8 months in the bevacizumab group. However, survival analysis showed that there was no significant difference in survival time between the anlotinib group and the bevacizumab group (P＝0.88). Further subgroup analysis showed that there was no significant difference in survival time between the two groups in all subgroups.

Conclusion: This study provided an initial indication of the efficacy of anlotinib in patients with recurrent glioblastoma and suggested that oral anlotinib may be a viable option for patients who were unable to tolerate bevacizumab or who had.

Objective: To investigate mechanisms whereby phospholipase D1 (PLD1) promotes pancreatic ductal adenocarcinoma (PDAC) progression.

Methods: Targets were identified by screening the Genomic Spatial Event (GSE) database for genes differentially expressed in metastatic and primary tumors. Xenograft models were constructed by orthotopic injection of KPC cells into the mouse pancreas. Differential PLD1 expression in paired primary tumors and liver metastases derived from C57 mice and PDAC patients was confirmed using immunohistochemical staining. The effect of PLD1 expression on PDAC prognosis was assessed using a PDAC tissue microarray and clinical data. The effect of PLD1 expression on PDAC metastasis was assessed using transwell migration and scratch assays of cell lines ectopically expressing/silencing PLD1. The role of PLD1 in tumor metastasis was investigated using xenograft models constructed by orthotopic injection of PLD1-overexpression cell lines or vector control into the pancreas of C57 mice. Growth of primary tumors and liver metastases was monitored using bioluminescent imaging. The role of PLD1 in tumor progression was assessed using western blotting, transwell migration and scratch assays, and PLD1 enzyme-mutation cell lines. Downstream PLD1 target genes were identified using quantitative real-time PCR (qPCR), transcriptome sequencing, and response blocking. The effect of downstream target FSTL1 on liver metastasis in mice was assessed using bioluminescent imaging.

Results: PLD1 expression was significantly higher in metastases than in primary tumors in KPC mice and patients.In the tissue microarray analysis, PLD1 expression was associated with diminished survival in PDAC patients; PLD1 overexpression in MIA PaCa-2 cells or knockdown in SW1990 cells could significantly affect the ability of invasion and migration.Xenograft models were established via orthotopic injections of the KPC cell line into the pancreas.Bioluminescent imaging demonstrated that PLD1 overexpression significantly increased signal intensity in the mouse liver (P<0.01);Treating the SW1990 cell line with PA and choline (PLD1 pathway products) did not restore loss of PDAC cell migration and invasion ability. Transwell and scratch assays in KRM, a PLD1 catalytic-mutation cell line, suggested that PLD1 activity is not required for PDAC metastasis;Transcriptome sequencing identified FSTL1 as a downstream molecule of PLD1. qPCR confirmed the consistency of mRNA levels between PLD1 and FSTL1. A blocking-rescue experiment suggested that FSTL1 is a downstream target of PLD1. A splenectomy metastasis model was constructed by injecting nude mice with tumor cells overexpressing FSTL1 and the results confirmed that overexpression of FSTL1 could induce liver metastases in PDAC cell due to tumor progression.

Conclusion: PLD1 upregulates FSTL1 expression, promotes epithelial-mesenchymal transition of tumor cells, and enhances PDAC metastasis. Thus, PLD1 blockade could inhibit PDAC progression.

The rapid development of the comprehensive intersection of oncology disciplines makes oncology teaching complex and challenging. In recent years, the deep integration of artificial intelligence (AI) and medical education has brought new opportunities for oncology teaching. Therefore, this paper proposes to construct a new teaching model of AI-enabled problem-based learning (PBL) fused with case-based learning (CBL), which fully combines PBL, CBL, virtual simulation technology, intelligent robots, AI models and other teaching methods, and integrates these innovative elements into all aspects of oncology teaching, including theoretical courses, laboratory operations and clinical practice, in order to provide a comprehensive and interactive oncology teaching system. This new teaching mode brings a new perspective and approach to theoretical, experimental, and clinical teaching in oncology, which not only helps to deepen students’ understanding of the basics of oncology, but also significantly improves their clinical thinking and problem-solving abilities. In addition, this new attempt at an integrated teaching method will provide a new teaching strategy for the development of medical oncology education.

Objective: To investigate the role of RASAL2 in vasculogenic mimicry in pancreatic cancer cells and to preliminarily explore the potential molecular mechanisms involved.

Methods: The clinical proteomic tumor analysis consortium (CPTAC) database was used to analyze the expression of RASAL2 in pancreatic cancer, and immunohistochemical method was used to detect the expression of RASAL2, β-catenin and Vimentin in pancreatic cancer and adjacent tissues. In the pancreatic cancer cell line, after lentivirus infection knockdown and overexpression of RASAL2, transcriptome sequencing was performed on pancreatic cancer cells silencing RASAL2 expression, and vasculogenic mimicry experiment was used to detect the effect of RASAL2 on angiogenesis of pancreatic cancer cells; The molecular mechanism of RASAL2 promoting vasculogenic mimicry in pancreatic cancer was studied by real-time fluorescent quantitative PCR and Western blotting detection.

Results: The analysis results of CPTAC database showed that the expression level of RASAL2 protein in pancreatic cancer tissue was significantly higher than that in normal pancreatic tissue. Immunohistochemical test results showed that the expression of RASAL2 in pancreatic cancer tissue was up-regulated, and the expression of β-catenin and Vimentin in pancreatic cancer tissue was also significantly up-regulated. The second-generation transcriptome sequencing results showed that RASAL2 may be involved in the biological behavior of intercellular connections and adhesion. After knocking down RASAL2 expression in pancreatic cancer cell PANC-1, the expression level of AKT/β-catenin signaling pathway related proteins and vasculogenic mimicry related proteins decreased, and the formation of vasculogenic mimicry structure was inhibited; After overexpression of RASAL2 in pancreatic cancer cell BxPC-3, the expression level of AKT/β-catenin signaling pathway related proteins and vasculogenic mimicry related proteins increased, promoting the formation of vasculogenic mimicry.

Conclusion: The effect of RASAL2 on vasculogenic mimicry in pancreatic cancer cells is related to AKT/β-catenin signaling pathway.

Objective: This study aims to construct a human peripheral blood mononuclear cell (PBMC)-NPSG-PDX (patient-derived xenograft) model, by transferring PBMCs into NPSG (NOD-Prkdc^scidIl2rg^null/Shjh) mice and transplanting human tumor tissues. This model mimics the human tumor microenvironment to investigate the interactions between tumors and the immune system.

Methods: PBMCs from healthy donors were transferred to NPSG mice to generate hPBMC-NPSG model. Patient-derived xenografts (PDX) were established in nude (BALB/c-nu) mice. Third-generation PDX tumors were then transplanted into hPBMC-NPSG mice to establish the hPBMC-NPSG-PDX model. Mouse body weight was monitored, and flow cytometry was used to analyze immune reconstitution and T cell function. Tumor growth was evaluated, and immunohistochemistry was performed to analyze tumor morphology and immune cell infiltration.

Results: Fourteen days after constructing the hPBMC-NPSG mouse model, the proportion of human hu-CD45⁺CD3⁺ T cells reached 97%. The proportions of human CD8⁺ T, CD4⁺ T, CD56⁺ natural killer (NK), and CD19⁺ B cells were 64%, 24%, 4.6%, and 1.0%, respectively. Human CD4⁺ and CD8⁺ cells secreted various cytokines (IL-2, IFN-γ, and TNF-α) and expressed cytotoxic molecules (FasL, granzyme B, and perforin) 28 days post reconstitution. Tumor growth in hPBMC-NPSG-PDX mice was rapid initially but then stabilized. Immunohistochemistry staining revealed typical tumor morphology, and tumor cell apoptosis was observed in areas with immune cell infiltration.

Conclusion: This study successfully constructed a hPBMC-NPSG-PDX model that effectively simulates the human tumor microenvironment, providing an ideal platform for tumor immunology research.

Pancreatic fibrosis is an important pathological feature of pancreatic cancer and chronic pancreatitis, and plays an important role in the progression of pancreatic cancer and chronic pancreatitis. Pancreatic fibrosis blocks the chemotherapy drugs from reaching the cancer cells to do their job and also affects the stiffness of the pancreatic tissue. Therefore, it is important to assess the degree of pancreatic fibrosis as an adjunct to surgical and chemotherapeutic treatments for pancreatic cancer and chronic pancreatitis. In recent years, there have been new research advances and technological breakthroughs in non-invasive diagnostic methods for pancreatic fibrosis. The fields of CT, ultrasound elastography and magnetic resonance imaging have extended new imaging techniques, yielded new imaging indices to assess the degree of pancreatic fibrosis. In this paper, we have collected relevant literatures since 2018 to describe the research progress related to non-invasive diagnostic methods for pancreatic fibrosis.

In 2024, Xue Jing's research team from Shanghai Jiao Tong University School of Medicine published a research paper in the journal Cancer Cell titled “Tumor Cell inflammatory dysregulation shapes cancer associated fibroblasts heterogeneity to metabolically support pancreatic cancer”. Studies have found that deletion of the tumor-intrinsic SET domain containing 2 (SETD2) releases bone morphogenetic protein 2 (BMP2) signals through abnormal increases in H3K27Ac, leading to the differentiation of cancer-associated fibroblasts (CAFs) cells toward a lipid-rich phenotype. Lipid-rich CAFs cells provide lipids to tumor cells through the ABCA8a transporter and enhance mitochondrial oxidative phosphorylation metabolism. Taken together, this study links epigenetic dysregulation of CAFs cells to tumor cells and highlights previously unrecognized metabolic crosstalk between CAFs cells and pancreatic tumor cells. In addition, the study also proposed using oxidative phosphorylation as a potential strategy for targeted treatment of patients with SETD2-deficient pancreatic ductal adenocarcinoma, providing new ideas for precise diagnosis and treatment.

The 5th edition of the World Health Organization (WHO) central nervous system (CNS) tumor classification (WHO CNS 2021), which was published in 2021, introduced a variety of molecular features that highlight the significance of molecular pathology in understanding the pathological mechanisms, diagnostic classification, prognosis assessment, and guidance of treatment for gliomas. This review aimed to summarize the significant advancements in molecular pathology and its practical applications in clinical settings. Moreover, the challenges faced during the development of molecular pathology and its implementation in clinical practice were discussed. Lastly, an outlook on forthcoming developments in this field for the future was provided.

Objective: To investigate the effect of copper chlorophyllin sodium salt (CHL) on the sensitivity of human pancreatic cancer cells in response to gemcitabine (GEM) therapy and on the therapeutic effect on pancreatic cancer cells that have developed GEM resistance.

Methods: MIA GR (a pancreatic cancer cell line resistant to GEM) was induced by a low-dose continuous incremental method, and the half inhibitory concentration (IC₅₀) of MIA WT and MIA GR to GEM treatment was detected by the CCK-8 method, and the resistance index was calculated; the difference in IC₅₀ of CHL on the two types of cells was detected by the CCK-8 method after treating MIA WT and MIA GR cells with different concentrations of CHL, CCK-8 method was used to detect the difference in IC₅₀ of CHL on the two types of cells; on the basis of IC₅₀, MIA WT and MIA GR cells were intervened with CHL and (or) GEM with different multiplicity of IC₅₀, respectively, and the growth inhibition curves of MIA WT and MIA GR cells were detected by the CCK-8 method under the intervention of CHL combined with GEM; After the intervention of MIA WT and MIA GR cells with CHL and (or) GEM at IC₅₀, respectively, the effects on the proliferation of the two different cells were detected using the clone formation assay; the effects on cytotoxicity/activity were observed under fluorescence microscopy; and the effects on apoptosis were detected using flow cytometry. Finally, western blotting was used to detect the effects of CHL and (or) GEM interventions on the drug resistance-associated molecules P-glycoprotein (P-gp) and ribonucleotide reductase regulatory subunit M2 (RRM2) in MIA GR cells, the and sensitivity-related molecule deoxycytidine kinase (DCK) on protein expression levels.

Results: MIA GR cells were verified to be well drug resistant, with resistance indices of 549.1 and 667.9 after 48 h and 96 h after GEM intervention compared to homologous wild-type MIA WT cells, respectively; CHL intervention inhibited the proliferation of MIA GR cells more significantly compared to that of MIA WT cells; and CHL in combination with GEM exerted a more significant growth inhibitory effect compared to GEM alone in both MIA WT cells (P<0.001) and MIA GR cells (P<0.01). CHL significantly inhibited the tumor proliferation of MIA GR cells, and the inhibitory effect was more pronounced in both cells when combined with GEM (P < 0.000 1); furthermore, compared to GEM alone, the intervention with CHL could cause more pronounced cytotoxicity (P < 0.000 1) in both MIA WT and MIA GR cells. caused more pronounced cytotoxicity (P < 0.000 1) and induced a higher percentage of apoptosis than GEM alone. The results of the western blotting assay showed that CHL intervention caused a decrease in the expression levels of P-gp and RRM2 proteins, as well as an increase in the protein expression level of DCK in MIA GR cells.

Conclusion: CHL increases the sensitivity of pancreatic cancer cells to GEM and also induces a decrease in the resistance of drug-resistant pancreatic cancer cells to GEM.

As a real-time, rapid and non-invasive method for monitoring the occurrence and development of various diseases and evaluating the health status of the body, breath detection has attracted wide attention in the application of early lung cancer screening. However, there is significant variability in the reported specific biomarkers of lung cancer, making it difficult to reach a unified consensus. Meanwhile, the pathways for the generation of volatile organic compounds (VOCs) in exhaled breath of lung cancer patients remain unclear, and further research on the detailed metabolic mechanisms is required. Therefore, this review comprehensively summarizes the VOCs detected in the exhaled breath of lung cancer patients from relevant literature in the past five years, deeply analyzes the production mechanism of these VOCs and the internal correlation with the disease, and evaluates the performance of the lung cancer prediction models constructed based on these VOCs, in order to provide reference for clinical and subsequent researches.

The incidence and mortality rates of gastrointestinal tumors account for 26% and 35% of global malignant tumors, respectively, and continue to rise annually. Elucidating the molecular mechanisms of occurrence and development of gastrointestinal tumors, as well as establishing precise molecularly targeted intervention strategies, have become critical scientific challenges in oncology research. Doublecortin-like kinase 1 (DCLK1), a type II transmembrane protein harboring serine/threonine kinase domains, is well-recognized as a specific molecular marker for cancer stem cells. DCLK1 has been demonstrated to directly promote tumor progression by enhancing the autonomous malignant phenotype of tumor cells, while also indirectly driving tumorigenesis through modulation of tumor immune microenvironment. In recent years, tissue-resident memory T cells (TRM), characterized by their sustained tissue residency and potent antitumor immune efficacy, have emerged as a novel avenue for cancer immunotherapy. This article systematically reviews the molecular regulatory mechanisms of DCLK1 in gastrointestinal tumors, with a focus on its potential association with TRM cell functional activation, aiming to provide a theoretical foundation for DCLK1-targeted inhibitors or monoclonal antibody-based immunotherapeutic strategies.

Ferroptosis is a form of iron dependent cell death, which is closely related to the progress and prognosis of bladder cancer (BCa). Among them, erroptosis related genes (FRGs) play an important role in the biological effects of BCa, such as participating in regulating the proliferation, migration, metastasis, drug resistance, immune regulation, and therapeutic efficacy of BCa cells. In addition, FRGs are also important biomarkers for predicting the prognosis of tumor patients. However, the specific mechanism of action of FRGs in BCa remains elusive. How to use FRGs to predict the prognosis of BCa and guide the treatment of BCa is still in the exploratory stage. Therefore, exploring the regulatory and predictive role of FRGs in BCa is particularly important for the diagnosis and treatment of BCa. This article aims to systematically elucidate the role of FRGs in the occurrence, development, treatment, and prognosis of BCa. To provide theoretical reference for further exploring the treatment of refractory and drug-resistant BCa patients, and constructing prognostic risk prediction models.

Meningioma is the most common primary intracranial tumor, of which about 20% are high-grade tumors, with a high recurrence rate after surgery and poorly controlled by radiotherapy, requiring adjuvant pharmacological treatment. Cytotoxic drugs were applied at the beginning, but the efficacy was poor with significant side effects. Subsequently, targeted drugs such as tyrosine kinase inhibitors and somatostatin analogs were used for treatment, and the prognosis of meningioma patients was improved.With the development of new technologies such as high-throughput sequencing, more potential targets have been revealed. There exists a suppressive immune microenvironment within meningiomas, and modulation of lymphocytes and myeloid cells can rescue the intrinsic immune function of the tumor, and relevant clinical trials are in progress. This article reviewed the research progress of pharmacological treatment of meningiomas, and the current situation and prospects of drug therapy ware discussed and prospected.

Currently, common primary malignant bone tumors in clinical practice include osteosarcoma, chondrosarcoma, Ewing's sarcoma, chordoma, and multiple myeloma. Malignant bone tumors often metastasize to the lungs through the bloodstream, but lymph node metastasis can also occur. Once lymph node metastasis occurs, the prognosis for patients is worse than with lung metastasis, making the study of lymph node metastasis in malignant bone tumors a growing research focus in recent years. According to current research, primary malignant bone tumors mainly metastasize to lymph nodes through two pathways: firstly, bone tumor cells break through the periosteum into the surrounding lymphatic tissue; secondly, they regulate the expression of VEGF-C by secreting factors like WISP-3, CCL5, BDNF, thus inducing the neogenesis of lymphatic vessels in malignant bone tumors. Past research on lymph node metastasis of primary malignant bone tumors has mostly focused on clinical studies of a single type of malignant bone tumor, lacking systematic basic research and reviews, and the mechanisms of metastasis are not yet fully elucidated. Moreover, different types of malignant bone tumors vary in their rates and sites of lymph node metastasis. Therefore, this article mainly reviews the rates, sites, diagnostic methods, potential mechanisms, and treatment methods of lymph node metastasis in these five common types of malignant bone tumors, aiming to deepen understanding of lymph node metastasis in primary malignant bone tumors and to provide new ideas for clinical treatment and drug development.

Objective: To evaluate the efficacy and safety of Qi Regulation and Detoxification Formula in the treatment of sputum and stasis in subsolid pulmonary nodules (5-8 mm), so as to explore the optimal treatment plan for subsolid pulmonary nodules.

Methods: A practical randomized control method was used to include 74 patients with sputum and stasis in the subsolid pulmonary nodules, and the patients were randomly divided into treatment group (n=37) and control group (n=37). The treatment group was given traditional Chinese medicine Qi Regulation and Detoxification Formula, and the control group only recommended regular follow-up observation according to the guidelines. The course of treatment was 24 weeks. The maximum diameter and number of lung nodules, TCM syndrome scores and TCM syndrome scores of the two groups before and after treatment were observed, and the clinical efficacy was evaluated. The adverse events were also recorded.

Results: The clinical effective rate of the treatment group was 22.9%, which was significantly higher than that of the control group of 2.9% (P<0.05), and the treatment group had obvious advantages in the maximum diameter, number of nodules and TCM syndrome score (P<0.05), and there was no significant statistical difference in the incidence of adverse events between the treatment group and the control group (P>0.05).

Conclusion: Qi Regulation and Detoxification Formula can effectively inhibit the progression of subsolid pulmonary nodules (5-8 mm), improve the clinical symptoms of patients, and be safe and feasible, which is worthy of further clinical research and application.

Colon cancer is a common malignant tumor in the gastrointestinal tract, with morbidity and mortality rates increasing every year. Currently, the etiology of colon cancer has not been fully elucidated. With the deepening of colon cancer research and treatment, it is especially important to establish corresponding preclinical in vivo models. In the treatment of colon cancer, Chinese medicine follows the principle of diagnosis and treatment, adopts the method of supporting the positive and dispelling the evil, adjusts the body's qi and blood, and the deficiency of internal organs to maintain the balance of the body's yin and yang, so as to achieve the purpose of anti-tumor. Chinese medicine animal models of colon cancer can be broadly divided into five categories: damp-heat accumulation, qi stagnation and blood stasis, qi and blood deficiency, spleen and kidney yang deficiency and liver and kidney yin deficiency. Western animal models of colon cancer are commonly divided into 4 categories: spontaneous, induced, transplanted and genetically engineered. The paper summarizes the construction methods and characteristics of colon cancer animal models currently commonly used in Chinese and western medicine, and summarizes, analyzes and concludes the colon cancer animal models based on three aspects: how to select animal models, comparison of Chinese and western medicine modeling methods and evaluation of modeling success, with a view to finding suitable modeling methods for preclinical experiments, so as to provide guidance for the selection of animal models of colon cancer.

Objective: To analyze the clinicopathological characteristics and incidence trend of primary breast cancer patients in Xinjiang Uygur Autonomous Region from 2015 to 2021, and provide references for clinical prevention and treatment of breast cancer in Xinjiang.

Methods: Retrospective analysis was made on the general demographic data, molecular typing, pathological typing and surgical types of 10 867 patients with primary breast cancer who were diagnosed, treated and hospitalized in The Affiliated Cancer Hospital of Xinjiang Medical University from 2015 to 2021, to explore the change trend with different periods.

Results: A total of 10 867 patients were included, with an average age of diagnosis of 51.34±10.96 years and a median age of diagnosis of 50 years. The average and median ages of diagnosis showed an upward trend with each year. The marital status is mainly married [9 854 patients (90.6%)]. The majority of patients are from northern Xinjiang (69.35%). The molecular typing is mainly Luminal type [5 665 patients (72%)], and the proportion of Luminal type and HER-2 overexpression type continues to increase over time, while the proportion of triple negative type significantly decreases. Clinical stage II was the most common [4 405 patients (41.7%)], followed by stage I [3 057 patients (29.0%)]. The pathological type is mainly invasive ductal carcinoma [9 307 patients (85.6%)]. The main surgical method is modified radical surgery [5 822 patients (74.6%)], while other surgical methods such as breast conserving surgery have shown an increasing trend over the years.

Conclusion: From 2015 to 2021, the number of breast cancer patients in Xinjiang will increase year by year, and the average age of diagnosis will be older. The molecular subtype is mainly Luminal B type, and the pathological type is mainly invasive ductal carcinoma; The proportion of early breast cancer patients increased with age. The main surgical method is modified radical surgery, which shows a decreasing trend with increasing years, while breast conserving surgery and other surgical procedures show an increasing trend.

Prolactinomas are the most common subtype of pituitary neuroendocrine tumors (PitNETs), which can be treated with drugs surgery, radiotherapy and so on. For invasive and non-invasive prolactinomas, there is still controversy on the treatment choice of drugs or surgery as the first-line option. In the past decade, with the progress of endoscopic transsphenoidal minimally invasive technology in-depth understanding of PitNETs pseudocapsule, and constructions of Pituitary Tumor Centers of Excellence (PTCOE), the biochemical remission rate by surgical treatment has been significantly improved. For some specific subtypes of prolactinomas, such as microadenomas and enclosed macroadenomas (Knosp grade 0-2), the biochemical remission rate can achieve 90% with the treatment of endoscopic transsphenoidal surgery, which was similar with the drug efficacy. Therefore, the International Pituitary Society made the latest consensus statement on the clinical treatment of prolactinomas suggested that surgery can be performed as first-line option for some selected prolactinomas. This shift of therapeutic strategy was determined in the form of consensus statement, which has a strong clinical guiding significance.

Objective: To describe the special molecular and histopathological transformation of recurrent tumor in a patient with primary hepatocellular carcinoma (HCC) after liver transplantation.

Methods: A case of HCC had recurrent tumor presenting special molecular and histopathological characteristics after liver transplantation. The diagnosis and treatment process of this case is reported.

Results: A case of highly differentiated HCC received immune checkpoint inhibitors combined with antiangiogenic therapy after liver malignant tumor resection. Nearly one year later, due to severe liver cirrhosis, the case accepted allogeneic orthotopic transplantation of liver. More than two years later, elevated level of serum alpha fetoprotein was detected, then the PET-CT examination showed multiple suspected lesions with increased ¹⁸F-FDG metabolism in the right lobe of the liver. Liver biopsy and high-throughput sequencing were performed, and the results revealed poorly differentiated HCC with YAP1-MAML2 fusion gene. Chemotherapy with XELOX regimen and radiotherapy were administered, and no tumor progression was observed during follow-up.

Conclusion: Recurrent tumors after liver transplantation in HCC patient developing into a special molecular and histopathological transformation is rarely reported. The underlying mechanism could be the dramatical alterations of immune microenvironment after liver transplantation, which consequently triggered genomic changes leading to generate novel YAP1-MAML2 fusion gene. The poor differentiation transformation after liver transplantation may be driven by YAP1-MAML2 fusion gene.

Primary retroperitoneal sarcomas, due to its special anatomical structure and lack of specific clinical manifestations in early stages, often leads to delayed diagnosis. because of the lack of specific clinical manifestations. By the time patients present with noticeable symptoms or palpable masses during clinical examination, the tumors has typically grown significantly in size and exhibits invasive growth patterns, frequently involving adjacent organs. Surgical treatment often necessitates multivisceral en bloc resection, with combined resection and functional reconstruction of gastrointestinal organs becoming critical components of the procedure. The surgical management of primary retroperitoneal sarcoma is characterized by extensive resection scope, technical complexity, and challenges in achieving complete tumor removal with wide clear negative margins. Additionally, the high propensity for local recurrence further increases the complexity of patient management. Current research on surgical treatment strategies for primary retroperitoneal sarcoma, particularly systematic studies focusing on combined gastrointestinal resection and functional reconstruction, remains insufficient. To enhance clinical understanding and optimize surgical approaches, this article systematically reviews domestic and international literature to summarize current research status and recent advancements in combined gastrointestinal resection and functional reconstruction for primary retroperitoneal sarcoma.

Objective: To investigate the regulatory mechanism of myoepithelial cells on glandular epithelial cells during the invasive process of ductal carcinoma in situ of breast.

Methods: A total of 157 patients with ductal carcinoma in situ of breast, treated at the Tianjin Medical University Cancer Hospital from May 2008 to July 2010, were randomly selected (including 63 high nuclear grade patients, 51 middle nuclear grade patients, and 43 low nuclear grade patients). Immunohistochemical staining for epithelial-mesenchymal transition (EMT)-related markers (Snail and ZEB1) was performed on tumor tissue specimens from these patients to explore the correlation between tumor cell nuclear grade, EMT process,and expression status of myoepithelial cells. To further investigate the regulatory role of myoepithelial cells on glandular epithelial cells during the invasive process of ductal carcinoma in situ of breast, a co-culture model of human myoepithelial cell line Hs578Bst and adenomatous epithelial cell line MCF-7 was established using Transwell chambers. Experimental, blank control, positive control, and negative control groups were designed by combining co-cultured Hs578Bst and MCF-7 cells with exogenous TGFβ1 and TGFβ1 inhibitors. After 72 hours of culture, morphological changes, migration and proliferation capabilities of MCF-7, as well as the changes in protein and mRNA expression levels of EMT-related genes (Snail and ZEB1), were observed in each group.

Results: Immunohistochemical staining results demonstrated a positive correlation between tumor nuclear atypia, EMT activation, and myoepithelial cell expression in ductal carcinoma in situ tissues. The model of ductal carcinoma in situ of breast demonstrated that myoepithelial cells Hs578Bst promoted morphological changes in glandular epithelial cells MCF-7 by stimulating TGFβ1 expression. Wound healing and cell proliferation assays revealed that myoepithelial cells Hs578Bst can enhance migration and proliferation of glandular epithelial cells MCF-7 via TGFβ1 activation. Western blot and real-time quantitative PCR confirmed that myoepithelial cells Hs578Bst can upregulate the protein and mRNA expression levels of EMT-related genes (Snail and ZEB1) in glandular epithelial cells MCF-7 by through TGFβ1 stimulation.

Conclusion: Breast myoepithelial cells promote EMT in glandular epithelial cells by secreting/stimulating TGFβ1, thereby contributing to the occurrence of invasion in ductal carcinoma in situ of the breast.

Objective: For small molecule drug 630120 based on proteolysis-targeting chimeras (PROTAC) that targets nicotinamide phosphoribosyltransferase (NAMPT), to explore its effect on the proliferation ability of colorectal cancer cells with low expression of nicotinate phosphoribosyltransferase (NAPRT).

Methods: This study detected the protein expression levels of NAMPT and Tubby in tumor tissues and adjacent normal tissues from 5 colorectal cancer patients by immunohistochemical staining. Additionally, the Gene Expression Profiling Interactive Analysis (GEPIA) platform was used to analyze the expression level of NAMPT mRNA in colorectal cancer tissues and corresponding adjacent normal tissues from The Cancer Genome Atlas (TCGA) database. Based on previous studies in hematologic malignancies, to detect the degradation of NAMPT protein in colorectal cancer (CRC) cell lines (SW480, HT29, RKO, SW620 and HCT116) treated with the drug PROTAC-630120. Furthermore, to create NAPRT knockdown and knockout colorectal cancer cell lines by using shNAPRT plasmids and CRISPR-Cas9 technology. The impact of different concentrations of PROTAC-630120 on the proliferation of NAPRT knockdown and knockout colorectal cancer cells was validated by Cell Titer-Glo (CTG) luminescence assay and colony formation assay. Finally, Western blotting was also used to detect the effect of PROTAC-630120 on the expression of downstream proteins in the MAPK signaling pathway in colorectal cancer cells.

Results: In colorectal cancer tissues, the expression levels of NAMPT protein and mRNA were significantly upregulated. The drug PROTAC-630120 can effectively degrade NAMPT protein in different colorectal cancer cells. Moreover, it can significantly inhibit the proliferation of NAPRT knockdown and knockout colorectal cancer cells. The IC₅₀ values (half-maximal inhibitory concentration) for different colorectal cancer cell lines treated with PROTAC-630120 were as follows: RKO^shNAPRT～49.03 nmol/L, HCT116^shNAPRT～42.28 nmol/L, SW620^shNAPRT～55.59 nmol/L, HT29^shNAPRT～29.66 nmol/L, SW480^shNAPRT～76.17 nmol/L, and SW480^sgNAPRT～27.01/34.23 nmol/L. Finally, the drug PROTAC-630120 can inhibit the MAPK-ERK signaling pathway in colorectal cancer cells.

Conclusion: The small molecule drug 630120 based on PROTAC that targets NAMPT protein, can inhibit the proliferation of NAPRT knockdown and knockout colorectal cancer cells, so it is expected to become a drug option for adjuvant therapy of cancer patients.

Objective: To explore the impact of the early warning model based on UpToDate on the adverse reactions and disease uncertainty of patients receiving AC-T chemotherapy after breast cancer surgery.

Methods: Two hundred patients with breast cancer who received AC-T chemotherapy after surgery in Gansu Cancer Hospital from October 2020 to October 2022 were included and randomly divided into control group and observation group (100 cases each). Both groups of patients underwent surgical treatment and received AC-T chemotherapy after surgery. During the treatment period, the control group received routine specialized nursing care, while the observation group received a warning mode based on UpToDate, with continuous intervention for 3 months. The psychological status, Hamilton anxiety scale (HAMA), Hamilton depression rating scale (HAMD), medical uncertainty inventory scale (MUIS), and European Organization for Research and Treatment of Cancer quality of life questionnaire core-30 (EORTC-QLQ-C30) scores and adverse reactions between two groups were compared.

Results: After 3 months of intervention, the HAMA, HAMD and MUIS scores of the observation group were 14.39±2.70, 10.91±2.22 and 66.36±7.55, respectively, which were significantly lower than those of the control group (17.76±4.15, 15.62±3.34 and 76.23±10.31, respectively), and the differences were statistically significant (all P<0.05). The total quality of life score of the observation group was 81.23±13.26, which was higher than that of the control group (73.69±8.45) (P<0.05). In the symptom scale, the fatigue, malignancy, vomiting, and pain scores of the observation group were 18.75±3.34, 24.72±5.18 and 22.26±3.04, respectively, which were lower than those of the control group (29.03±6.07, 35.07±8.15 and 28.31±5.16, respectively) (all P<0.05). In the individual test, the insomnia score of the observation group was 18.65±3.37, which was lower than that of the control group (22.60±5.24) (P<0.05). The incidence rates of nausea and vomiting, decreased appetite, abdominal pain and diarrhea, and decreased blood cells in the observation group were lower than those in the control group (all P<0.05).

Conclusion: The early warning mode based on UpToDate can improve the psychological status of breast cancer patients receiving chemotherapy after surgery, reduce adverse reactions and the uncertainty of disease, and improve the quality of life.

Vestibular schwannomas (VS) is a benign tumor originating from Schwann cells in the vestibular nerve sheath of the internal auditory canal, often causing symptoms such as hearing loss and tinnitus in patients. With the significant increase in early detection rate of tumors, treatment goals are shifting towards preserving and rebuilding neurological function, improving patients’ quality of life, and individualized treatment strategies. For those with functional hearing, hearing preservation surgery (HPS) is preferred. For patients who failed to do HPS or have no functional hearing before surgery, auditory restoration can be performed simultaneously or later. In terms of restoration approaches, for individuals whose cochlear nerve can be preserved, cochlear implant (CI) may be a viable option. CI not only provides good auditory perception but also effectively suppresses tinnitus. When the cochlear nerve cannot be preserved, BoneBridge implantation are considered. Although BoneBridge implantation cannot completely restore normal auditory function, it significantly improves speech recognition and quality of life. For patients with bilateral acoustic neuromas (as seen in neurofibromatosis type 2), although the effect of artificial auditory brainstem implantation (ABI) on auditory reconstruction varies greatly, it can help most patients regain auditory perception and improve communication skills, which is of great significance. Further research is needed in the future to investigate the influencing factors of auditory preservation and reconstruction effects, in order to maximize the hearing recovery and quality of life improvement for each patient.

The ataxia telangiectasia mutated (ATM) gene is an important tumor suppressor gene and a key effector gene in regulating the repair of double-strand DNA breaks. It plays an indispensable role in maintaining genetic stability, facilitating cell cycle arrest, and modulating cell apoptosis. When the ATM gene mutates, it fails to effectively induce the phosphorylation of downstream targets, leading to impaired DNA repair mechanisms, genetic instability, and chromosomal structural abnormalities, ultimately promoting abnormal proliferation of tumor cells. Analysis of next-generation sequencing (NGS) datas reveals a relatively high mutation rate of the ATM gene in bladder cancer cells. Relevant studies have shown that ATM gene regulates the proliferation, invasion, and metastasis of bladder cancer cells through the signaling pathways such as nuclear transcription factor-κB (NF-κB) and Interferon-γ (IFNγ). Mutanted ATM gene can enhance patients’ sensitivity to radiotherapy and chemotherapy, and boost the efficacy of immunotherapy, resulting in a generally better prognosis for patients with ATM gene mutation. This finding marks ATM gene as a potential therapeutic target and predictive prognosis biomarker for bladder cancer patients. Therefore, this article will comprehensively review the research on the ATM gene in bladder cancer from 3 aspects: the structural characteristics of the ATM gene and its tumor-suppressing and tumor-promoting functions, the mechanism of action of the ATM gene in the occurrence and development of bladder cancer, and the impact of the ATM gene on the treatment and prognosis of bladder cancer patients. Additionally, the future research directions of the ATM gene was prospected, with the aim of providing new targets for the drug treatment of bladder cancer, and bringing new hope for the treatment of bladder cancer patients.

Objective: To investigate the incidence of non-alcoholic fatty liver disease (NAFLD) in breast cancer patients and healthy individuals, and assess liver fibrosis in breast cancer patients with NAFLD.

Methods: Propensity score matching (PSM) was used to match 194 breast cancer patients who were treated in the Department of Thyroid and Breast Surgery of Huai’an No.1 People’s Hospital between May 2021 and December 2021, with 1 138 people who underwent physical examination during the same period. The effect of NAFLD on the risk of breast cancer was investigated by univariate and multivariate logistic regression analysis. Liver fibrosis in NAFLD patients with breast cancer was assessed by serum fibrosis markers. Differences in NAFLD status were compared in patients of different breast cancer molecular subtypes, expression of human epidermal growth factor receptor 2 (HER2) and clinical staging.

Results: The PSM successfully matched 164 pairs. Whether or not in menopause, the prevalence of NAFLD in the breast cancer group was significantly higher than that in the health examination group (premenopausal: 12/61 vs 5/67, P = 0.042; postmenopausal: 27/103 vs 9/97, P = 0.002). Multivariate logistic regression analysis showed that the risk of breast cancer in premenopausal NAFLD patients was 4.05 times higher than that without NAFLD [relative risk (RR) = 4.05, 95% confidence interval (CI): 1.22-13.47, P=0.023]. The same phenomenon can be observed in postmenopausal patients (RR = 5.86, 95% CI: 2.06-16.62, P < 0.001). For patients with NAFLD, those with concurrent breast cancer have a higher risk of liver fibrosis than those without breast cancer. The incidence of NAFLD is not related to breast cancer molecular subtypes and HER2 expression, but exhibits a higher incidence in stage Ⅱ patients.

Conclusion: NAFLD is closely associated with breast cancer. Patients with breast cancer have a higher proportion of NAFLD than healthy people, and NAFLD patients have an increased risk of breast cancer compared with non-NAFLD patients. Attention should be paid to the screening and management of NAFLD in breast cancer patients to prevent the incidence and progression of liver fibrosis in early stage.

Digestive system tumors are malignant tumors with high malignancy, easy metastasis, and poor prognosis, which are difficult to diagnose due to the insidious onset. Most of the patients have reached the middle and advanced stages at the time of diagnosis, so the effect of treatment is usually not good. Studies have shown that the long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) is highly expressed in a variety of solid tumors, and can participate in malignant biological processes such as tumor proliferation, invasion and migration. SNHG6 is closely related to the emergence of chemotherapy drug resistance. This article reviews the biological function and clinical significance of SNHG6 in 6 different tumors of the digestive system, and discusses its mechanism of action in tumorigenesis and development, in the hope to search for effective early diagnosis and treatment targets and thereby improve the survival rate of cancer patients.

Objective: To explore potential biomarkers of biliary tract carcinoma (BTC) by proteomic techniques based on isobaric tags for relative and absolute quantitation (iTRAQ).

Methods: Bile samples from 4 patients with BTC and 4 patients with benign biliary tract disease (BBD) were randomly selected from sample library of central laboratory, Qingpu branch of Zhongshan Hospital, Fudan University. After mixing samples within each group, iTRAQ labeling technology combined with two-dimensional liquid chromatography-tandem mass spectrometry (2D-LC-MS/MS) was used for quantitative proteomic analysis. Then, differentially expressed proteins between the BTC and BBD groups were screened and subjected to bioinformatic analysis, including KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis, GO (Gene Ontology) enrichment analysis and protein-protein interaction (PPI) network analysis. The candidate protein with the largest fold change in expression abundance selected from the differentially expressed proteins as a potential diagnostic biomarker for BTC. Enzyme-linked immunosorbent assay (ELISA) validation and receiver operating characteristic (ROC) cure analysis were performed on this candidate protein using bile samples form 50 BTC patients and 50 BBD patients.

Results: A total of 12 differential expressed proteins were screened from the bile samples of 4 BTC patients and 4 BBD patients (FDR<1%). Haptoglobin (Hp) and Complement Factor H (CFH), as hub proteins in the PPI network, were significantly upregulated in the bile of BBD patients. ELISA results showed that Hp and CFH were significantly upregulated in the bile of patients with various subtypes of BTC (P<0.01).ROC curve analysis indicated that Hp and CFH in bile exhibited significant specificity and sensitivity in the diagnosis of BTC, and their diagnostic performance was superior to that of serum protein CA19-9.

Conclusion: In this study, iTRAQ labeling technology combined with 2D-LC-MS/MS was used to systematically analyze the proteomic differences between bile samples from BTC and BBD patients. Hp and CFH were identified as core differentially expressed proteins, and their diagnostic efficiency for BTC was significantly better than that of serum potein CA19-9. They can serve as potential biomarkers for early diagnosis and therapeutic targets of BTC.

In the past decade, the application and development of artificial intelligence in the diagnosis and treatment of nervous system tumors have entered an organized, rapid, and systematic trajectory. Currently, technologies such as big data mining, machine learning, computer vision, image recognition, and surgical robots have been incorporated into various aspects including tumor screening, clinical diagnosis, tumor classification, drug discovery, treatment decision-making, surgical assistance, prognosis assessment, precision medicine, and simulation-based education for nervous system tumors. However, these technologies are still in their early stages. Therefore, a comprehensive, rational, and objective examination of the application of artificial intelligence in the diagnosis and treatment of nervous system tumors is crucial. Such scrutiny aims to assess the current status of relevant achievements, holds significance for disciplinary innovation, avoidance of research and development pitfalls, and overcoming developmental bottlenecks.

Multiple genetic tumor susceptibility syndromes are associated with the development of neurological tumors. The classification of hereditary tumor syndromes has changed in the past few years, and there is now a clear understanding of the pathogenic mechanisms of these syndromes and they are classified into eight pathogenic mechanisms. In 2007, our team first published a special issue on “Genetic tumour syndromes of the nervous system” in China, which provided a detailed introduction to 8 types of hereditary neurological tumor syndromes. Based on this, the newly included susceptible neurological tumor syndromes was introduced and the research and care points that should be paid attention to in the next step were emphasized.