Chinese Medical Journal最新文献

{"title":"Intratumoral microbiota in tumorigenesis: A double-edged sword.","authors":"Xinyue Fu, Hao Chen, Meihang Du, Peiheng Li, Yue Zhao, Huanzuo Yang, Hancong Li, Gongshuang Zhang, Puxing He, Shuang Wu, Miao Zhang, Zhenmei An, Zhihui Li, Binwu Ying, Juan Rául Hernandez Silva, Liwei An, Han Luo","doi":"10.1097/CM9.0000000000004178","DOIUrl":"10.1097/CM9.0000000000004178","url":null,"abstract":"<p><strong>Abstract: </strong>The rapid development of high-throughput sequencing technologies and bioinformatics has enabled the identification of diverse microbial communities within tumor tissues, giving rise to the concept of intratumoral microbiota. Comprising bacteria, viruses, fungi, and archaea, the intratumoral microbiota has been shown to play critical roles in tumor initiation, progression, and therapeutic responses. This review systematically summarizes the composition, ecological characteristics, and functional roles of intratumoral microbiota, with particular emphasis on its dual regulatory mechanisms in tumorigenesis, progression, metastasis, and recurrence. We further delineate four principal mechanistic pathways through which intratumoral microbiota influence tumor biology, including receptor-mediated signaling, metabolic reprogramming, effector molecule secretion, and intracellular invasion. Additionally, we evaluate the translational potential of these findings in clinical oncology, offering innovative perspectives for tumor diagnosis, therapeutic intervention, and preventive strategies.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2706-2720"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148396043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spesolimab for patients with generalized pustular psoriasis flares: Real-world experience in China.","authors":"Min Zheng, Furen Zhang, Yuling Shi, Xiaoming Liu, Ai'e Xu, Qianjin Lu, Xian Jiang, Bin Yang, Juan Tao, Linfeng Li, Nichiren Pillai, Fan Chen, Yijun Zhou, Yuexiao Xu, Xinghua Gao","doi":"10.1097/CM9.0000000000003774","DOIUrl":"10.1097/CM9.0000000000003774","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2821-2823"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characteristics, prognosis, and risk factors for relapse in patients with cryptogenic organizing pneumonia: A prospective cohort study in China.","authors":"Weiqing Meng, Bingbing Xie, Shu Zhang, Xinran Zhang, Jing Geng, Yinan Hu, Xueying Chen, Ling Zhao, Yanhong Ren, Xiaojuan Guo, Min Liu, Sheng Xie, Huaping Dai","doi":"10.1097/CM9.0000000000004247","DOIUrl":"10.1097/CM9.0000000000004247","url":null,"abstract":"<p><strong>Background: </strong>Cryptogenic organizing pneumonia (COP) is classified as a subtype of idiopathic interstitial pneumonia (IIP), which has a good prognosis. Relapse remains one of the most challenging and intriguing aspects of COP. This study aimed to characterize the clinical features, prognosis, and relapse patterns of COP.</p><p><strong>Methods: </strong>In this prospective cohort study, patients diagnosed with COP between March 1, 2004 and June 30, 2022 at China-Japan Friendship Hospital and Beijing Chao-Yang Hospital were enrolled after a comprehensive multidisciplinary review. Patients were followed up through regular clinical visits every 3-6 months until October 30, 2023. Data collected included demographic characteristics, clinical presentation, laboratory findings, radiologic features, and prognostic outcomes. The primary outcome measure was relapse. Cox regression analyses were performed to explore factors related to the presence of relapse.</p><p><strong>Results: </strong>This study included 268 patients with a final diagnosis of COP based on multidisciplinary discussion. After diagnosis, the one-year survival rate was 99.6%, decreasing to 97.7% at 3 years, 94.5% at 5 years, and 81.7% at 10 years. Relapses occurred in 20.9% (56/268) of patients, with a median time to relapse of 12 months. Of these relapses, 28.6% (16/56) occurred when prednisone was tapered to below 10 mg/day, and 62.5% (35/56) occurred after discontinuation of prednisone therapy; fewer than 10% of relapses occurred at prednisone doses above 15 mg/day. Ground-glass opacities (GGOs) (225/268, 84.0%) and consolidations (212/268, 79.1%), predominantly with bilateral lung distribution, were the most common computed tomography (CT) features at diagnosis. No patient developed residual lung fibrosis on high-resolution CT, regardless of relapse status. Furthermore, no deaths were attributable to COP progression or relapse, and all-cause mortality was unrelated to COP itself.</p><p><strong>Conclusion: </strong>This study indicated that patients with COP had a good prognosis with favorable survival outcomes. However, relapse was relatively common, occurring in more than 20% of patients. Therefore, close follow-up is essential for early detection of relapses, particularly during corticosteroid tapering or after treatment discontinuation.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":"2750-2759"},"PeriodicalIF":9.1,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancements and future directions in transforming therapies of prostate cancer.","authors":"Jinge Zhao, Bo Tang, Hao Zeng, Qiang Wei","doi":"10.1097/CM9.0000000000004322","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004322","url":null,"abstract":"<p><strong>Abstract: </strong>The treatment landscape for advanced prostate cancer (PCa) has significantly evolved in recent years, marked by the introduction of several novel therapies. Targeting the androgen receptor (AR) remains a cornerstone of treatment, with drugs, such as abiraterone and next-generation antiandrogens, providing substantial benefits. Poly (ADP-ribose) polymerase (PARP) inhibitors, both as monotherapies and in combination with other agents, have demonstrated promise, particularly for patients with deoxyribonucleic acid (DNA) repair defects. While immunotherapy has historically shown limited efficacy in the treatment of PCa, recent findings from the CONTACT‑02 study suggest a potential breakthrough, demonstrating improved patient outcomes with the combined use of atezolizumab and cabozantinib. Additionally, emerging therapies targeting cyclin-dependent kinases 4 and 6 (CDK4/6), the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway, and epigenetic modifications offer new treatment possibilities. These advancements, coupled with ongoing research into combination therapies and novel drug targets, hold the potential to further enhance outcomes for patients with advanced PCa. This article review summarizes the latest transformative therapies in PCa care.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacteriophages in humans: From discovery and mechanisms to therapeutic promise in combating disease.","authors":"Xiaoming Yuan, Nengneng Li, Shengtao Zhu, Tao Zuo","doi":"10.1097/CM9.0000000000004296","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004296","url":null,"abstract":"<p><strong>Abstract: </strong>Since the discovery of bacteriophages over a century ago, bacteriophages have evolved from fundamental biological models into promising therapeutic agents, especially in the era of antimicrobial resistance and in the treatment of human diseases. This article systematically reviews the key milestones in phage research and application at both international and Chinese fronts. It examines the evolving understanding of phage-bacterium interactions, which provides the development of targeted phage-based biocontrol and therapeutic strategies. Particular emphasis is placed on recent advances linking phages to human diseases, including their potential roles in gut microbiota modulation and chronic disease contexts. Despite promise, substantial challenges remain. The article concludes by discussing critical future directions, emphasizing the need for identifying key microbial targets in diseases, integrating phage therapy with emerging technologies to accelerate clinical translation, and exploring dietary phage interventions for disease prevention.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improved diagnostic capability, rather than biologics, reduces surgical rates in Chinese Crohn's disease patients: A multicenter study.","authors":"Jian Wan, Zhuo Wang, Jun Shen, Jie Zhong, Naizhong Hu, Lanxiang Zhu, Yinglei Miao, Wensong Ge, Zhonghui Wen, Yufang Wang, Jiaming Zhou, Yong Lyu, Jie Liang, Kaichun Wu","doi":"10.1097/CM9.0000000000004315","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004315","url":null,"abstract":"<p><strong>Background: </strong>Surgical rates for Crohn's disease (CD) are declining globally. However, the driving factors remain unclear, particularly in newly industrialized countries. We aimed to evaluate the impact of diagnostic capacity and treatment with biologics on surgical rates among Chinese CD patients.</p><p><strong>Methods: </strong>Data of CD patients from January 2000 to January 2024 were extracted from 8 sites of the Chinese database for inflammatory bowel disease. Trends in cross-sectional imaging use, surgically diagnosed proportion, medical treatment, and surgery for CD were described. Cumulative surgical rates were compared using Kaplan-Meier method with log-rank test. Time-dependent Cox models were used to identify factors associated with surgery risk, and propensity score matching (PSM) was applied to validate the findings.</p><p><strong>Results: </strong>In total, 1354 patients were included, with a median follow-up of 5.99 years. The cumulative 5-year surgical rate decreased from 30.96% in 2000-2012 to 21.57% in 2013-2024 (log-rank P <0.001). The use of cross-sectional imaging increased from 2.00% in 2000-2004 to 82.81% in 2020-2024. The proportion of surgically diagnosed patients declined from 13.68% in 2000-2012 to 6.21% in 2013-2024. Multivariate Cox analysis showed that diagnosis in 2013-2024 (hazard ratio [HR] 0.74, 95% confidence interval [CI]: 0.59-0.91, P = 0.006) was independently associated with a lower risk of surgery, whereas biologic use (HR 0.93, 95% CI: 0.71-1.22, P = 0.604) was not. Sensitivity analyses excluding surgically diagnosed patients demonstrated similar surgical rates between the two cohorts. PSM and subgroup analyses confirmed these trends.</p><p><strong>Conclusions: </strong>Surgical rates among Chinese CD patients have significantly decreased over the past two decades, in parallel with improvements in diagnosis. Enhancements in diagnostic pathways within broader systemic healthcare upgrades are strongly associated with reduced surgical risk, whereas increased use of biologics is not.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-11 drives Treg cell differentiation by activating the MBD3/APOH-mediated fatty acid oxidation axis to promote hepatocellular carcinoma.","authors":"Yang Gao, Xijuan Yao, Xing Huang, Lian Wang, Yong Wang, Guangyu Zhu, Zhen Wang, Lu Li, Jinhe Guo, Jian Lu","doi":"10.1097/CM9.0000000000004371","DOIUrl":"10.1097/CM9.0000000000004371","url":null,"abstract":"<p><strong>Background: </strong>The immunosuppressive tumor microenvironment (TME) represents a major barrier to effective hepatocellular carcinoma (HCC) therapy. While interleukin-11 (IL-11) has been implicated in cancer progression, its immunomodulatory functions and underlying mechanisms in HCC remain poorly understood.</p><p><strong>Methods: </strong>We evaluated IL-11 expression and its clinical relevance using data from public databases and clinical HCC specimens. Functional effects of IL-11 were assessed through in vitro cell culture models and in vivo orthotopic tumor experiments in mice. Regulatory T (Treg) cell differentiation and TME composition were analyzed via flow cytometry and immunohistochemistry. Molecular mechanisms were explored using Western blotting, quantitative reverse transcription polymerase chain reaction (qRT-PCR), chromatin immunoprecipitation, and metabolic assays, focusing on the IL-11/methyl-CpG binding domain protein 3 (MBD3)/apolipoprotein H (APOH) pathway.</p><p><strong>Results: </strong>IL-11 was significantly overexpressed in HCC tissues and correlated with poor patient survival. Functionally, IL-11 enhanced the malignant phenotypes of HCC cells in vitro and in vivo , whereas its knockdown suppressed tumor migration and growth. Importantly, IL-11 increased the proportion of Treg cells in the HCC microenvironment by driving their differentiation, thereby fostering an immunosuppressive TME. Mechanistically, IL-11 upregulated MBD3, which transcriptionally repressed APOH. This downregulation activated the AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ (PPARγ)-mediated fatty acid oxidation (FAO) pathway, and pharmacological inhibition of FAO effectively reversed IL-11-induced Treg differentiation and tumor growth.</p><p><strong>Conclusion: </strong>We have identified a novel IL-11/MBD3/APOH/FAO regulatory axis that promotes HCC progression by enhancing Treg cell differentiation and establishing an immunosuppressive microenvironment. These results nominate IL-11 as a promising therapeutic target for HCC immunotherapy and shed new light on the metabolic basis of immune evasion in liver cancer.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sublethal heat stress-induced HSF4 upregulation via GRSF1 in an m6A-dependent manner in hepatocellular carcinoma.","authors":"Jie Chen, Yan Tan, Wei Xie, Lei Shi, Hu Quan, Hua Xiao, Jia Liu, Xianhai Mao, Pan Chen, Jia Luo","doi":"10.1097/CM9.0000000000004188","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004188","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Sublethal heat stress exacerbates hepatocellular carcinoma (HCC) by promoting recurrence and metastasis. This study aimed to investigate the molecular mechanisms by which sublethal heat stress enhances HCC progression to improve therapeutic strategies and patient outcomes in HCC management.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Cell-based and mouse models of insufficient thermal ablation in HCC were established via sublethal heat stress treatment. Twenty-four BALB/c nude mice were randomly divided into four groups, with six mice per group. RNA sequencing was used for transcriptional profiling. Messenger RNA (mRNA) and protein levels were quantified using quantitative reverse transcription polymerase chain reaction, Western blotting, and immunohistochemistry. Metastatic lesions in mouse liver and lung tissues were identified by hematoxylin and eosin staining. Proliferative, migratory, and invasive characteristics of tumor cells were probed via colony formation, 5-ethynyl-2'-deoxyuridine incorporation, scratch wound healing, and Transwell assays. Interactions between related genes were determined using dual-luciferase reporter, chromatin immunoprecipitation, co-immunoprecipitation, and RNA immunoprecipitation assays. Methylated RNA immunoprecipitation was used to detect N6-methyladenosine (m6A) levels in heat shock transcription factor 4 (HSF4).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;HSF4 was identified as a key gene that was upregulated in sublethal heat stress-treated cells (6.20-fold increase in Huh7 cells and 8.34-fold increase in Hep3B cells; P &lt;0.001). HSF4 knockdown inhibited sublethal heat stress-induced cell proliferation by 61.09% in Huh7 cells and 47.28% in Hep3B cells (P &lt;0.001 and P &lt;0.01), migration by 31.64% in Huh7 cells and 17.01% in Hep3B cells (P &lt;0.05), invasion by 29.68% in Huh7 cells and 47.03% in Hep3B cells (P &lt;0.05 and P &lt;0.001), and epithelial-mesenchymal transition (EMT). Furthermore, HSF4 knockdown repressed liver (reduced liver weight-to-body weight ratio by 32.46%, P &lt;0.001) and lung (decreased metastatic nodules from 10.5 to 5.17 per section, P &lt;0.001) metastases in vivo. Mechanistically, HSF4 increased cell cycle and apoptosis regulator 1 (CCAR1) levels and activated β-catenin pathway by binding to CCAR1 promoter. CCAR1 overexpression counteracted the suppressive effects of HSF4 knockdown on cell proliferation, migration, invasion, and EMT following sublethal heat stress. In addition, sublethal heat stress increased the HSF4 levels by upregulating guanine-rich RNA sequence binding factor 1 (GRSF1) (2.92-fold in Huh7 cells and 2.87-fold in Hep3B cells, P &lt;0.001) in an insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)-m6A-dependent manner. HSF4 overexpression blocked the inhibitory effects of GRSF1 knockdown on HCC cell proliferation and metastasis following sublethal heat stress.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Sublethal heat stress increased HSF4 expression by upregulating GRSF1 thro","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E2F7 promotes lung adenocarcinoma progression by affecting phosphorylation and stabilization of β-catenin.","authors":"Sisi Chen, Manxiang Li, Jian Liu, Kai Li, Jiaojiao Zhang, Xinming Xie, Yamei Pang","doi":"10.1097/CM9.0000000000004312","DOIUrl":"https://doi.org/10.1097/CM9.0000000000004312","url":null,"abstract":"<p><strong>Background: </strong>E2F transcription factor 7 (E2F7) has been implicated in the tumorigenesis and progression of multiple cancer types; however, the molecular mechanisms through which E2F7 regulates malignant phenotypes in cancer cells remain largely undefined. In this study, we investigated the biological functions and underlying mechanisms of E2F7 in lung adenocarcinoma (LUAD).</p><p><strong>Methods: </strong>E2F7 expression in LUAD was analyzed using The Cancer Genome Atlas (TCGA) datasets and further validated in clinical specimens via quantitative real-time polymerase chain reaction (PCR) and immunohistochemistry. The effects of E2F7 on cancer cell self‑renewal and epithelial-mesenchymal transition (EMT) were assessed using sphere formation and Transwell assays, respectively. In vivo tumorigenicity and metastasis were evaluated using xenograft models combined with extreme limiting dilution analysis to assess tumor-initiating capacity. Wnt/β‑catenin pathway activity was measured using T-cell factor optimal promoter luciferase reporter plasmid/far-from optimal promoter luciferase reporter plasmid (TOP/FOP) flash reporter assays. β‑Catenin expression, stability, and ubiquitination were examined via western blotting, cycloheximide chase assays, and ubiquitination assays. Protein-protein interactions among E2F7, β‑catenin, and glycogen synthase kinase 3 beta (GSK3β) were verified through co‑immunoprecipitation (Co‑IP), glutathione S‑transferase (GST) pull‑down, and immunofluorescence assays. Truncated mutants were generated to map the functional binding domains of E2F7. In vitro immunoprecipitation and kinase assays were further performed to confirm that E2F7 regulates GSK3β autophosphorylation and β‑catenin phosphorylation.</p><p><strong>Results: </strong>Bioinformatic analyses revealed that E2F7 was significantly upregulated in LUAD tissues, and elevated E2F7 expression correlated with poor patient prognosis. Functional assays demonstrated that E2F7 promoted LUAD cell self‑renewal and EMT. Mechanistically, cytoplasmic E2F7 directly associated with β‑catenin through its DNA‑binding domain (DBD) and PHA03247 domain. E2F7 modulated β‑catenin phosphorylation at Ser675 and Ser33/37/T41, thereby inhibiting ubiquitin‑mediated degradation and enhancing β‑catenin protein stability. Furthermore, E2F7 interacted with GSK3β and suppressed its autophosphorylation at Tyr216, concomitant with reduced β-catenin phosphorylation at Ser33/37/T41 and its accumulation.</p><p><strong>Conclusion: </strong>Collectively, these findings indicate that E2F7 drives LUAD malignant progression through regulation of the GSK3β/β‑catenin signaling axis and stabilization of β‑catenin. This study unveils a novel oncogenic mechanism of E2F7 in LUAD and identifies E2F7 as a promising therapeutic target for clinical intervention in LUAD.</p>","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning for early post-ESWL risk stratification of pancreatitis in chronic pancreatitis.","authors":"Sihuai Xiong, Wenda Sheng, Wenbin Zou, Nan Ru, Hui Chen, Hao Wu, Jun Pan, Bo Li, Lei Xin, Xinying Tang, Lianghao Hu, Zhendong Jin, Yiqi Du, Luowei Wang, Zhaoshen Li, Yangyang Qian, Zhuan Liao","doi":"10.1097/CM9.0000000000004320","DOIUrl":"10.1097/CM9.0000000000004320","url":null,"abstract":"","PeriodicalId":10183,"journal":{"name":"Chinese Medical Journal","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}