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    25 December 2025, Volume 17 Issue 6 Previous Issue    Next Issue
    Current status and future prospects of cardio⁃oncology
    LIU Zhaozhe, XIE Xiaodong
    2025, 17 (6):  653-659.  doi: 10.3969/j.issn.1674-5671.2025.06.01
    Abstract ( 59 )   PDF (706KB) ( 28 )   Save
    Tumors and cardiovascular diseases are regarded as two major "killers" threatening human health and have traditionally been studied as separate disciplines in the medical field. With continuous advancements in tumor diagnosis and treatment, the long⁃term survival rates of patients have significantly improved. Various malignant tumors and the corresponding therapeutic drugs affect cardiac metabolism, biochemical properties, and structural functions through diverse mechanisms. Related cardiovascular toxicities increasingly compromise patients' quality of life, leading to the emergence of the interdisciplinary field of cardio⁃oncology. Over nearly two decades, this discipline has evolved from a conceptual consensus to clinical practice, establishing a comprehensive diagnosis and treatment system centered on multidisciplinary collaboration, holistic management, and technological innovation. It provides a scientific pathway to achieve the dual goals of "cancer treatment" and "heart protection". This article reviews the developmental history, mechanistic research, risk assessment and prevention, as well as future directions of cardio⁃oncology.
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    Evidence⁃based update and recommendations for perioperative antiplatelet therapy of transurethral resection of bladder tumor for patients with bladder cancer complicated by coronary heart disease
    MIAO Qi, ZHANG Ning
    2025, 17 (6):  660-664.  doi: 10.3969/j.issn.1674-5671.2025.06.02
    Abstract ( 37 )   PDF (592KB) ( 22 )   Save
    The decision⁃making process for the comprehensive treatment of cancer patients with concurrent  cardiovascular diseases remains in the preliminary exploration phase. Taking transurethral resection of bladder tumor (TURBT) in bladder cancer patients with concomitant coronary atherosclerotic heart disease (CAD) as an example, the choice of perioperative antiplatelet therapy poses a clinical dilemma: discontinuing antiplatelet therapy elevates the risk of perioperative adverse cardiovascular events, while continuing antiplatelet therapy increases the likelihood of surgical bleeding. For an extended period, bridging therapy with anticoagulants such as low⁃molecular⁃weight heparin (LMWH) has been routinely administered preoperatively to patients on antiplatelet treatment. However, anticoagulants and antiplatelet agents exert distinct mechanisms on the coagulation system, and there is currently a paucity of high⁃quality evidence. Based on recent research findings, this article proposed the following perspective: For patients with mild⁃to⁃moderate coronary artery stenosis, no history of percutaneous coronary intervention (PCI), and who are scheduled to undergo TURBT, those with low thromboembolic risk and moderate surgical bleeding risk, discontinuing their prior antiplatelet therapy. In contrast, for patients with severe coronary artery stenosis, a history of PCI, and who are planned for TURBT, those with high thromboembolic risk and moderate surgical bleeding risk, continuing the previous antiplatelet therapy or implementing bridging therapy with short⁃acting antiplatelet agents may represent a more rational clinical decision.
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    New breakthroughs and future trends in renal cell carcinoma treatment: based on the ESMO 2025
    YU Jingxuan, GAO Lei, LIU Zhenyu, ZHOU Yu, WANG Min, WANG Lin, ZHAO Fuhan, XIE Sen, PAN Tiejun
    2025, 17 (6):  665-671.  doi: 10.3969/j.issn.1674-5671.2025.06.03
    Abstract ( 57 )   PDF (574KB) ( 21 )   Save
    The 2025 European Society for Medical Oncology (ESMO) Annual Meeting was convened in Berlin, Germany on October 17, 2025. Significant advancements were report in the field of renal cell carcinoma (RCC), covering several aspects such as postoperative adjuvant therapy, neoadjuvant therapy, the optimization of first⁃line regimens for advanced disease, treatment options following drug resistance, and the exploration of biomarkers. These studies not only demonstrated the deepening  application of immune⁃targeted combination therapies in RCC, but also highlighted the trend toward personalized treatment based on risk stratification and molecular biomarkers. They provided new evidence for the development of  precise clinical strategies and indicated the future research directions focused on biomarkers, novel combination therapies, and multidisciplinary integration. This review systematically summarized the key studies presented at the meeting, aiming to provide clinicians with the latest academic developments and explore future treatment directions and clinical translation prospects for RCC.
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    Research progress on targets for antibody⁃drug conjugate in urothelial carcinoma: clinical value and future challenges of NECTIN⁃4,HER⁃2,and TROP⁃2
    ZHANG Wentao, LIU Yongqiang, WU Yang, CHEN Haotian, GUO Yadong, ZHANG Junfeng, MAO Shiyu, SHEN Liliang, MA Wenchao, WANG Ruiliang, XU Tianyuan, GENG Jiang, SHEN
    2025, 17 (6):  672-682.  doi: 10.3969/j.issn.1674-5671.2025.06.04
    Abstract ( 75 )   PDF (654KB) ( 24 )   Save
    Antibody⁃drug conjugate (ADC) have revolutionized the treatment paradigm for advanced urothelial carcinoma (UC) through their dual mechanism of precise targeting and effective cytotoxicity. This article examines the expression profiles of NECTIN⁃4,  HER⁃2 and TROP⁃2 in UC and their biological basis as ADC targets. By integrating key clinical trial data from recent years, it thoroughly explores the breakthrough advances of ADCs therapy of locally advanced/metastatic UC, the challenges related to biomarkers, and future development directions. This study provides new insights for the precise diagnosis and treatment of UC and provides evidence⁃based support for clinical practice.
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    Advances in the clinical diagnosis and treatment of prostate cancer in 2025
    ZENG Bin, XU Hang, LIAO Xinyang, TU Xiang, LI Jiakun, WEI Qiang, YANG Lu
    2025, 17 (6):  683-689.  doi: 10.3969/j.issn.1674-5671.2025.06.05
    Abstract ( 48 )   PDF (470KB) ( 25 )   Save
    In recent years, the incidence and mortality rates of prostate cancer in China have continued to rise, leading to an increased disease burden. The widespread adoption of precision medicine principles, coupled with advancement of drug research, has significantly transformed the management of prostate cancer at each stage. This article systematically reviews and summarizes the key clinical research progress in 2025 around three major themes: the innovation of precision diagnosis and treatment for localized prostate cancer, the forward⁃moving of intensified treatment and precision stratification for metastatic hormone⁃sensitive prostate cancer (mHSPC), and the breakthrough of new mechanism for metastatic castration⁃resistant prostate cancer (mCRPC).
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    Analysis of lung cancer incidence and mortality in Gansu Province from 2010 to 2021 and the future trend prediction
    WANG Jia, ZHANG Bolun, DING Gaoheng, LIU Yuqin
    2025, 17 (6):  690-696.  doi: 10.3969/j.issn.1674-5671.2025.06.06
    Abstract ( 40 )   PDF (679KB) ( 17 )   Save
    Objective To analyze the incidence and mortality of lung cancer in Gansu Province from 2010 to 2021 and predict its trends from 2022 to 2030. Methods Lung cancer registration data from 15 cancer registries in Gansu Province between 2010 and 2021 were collected and collated. The study calculated the age⁃standardized incidence rate by Chinese standard population (ASIRC), and age⁃standardized mortality rate by Chinese standard population (ASMRC) by age group, gender and urban⁃rural distribution. Joinpoint software was used to calculate annual percentage change (APC) and average annual percentage change (AAPC). Bayesian age⁃period⁃cohort (BAPC) model was employed to forecast trends in lung cancer incidence and mortality from 2022 to 2030.  Results From 2010 to 2021, both the ASIRC and ASMRC for lung cancer in Gansu Province showed a sustained upward trend. ASIRC rose by an average of 0.85% annually (AAPC=0.85%, 95%CI: -0.81% to 2.54%, P=0.283), with a 2.44% increase in urban (AAPC=2.44%, 95%CI: 0.71% to 4.19%, P=0.010), a 0.61% decline in rural (AAPC=-0.61%, 95%CI: -4.39% to 3.31%, P=0.756); a 0.69% increase among males (AAPC=0.69%, 95%CI: -0.97% to 2.38%, P=0.381) , and a 1.29% increase among females (AAPC=1.29%, 95%CI: -0.72% to 3.33%, P=0.184). ASMRC by an average of 1.56% annually (AAPC=1.56%, 95%CI: -2.77% to 6.07%, P=0.447), with a 3.28% increase in urban (AAPC=3.28%, 95%CI: -6.58% to 14.17%; P=0.529), a 2.11% decline in rural (AAPC=-2.11%, 95%CI:-5.77% to 1.68%, P=0.271), a 2.30% increase among males (AAPC=2.30%, 95%CI: -2.06% to 6.86%, P=0.271), and a 0.27% decline among females (AAPC=-0.27%, 95%CI: -6.99% to 6.93%, P=0.939). Both ASIRC and ASMRC showed fluctuating upward trend with age across all age groups ≥40 years. BAPC projections indicated that the ASIRC of lung cancer in Gansu Province would rise while ASMRC would decline during 2022 to 2030. Conclusions From 2010 to 2021, the ASIRC and ASMRC of lung cancer in Gansu Province continued to rise, with the risk of lung cancer occurrence and death among residents aged 40 and above fluctuating and increasing with age. The BAPC model predicts that by 2030, the ASIRC will persistently rise, while the ASMRC is expected to decline. It is necessary to strengthen the prevention and control of lung cancer in order to reduce the risks of lung cancer.
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    Clinical efficacy and safety of BAI/BACE combined with platinum⁃based dual⁃drug chemotherapy and PD⁃1 inhibitor in stage Ⅳ driver gene⁃negative non⁃small cell lung cancer
    QUAN Xiaoying, CHEN Xiaoyan, LEI Lei, JIA Xiaoli, WU Chunzhi, YE Bin, HUANG Qiyue, LUO Min, WANG Ning, YU Jiayang, FENG Lifu
    2025, 17 (6):  697-704.  doi: 10.3969/j.issn.1674-5671.2025.06.07
    Abstract ( 52 )   PDF (935KB) ( 16 )   Save
    Objective To investigate the clinical efficacy of bronchial arterial infusion (BAI) / bronchial arterial chemoembolization (BACE) combined with platinum⁃based dual⁃drug chemotherapy and PD⁃1 inhibitor as first⁃line treatment for stage Ⅳ driver gene⁃negative non⁃small cell lung cancer (NSCLC). Methods Clinical data of 91 patients with stage Ⅳ driver gene⁃negative NSCLC treated at the Chengdu Sixth People's Hospital between April 2020 and October 2024 were analyzed. Patients were categorized into two cohorts based on their treatment regimen: the BAI group (n=47) received BAI/BACE combined with platinum⁃based dual⁃drug chemotherapy and PD⁃1 inhibitor, and the non⁃BAI group (n=44) received platinum⁃based dual⁃drug chemotherapy and PD⁃1 inhibitor alone. Short⁃term efficacy, progression⁃free survival (PFS), overall survival (OS), and the incidence of adverse events (≥grade 1) within 90 days post⁃treatment were compared between the two groups. Results The objective response rate was significantly higher in the BAI group than in the non⁃BAI group (68.1% vs 47.7%, P=0.049). Additionally, the BAI group showed significantly better PFS (P=0.021)and OS (P=0.012), with median PFS of 12 months vs 8 months and median OS of 18 months vs 11 months. Two⁃stage analysis revealed that during the early stage (≤12 months), the BAI group demonstrated significantly superior PFS and OS compared to the non⁃BAI group (all P=0.003). Subgroup analysis of the BAI group showed a trend toward better PFS and OS in patients with central⁃type tumors compared to those with peripheral⁃type tumors (median PFS: 15 months vs 11 months; median OS: 21 months vs 16 months). Furthermore, in the advanced stage (>12 months), patients with central⁃type tumors demonstrated significantly better PFS (P=0.022) and OS (P=0.037) than those with peripheral⁃type tumors (median PFS: 7 months vs 2 months; median OS: 14 months vs 6 months). Multivariate Cox proportional hazards regression analysis confirmed that treatment with BAI/BACE combined with platinum⁃based dual⁃drug chemotherapy and PD⁃1 inhibitor was an independent protective factor for both PFS and OS (all P<0.05). Adverse reactions in both groups were predominantly grade Ⅰ-Ⅱ, with no significant difference in incidence rates. Conclusions BAI/BACE combined with platinum⁃based dual⁃drug chemotherapy and PD⁃1 inhibitor demonstrated favorable efficacy and manageable safety in first⁃line treatment for stage Ⅳ driver gene⁃negative NSCLC patients, delivering significant survival benefits.
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    Multi⁃omics analysis reveals the role and clinical significance of the loss of Y chromosome in bladder cancer
    LIU Tao, QIN Zezu, FENG Chao, ZHENG Youwen, TANG Shaomei, WANG Qiuyan, LI Tianyu
    2025, 17 (6):  705-714.  doi: 10.3969/j.issn.1674-5671.2025.06.08
    Abstract ( 40 )   PDF (3771KB) ( 11 )   Save
    Objective To investigate the role and clinical significance of the loss of  Y chromosome (LOY) in bladder cancer. Methods  Tissue samples and clinical data were collected from 44 male patients with bladder cancer undergoing radical cystectomy at the First Affiliated Hospital of Guangxi Medical University between January 2018 and October 2019. Whole⁃transcriptome sequencing data were analyzed and scored based on Y chromosome transcriptional signature (YchrS) using single⁃sample gene set enrichment analysis (ssGSEA). Patients were stratified into high and low YchrS score groups. The prognosis of the two groups were evaluated using the Kaplan⁃Meier method, and the potential molecular characteristics were revealed via differential expression analysis and gene set enrichment analysis (GSEA). The diversity of immune cells in the two groups was analyzed using cytometry by time of flight (CyTOF). Single⁃cell transcriptomic sequencing data from a public database (HRA000212) was used to characterize LOY epithelial cells through cell differentiation trajectories and cell communication analysis. The CMap  database was utilized to identify potential therapeutic agents. Results  Patients with bladder cancer in the low YchrS score group exhibited shorter overall survival (P=0.006) and higher tumor grade (P=0.036). Upregulated genes in low YchrS score group were enriched in biological processes related to the cell cycle regulation, DNA replication, and chromosome segregation (P<0.05), showing elevated scores for p53⁃repressed genes and reduced scores for p53⁃induced genes (all P<0.001). Compared with other epithelial cells, LOY epithelial cells displayed activation of immune⁃related signaling pathways and stronger interactions with myeloid cells and T cells. CyTOF analysis revealed an enrichment of regulatory T (Treg) cells and upregulated expression of CD279 (PD⁃1) on CD4+ T cells in the low YchrS score group. CMap analysis indicated that cyclin⁃dependent kinase (CDK) inhibitors (e.g., Palbociclib) and histone deacetylase (HDAC) inhibitors were potential therapeutic agents for bladder cancer patients in the low YchrS score group. Conclusions LOY is strongly associated with poor prognosis in bladder cancer patients, with its tumorigenic mechanism may involve p53 suppression and immune suppression. CDK inhibitors and HDAC inhibitors serve as potential therapeutic agents for the LOY bladder cancer patients.
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    Mestranol enhances CD8+ T cell effector functions by promoting expression of AGK
    ZHUO Fangqi, WANG Ruikun, WU Guanglong, HAN Juqiang, WANG Xiaoyu, XU Kaiyue, LIU Sihan, XIAO Xiaoyinan, DU Yimeng, CHE Yongsheng, XU Xiaojie
    2025, 17 (6):  715-721.  doi: 10.3969/j.issn.1674-5671.2025.06.09
    Abstract ( 35 )   PDF (868KB) ( 7 )   Save
    Objective To investigate the transcriptional activation potential of Mestranol (Mes) on acylglycerol Kinase (AGK) and its role in enhancing CD8+ T cell effector function. Methods Public databases were utilized to analyze the correlation between AGK expression and CD8+ T cell effector function genes, and its association with CD8+ T cell infiltration levels across the tumor microenvironments. The effects of Mestranol on AGK mRNA and protein expression levels, as well as on the activation of the AGK downstream signaling pathway were assessed using quantitative PCR (qPCR) and Western blot. The half maximal inhibitory concentration (IC50) of Mestranol was determined using the CCK⁃8 assay. An AGK overexpression plasmid was transfected into human T lymphocyte leukemia Jurkat cells and CD8⁺ T cells by electroporation, and a luciferase reporter gene assay was employed to examine the impact of Mestranol on AGK promoter transcriptional activity. Enzyme⁃linked immunosorbent assay (ELISA) was used to quantify the levels of  interferon⁃γ (IFN⁃γ) and tumor necrosis factor⁃α (TNF⁃α) secreted by CD8+ T cells under following AGK overexpression, along with Mestranol's effects on these parameters. The effects of Mestranol on the cytotoxic activity of CD8+ T cells was assessed in vitro using flow cytometry.  Results Public databases analysis revealed that AGK expression was significantly positively correlated with CD8+T cell effector function genes, negatively correlated with inhibitory function genes, and positively associated with CD8+ T cell infiltration levels in various tumor microenvironments (all P<0.05). The IC50 of Mestranol was 36 μmol/L. Mestranol significantly upregulated AGK expression at both mRNA and protein levels in Jurkat cells in a dose⁃dependent manner across various concentrations (all P<0.01). Furthermore, luciferase reporter assays demonstrated that Mestranol significantly enhanced the transcriptional activity of the AGK promoter(P<0.001). Mestranol elevated the phosphorylation levels of AKT protein at Ser473, enhanced the secretion of IFN⁃γ and TNF⁃α in treated CD8⁺T cells (all P<0.001), and increased their tumor⁃killing capacity in vitro (P<0.01).  Conclusions Mestranol up⁃regulates AGK expression by enhancing the transcriptional activity of the AGK promoter, thereby augmenting CD8+ T cell effector function, which provides a new insight for tumor immunotherapy targeting AGK.

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    miR⁃130a⁃3p targets ATG2B to regulate autophagy in cisplatin⁃resistance small cell lung cancer 
    AIHEMAITI Mikeriayi, AOSIMAN Aliya, LIU Junyuan, AERXIDING Patiguli
    2025, 17 (6):  722-729.  doi: 10.3969/j.issn.1674-5671.2025.06.10
    Abstract ( 53 )   PDF (2023KB) ( 29 )   Save
    Objective To investigate the role of miR⁃130a⁃3p in cisplatin⁃resistant  small cell lung cancer (SCLC) and explore its underlying molecular mechanisms. Methods Cisplatin⁃resistant SCLC cell line (H446/EP) was established using a concentration⁃gradient induction method. The SCLC cells were transfected with miR⁃130a⁃3p mimics via lipofection. Cell proliferation viability was assessed using the CCK⁃8 assay, while apoptosis rates and cell cycle distribution were analyzed by flow cytometry. Bioinformatics analysis was performed using TargetScan, TarBase, and miRWalk databases to predict the targeting relationship between miR⁃130a⁃3p and ATG2B. The expression levels of miR⁃130a⁃3p and ATG2B mRNA were detected by quantitative real⁃time PCR (qRT⁃PCR). Protein expression of autophagy⁃related proteins, including ATG2B, LC3B, p62, and Beclin1 were measured by Western blot. The fluorescence intensity of LC3B and p62 proteins was quantified by immunofluorescence to evaluate cellular autophagy activity. Results The resistance index of H446/EP cells was 6.465, with miR⁃130a⁃3p expression was significantly lower than in the sensitive parent cells. Restoring miR⁃130a⁃3p expression effectively inhibited proliferation and promoted apoptosis in the resistant cells (all P<0.05). Bioinformatics prediction indicated that ATG2B is a high⁃confidence target gene of miR⁃130a⁃3p. Overexpression of with miR⁃130a⁃3p suppressed the expression of the autophagy⁃related gene ATG2B, leading to decreased LC3B⁃Ⅱ/LC3B⁃Ⅰ ratio and Beclin1 levels (all P<0.05), while upregulating p62 levels (P<0.05). Conclusions miR⁃130a⁃3p mediates cisplatin resistance in SCLC cells through regulating ATG2B expression. Enhancing miR⁃130a expression may provide a novel strategy for overcoming platinum resistance in SCLC.
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    M2⁃type tumor⁃associated macrophages promote the proliferation and epithelial⁃mesenchymal transition of gastric cancer MKN⁃45 cells by regulating CTHRC1 expression
    SUO Feiya, TIAN Lili, YAN Quanzhi, SU Rina, XING Hongjun, ZHAO Huiying
    2025, 17 (6):  730-738.  doi: 10.3969/j.issn.1674-5671.2025.06.11
    Abstract ( 64 )   PDF (2623KB) ( 30 )   Save
    Objective To investigate the effects of M2⁃type tumor⁃associated macrophages (TAMs) on the proliferation of gastric cancer cells and epithelial⁃mesenchymal transition (EMT) , along with possible mechanisms. Methods THP⁃1 cells were differentiated into M2⁃type macrophages in vitro and treated with conditioned medium from gastric cancer MKN⁃45 cells to obtain M2⁃type TAMs (M2⁃TAMs). M2⁃TAMs were co⁃cultured with MKN⁃45 cells (MKN⁃45 group and M2⁃TAMs/MKN⁃45 group). In addition, siRNA technology was used to silence collagen triple helix repeat containing 1 (CTHRC1) in MKN⁃45 cells, the cells were co⁃cultured with or without M2⁃TAMs (si⁃NC group, si⁃CTHRC1 group, M2⁃TAMs/si⁃NC group, and M2⁃TAMs/si⁃CTHRC1 group). Cell proliferation, invasion and migration abilities were detected by CCK⁃8, colony formation, Transwell and scratch test. The levels of matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9) in cell supernatant were detected by ELISA. qRT⁃PCR was used to detect the expression level of CTHRC1 mRNA in cells. Western blot was used to detect the protein expression levels of E⁃cadherin, N⁃cadherin, Vimentin and CTHRC1. Results Compared with the MKN⁃45 group, the M2⁃TAMs/MKN⁃45 group showed significantly increased cell proliferation, migration and invasion abilities (all P<0.05), upregulated MMP2 and MMP9 levels (all P<0.01), decreased E⁃cadherin expression(P<0.001), and increased N⁃cadherin, Vimentin and CTHRC1 expression (all P<0.01). Compared with the si⁃NC group, the si⁃CTHRC1 group exhibited significantly reduced cell proliferation, migration and invasion abilities (all P<0.05), increased E⁃cadherin expression (P<0.001), and decreased CTHRC1, N⁃cadherin and Vimentin expression (all P<0.01). Compared with the M2⁃TAMs/si⁃NC group, the M2⁃TAMs/si⁃CTHRC1 group showed significantly decreased cell proliferation, migration and invasion abilities (all P<0.05), increased E⁃cadherin expression (P<0.001), and decreased CTHRC1, N⁃cadherin and Vimentin expression (all P<0.01). Conclusions M2⁃type TAMs may promote the proliferation and EMT of gastric cancer MKN⁃45 cells by upregulating CTHRC1 expression.
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    Clinical practice and challenges of antibody⁃drug conjugate in combination therapy for non⁃small cell lung cancer
    ZHANG Yeran, TAN Yuanyuan, XU Yali
    2025, 17 (6):  739-746.  doi: 10.3969/j.issn.1674-5671.2025.06.11
    Abstract ( 17 )   PDF (577KB) ( 1 )   Save
    Antibody⁃drug conjugate (ADC) facilitate precise targeting of non⁃small cell lung cancer (NSCLC) by delivering potent cytotoxic agents directly to tumor cells, but monotherapy with ADC limited by tumor heterogeneity and acquired resistance. In recent years, combination therapy strategies that integrate ADC with immune checkpoint inhibitors and targeted agents have demonstrated superior efficacy in driver gene⁃negative NSCLC. This approach not only offers a chemotherapy⁃sparing treatment model, but also significantly transforms the therapeutic landscape for advanced NSCLC. This review aims to systematically summarize the biological mechanisms and the latest clinical advances of ADC⁃based combination therapy, while also exploring key challenges and future directions. It seeks to provide a theoretical foundation and clinical practical insights for precision treatment in advanced NSCLC.

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    Research progress of CAR⁃NK cell therapy in abdominal tumors
    NIU Xudong, WANG Bingping, HAN Jingjing, JI Yadong, ZHOU Jie, MING Xing, GAO Yanwei
    2025, 17 (6):  747-754.  doi: 10.3969/j.issn.1674-5671.2025.06.13
    Abstract ( 50 )   PDF (948KB) ( 17 )   Save
    As an emerging immunotherapy modality, chimeric antigen receptor (CAR)⁃natural killer (NK) cell therapy demonstrates significant potential in tumor treatment, achieving a pivotal breakthrough from foundational research to clinical application, particularly in the treatment of abdominal malignancies. This article provides an overview of CAR⁃NK cell therapy and systematically summarizes the research progress in its application to abdominal tumors, including hepatocellular carcinoma (HCC), gastric cancer, colorectal cancer, and pancreatic cancer. It also explores the potential of key receptors including HER2, MSLN, CEA, and EGFR in developing novel CAR⁃NK therapies. This aims to explore new treatment pathways for patients with abdominal tumors, improve their clinical prognosis, and promote the field of molecular oncology towards precision diagnosis and treatment.
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    Mechanisms and advances in targeted therapeutic strategies of lactylation in cancer
    LIN Jinquan, ZHAO Zhi, WANG Xing
    2025, 17 (6):  755-762.  doi: 10.3969/j.issn.1674-5671.2025.06.14
    Abstract ( 44 )   PDF (796KB) ( 19 )   Save
    Lactylation is a novel post⁃translational modification, plays a crucial role in cancer development by regulating metabolic and epigenetic reprogramming, as well as the immunosuppressive tumour microenvironment. The interaction between lactylation and immune cells modulates tumor differentiation, immune responses, and drug sensitivity, highlighting its significant potential as a therapeutic target. This review summarizes the molecular mechanisms of lactylation in cancer, its clinical research progress, and future therapeutic prospects. The aim is to promote innovative research in the development of tumor treatment targets, thereby accelerating the clinical application of lactylation⁃based treatments.
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    Research advances on m6A methylation modification in osteosarcoma metastasis
    QIN Xiong, ZHU Bo
    2025, 17 (6):  763-769.  doi: 10.3969/j.issn.1674-5671.2025.06.15
    Abstract ( 36 )   PDF (474KB) ( 7 )   Save
    Osteosarcoma is a common primary malignant bone tumor characterized by high invasiveness and metastatic potential. Pulmonary metastasis is the primary cause of treatment failure and poor prognosis in patients. N6⁃methyladenosine (m6A) is the most abundant epigenetic modification in eukaryotic mRNA, has been confirmed to be deeply involved in the metastatic progression of osteosarcoma. This article systematically reviews the dynamic modification mechanism of m6A methylation and the functions of its core regulatory components. It elucidates the molecular mechanisms through which these regulatory factors,  by mediating RNA splicing, transport, translation, and degradation to regulate downstream target genes and related signaling pathways, ultimately driving osteosarcoma migration, invasion, and epithelial⁃mesenchymal transition. Additionally, explores the clinical potential of m6A modification as a diagnostic biomarker and therapeutic target for osteosarcoma metastasis, aiming to provide new directions for mechanistic research and clinical intervention of osteosarcoma metastasis.
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     A case report and literature review of primary hepatic perivascular epithelioid cell tumor 
    LIU Zhidong, MAI Rongyun, MA Liang, ZHANG Yu
    2025, 17 (6):  770-774. 
    Abstract ( 54 )   PDF (702KB) ( 19 )   Save
    Primary hepatic perivascular epithelioid cell tumor (PEComa) is a rare mesenchymal neoplasm, typically presenting benign or indolent biological behavior. However, its clinical and radiological manifestations are non⁃specific, often leading to misdiagnosis as hepatocellular carcinoma (HCC), hepatic adenoma or other metastatic lesions. This report describes a case of primary hepatic PEComa in a patient who presented with a hepatic space⁃occupying lesion persisting for over a year, without typical clinical or imaging features, and was initially misdiagnosed as HCC. Following multi⁃disciplinary team (MDT) consultation, the patient underwent radical hepatectomy. Postoperative pathological examination showed positive expression of SMA, HMB⁃45 and Melan⁃A, confirming epithelioid⁃type PEComa. There was no recurrence sign during the 6⁃month postoperative follow⁃up. This case underscores the importance of considering liver biopsy and immunohistochemistry in atypical cases, even when imaging suggests HCC. Furthermore, it advocates for the establishment of an individualized treatment approach centered on MDT collaboration to achieve precise therapeutic outcomes.
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