Frontiers of Medicine最新文献_第3页

Non small cell lung cancer with SMARCA4 deficiency harboring rare EGFR mutations exhibited significant tumor response when treated with afatinib: a case report. 携带罕见EGFR突变的SMARCA4缺乏症的非小细胞肺癌在使用阿法替尼治疗时表现出显著的肿瘤反应：一份病例报告。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2025-02-01 Epub Date: 2025-01-14 DOI: 10.1007/s11684-024-1118-y

Xiaotong Qiu, Liangkun You, Chongwei Wang, Jin Sheng

引用次数: 0

Mitochondrial-associated programmed-cell-death patterns for predicting the prognosis of non-small-cell lung cancer. 用于预测非小细胞肺癌预后的线粒体相关程序性细胞死亡模式。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2025-02-01 Epub Date: 2024-11-22 DOI: 10.1007/s11684-024-1093-3

Xueyan Shi, Sichong Han, Guizhen Wang, Guangbiao Zhou

{"title":"Mitochondrial-associated programmed-cell-death patterns for predicting the prognosis of non-small-cell lung cancer.","authors":"Xueyan Shi, Sichong Han, Guizhen Wang, Guangbiao Zhou","doi":"10.1007/s11684-024-1093-3","DOIUrl":"10.1007/s11684-024-1093-3","url":null,"abstract":"Mitochondria are the convergence point of multiple pathways that trigger programmed cell death (PCD). Mitochondrial-associated PCD (mtPCD) is involved in the pathogenesis of several diseases. However, the role of mtPCD in the prognostic prediction of cancers including non-small-cell lung cancer (NSCLC) remains to be investigated. Here, 12 mtPCD patterns were analyzed in transcriptomics, genomics, and clinical data collected from 4 datasets containing 977 patients. A risk-score assessment system containing 18 genes was established. We found that NSCLC patients with a high-risk score had a poorer prognosis. A nomogram was constructed by incorporating the risk score with clinical features. The risk score was further associated with clinicopathological information, tumor-mutation frequency, and immunotherapy responses. NSCLC patients with a high risk score had more Treg cells infiltration. However, these patients had higher tumor-mutation burden scores and may be more sensitive to immunotherapy. Moreover, receptor-interacting serine/threonine protein kinase 2 (RIPK2) was selected from mtPCD gene model for validation. We found that RIPK2 exhibited oncogenic function, and its expression level was inversely associated with the overall survival of NSCLC. Taken together, our results indicated the accuracy and practicability of the mtPCD gene model and RIPK2 in predicting the prognosis of NSCLC.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"101-120"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686518","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}

引用次数: 0

TRIM4 modulates the ubiquitin-mediated degradation of hnRNPDL and weakens sensitivity to CDK4/6 inhibitor in ovarian cancer. TRIM4在卵巢癌中调节泛素介导的hnRNPDL降解并减弱对CDK4/6抑制剂的敏感性。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2025-02-01 Epub Date: 2024-12-07 DOI: 10.1007/s11684-024-1103-5

Xiaoxia Che, Xin Guan, Yiyin Ruan, Lifei Shen, Yuhong Shen, Hua Liu, Chongying Zhu, Tianyu Zhou, Yiwei Wang, Weiwei Feng

{"title":"TRIM4 modulates the ubiquitin-mediated degradation of hnRNPDL and weakens sensitivity to CDK4/6 inhibitor in ovarian cancer.","authors":"Xiaoxia Che, Xin Guan, Yiyin Ruan, Lifei Shen, Yuhong Shen, Hua Liu, Chongying Zhu, Tianyu Zhou, Yiwei Wang, Weiwei Feng","doi":"10.1007/s11684-024-1103-5","DOIUrl":"10.1007/s11684-024-1103-5","url":null,"abstract":"Ovarian cancer is the most lethal malignancy affecting the female reproductive system. Pharmacological inhibitors targeting CDK4/6 have demonstrated promising efficacy across various cancer types. However, their clinical benefits in ovarian cancer patients fall short of expectations, with only a subset of patients experiencing these advantageous effects. This study aims to provide further clinical and biological evidence for antineoplastic effects of a CDK4/6 inhibitor (TQB4616) in ovarian cancer and explore underlying mechanisms involved. Patient-derived ovarian cancer organoid models were established to evaluate the effectiveness of TQB3616. Potential key genes related to TQB3616 sensitivity were identified through RNA-seq analysis, and TRIM4 was selected as a candidate gene for further investigation. Subsequently, co-immunoprecipitation and GST pull-down assays confirmed that TRIM4 binds to hnRNPDL and promotes its ubiquitination through RING and B-box domains. RIP assay demonstrated that hnRNPDL binded to CDKN2C isoform 2 and suppressed its expression by alternative splicing. Finally, in vivo studies confirmed that the addition of siTRIM4 significantly improved the effectiveness of TQB3616. Overall, our findings suggest that TRIM4 modulates ubiquitin-mediated degradation of hnRNPDL and weakens sensitivity to CDK4/6 inhibitors in ovarian cancer treatment. TRIM4 may serve as a valuable biomarker for predicting sensitivity to CDK4/6 inhibitors in ovarian cancer.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"121-133"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791662","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}

引用次数: 0

CHAF1B promotes the progression of lung squamous-cell carcinoma by inhibiting SETD7 expression. CHAF1B通过抑制SETD7的表达促进肺鳞状细胞癌的进展。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2025-01-25 DOI: 10.1007/s11684-024-1122-2

Zhuo Zheng, Yongfang Lin, Hua Guo, Zheng Liu, Xiaoliang Jie, Guizhen Wang, Guangbiao Zhou

{"title":"CHAF1B promotes the progression of lung squamous-cell carcinoma by inhibiting SETD7 expression.","authors":"Zhuo Zheng, Yongfang Lin, Hua Guo, Zheng Liu, Xiaoliang Jie, Guizhen Wang, Guangbiao Zhou","doi":"10.1007/s11684-024-1122-2","DOIUrl":"https://doi.org/10.1007/s11684-024-1122-2","url":null,"abstract":"The p60 subunit of the chromatin assembly factor-1 complex, that is, chromatin assembly factor-1 subunit B (CHAF1B), is a histone H3/H4 chaperone crucial for the transcriptional regulation of cell differentiation and self-renewal. CHAF1B is overexpressed in several cancers and may represent a potential target for cancer therapy. However, its expression and clinical significance in lung squamous-cell carcinoma (LUSC) remain unclear. In this study, we performed weighted gene correlation network analysis to analyze the Gene Expression Omnibus GSE68793 LUSC dataset and identified CHAF1B as one of the most important driver gene candidates. Immunohistochemical analysis of 126 LUSC tumor samples and 80 adjacent normal lung tissues showed the marked upregulation of CHAF1B in tumor tissues and the negative association of its expression level with patient survival outcomes. Silencing of CHAF1B suppressed LUSC proliferation in vitro and LUSC tumor growth in vivo. Furthermore, bulk RNA sequencing of CHAF1B knockdown cells indicated SET domain containing 7 (SETD7) as a significant CHAF1B target gene. In addition, CHAF1B competitively binds to the SETD7 promoter region and represses its transcription. Altogether, these results imply that CHAF1B plays a vital role in LUSC tumorigenesis and may represent a potential molecular target for this deadly disease.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037894","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}

引用次数: 0

Intracellular concentration of ADA2 is a marker for monocyte differentiation and activation. 细胞内ADA2浓度是单核细胞分化和活化的标志。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2025-01-20 DOI: 10.1007/s11684-024-1110-6

Liang Dong, Bingtai Lu, Wenwen Luo, Xiaoqiong Gu, Chengxiang Wu, Luca Trotta, Mikko Seppanen, Yuxia Zhang, Andrey V Zavialov

{"title":"Intracellular concentration of ADA2 is a marker for monocyte differentiation and activation.","authors":"Liang Dong, Bingtai Lu, Wenwen Luo, Xiaoqiong Gu, Chengxiang Wu, Luca Trotta, Mikko Seppanen, Yuxia Zhang, Andrey V Zavialov","doi":"10.1007/s11684-024-1110-6","DOIUrl":"https://doi.org/10.1007/s11684-024-1110-6","url":null,"abstract":"Adenosine, a critical molecule regulating cellular function both inside and outside cells, is controlled by two human adenosine deaminases: ADA1 and ADA2. While ADA1 primarily resides in the cytoplasm, ADA2 can be transported to lysosomes within cells or secreted outside the cell. Patients with ADA2 deficiency (DADA2) often suffer from systemic vasculitis due to elevated levels of TNF-α in their blood. Monocytes from DADA2 patients exhibit excessive TNF-α secretion and differentiate into pro-inflammatory M1-type macrophages. Our findings demonstrate that ADA2 localizes to endolysosomes within macrophages, and its intracellular concentration decreases in cells secreting TNF-α. This suggests that ADA2 may function as a lysosomal adenosine deaminase, regulating TNF-α expression by the cells. Interestingly, pneumonia patients exhibit higher ADA2 concentrations in their bronchoalveolar lavage (BAL), correlating with elevated pro-inflammatory cytokine levels. Conversely, cord blood has low ADA2 levels, creating a more immunosuppressive environment. Additionally, secreted ADA2 can bind to apoptotic cells, activating immune cells by reducing extracellular adenosine levels. These findings imply that ADA2 release from monocytes during inflammation, triggered by growth factors, may be crucial for cell activation. Targeting intracellular and extracellular ADA2 activities could pave the way for novel therapies in inflammatory and autoimmune disorders.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003834","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}

引用次数: 0

Inhibition of cap-dependent endonuclease in influenza virus with ADC189: a pre-clinical analysis and phase I trial. ADC189抑制流感病毒帽盖依赖性核酸内切酶：临床前分析和I期试验

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2025-01-20 DOI: 10.1007/s11684-024-1115-1

Jing Wei, Yaping Deng, Xiaoyun Zhu, Xin Xiao, Yang Yang, Chunlei Tang, Jian Chen

{"title":"Inhibition of cap-dependent endonuclease in influenza virus with ADC189: a pre-clinical analysis and phase I trial.","authors":"Jing Wei, Yaping Deng, Xiaoyun Zhu, Xin Xiao, Yang Yang, Chunlei Tang, Jian Chen","doi":"10.1007/s11684-024-1115-1","DOIUrl":"https://doi.org/10.1007/s11684-024-1115-1","url":null,"abstract":"ADC189 is a novel drug of cap-dependent endonuclease inhibitor. In our study, its antiviral efficacy was evaluated in vitro and in vivo, and compared with baloxavir marboxil and oseltamivir. A first-in-human phase I study in healthy volunteers included single ascending dose (SAD) and food effect (FE) parts. In the preclinical study, ADC189 showed potent antiviral activity against various types of influenza viruses, including H1N1, H3N2, influenza B virus, and highly pathogenic avian influenza, comparable to baloxavir marboxil. Additionally, ADC189 exhibited much better antiviral efficacy than oseltamivir in H1N1 infected mice. In the phase I study, ADC189 was rapidly metabolized to ADC189-I07, and its exposure increased proportionally with the dose. The terminal elimination half-life (T1/2) ranged from 76.69 to 98.28 hours. Of note, food had no effect on the concentration, clearance, and exposure of ADC189. It was well tolerated, with few treatment-emergent adverse events (TEAEs) reported and no serious adverse events (SAEs). ADC189 demonstrated excellent antiviral efficacy both in vitro and in vivo. It was safe, well-tolerated, and had favorable pharmacokinetic characteristics in healthy volunteers, supporting its potential for single oral dosing in clinical practice.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003832","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}

引用次数: 0

Cardiomyocyte-specific long noncoding RNA Trdn-as induces mitochondrial calcium overload by promoting the m⁶A modification of calsequestrin 2 in diabetic cardiomyopathy. 心肌细胞特异性长链非编码RNA Trdn-as在糖尿病心肌病中通过促进钙sequestrin 2的m6A修饰诱导线粒体钙超载

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2025-01-17 DOI: 10.1007/s11684-024-1102-6

Xiaohan Li, Ling Liu, Han Lou, Xinxin Dong, Shengxin Hao, Zeqi Sun, Zijia Dou, Huimin Li, Wenjie Zhao, Xiuxiu Sun, Xin Liu, Yong Zhang, Baofeng Yang

{"title":"Cardiomyocyte-specific long noncoding RNA Trdn-as induces mitochondrial calcium overload by promoting the m6A modification of calsequestrin 2 in diabetic cardiomyopathy.","authors":"Xiaohan Li, Ling Liu, Han Lou, Xinxin Dong, Shengxin Hao, Zeqi Sun, Zijia Dou, Huimin Li, Wenjie Zhao, Xiuxiu Sun, Xin Liu, Yong Zhang, Baofeng Yang","doi":"10.1007/s11684-024-1102-6","DOIUrl":"https://doi.org/10.1007/s11684-024-1102-6","url":null,"abstract":"Diabetic cardiomyopathy (DCM) is a medical condition characterized by cardiac remodeling and dysfunction in individuals with diabetes mellitus. Sarcoplasmic reticulum (SR) and mitochondrial Ca2+ overload in cardiomyocytes have been recognized as biological hallmarks in DCM; however, the specific factors underlying these abnormalities remain largely unknown. In this study, we aimed to investigate the role of a cardiac-specific long noncoding RNA, D830005E20Rik (Trdn-as), in DCM. Our results revealed the remarkably upregulation of Trdn-as in the hearts of the DCM mice and cardiomyocytes treated with high glucose (HG). Knocking down Trdn-as in cardiac tissues significantly improved cardiac dysfunction and remodeling in the DCM mice. Conversely, Trdn-as overexpression resulted in cardiac damage resembling that observed in the DCM mice. At the cellular level, Trdn-as induced Ca2+ overload in the SR and mitochondria, leading to mitochondrial dysfunction. RNA-seq and bioinformatics analyses identified calsequestrin 2 (Casq2), a primary calcium-binding protein in the junctional SR, as a potential target of Trdn-as. Further investigations revealed that Trdn-as facilitated the recruitment of METTL14 to the Casq2 mRNA, thereby enhancing the m6A modification of Casq2. This modification increased the stability of Casq2 mRNA and subsequently led to increased protein expression. When Casq2 was knocked down, the promoting effects of Trdn-as on Ca2+ overload and mitochondrial damage were mitigated. These findings provide valuable insights into the pathogenesis of DCM and suggest Trdn-as as a potential therapeutic target for this condition.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143003686","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}

引用次数: 0

Metabolism and metabolomics in senescence, aging, and age-related diseases: a multiscale perspective. 衰老、衰老和年龄相关疾病的代谢和代谢组学：多尺度视角。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2025-01-17 DOI: 10.1007/s11684-024-1116-0

Ziyi Wang, Hongying Zhu, Wei Xiong

引用次数: 0

The novel anthraquinone compound Kanglexin prevents endothelial-to-mesenchymal transition in atherosclerosis by activating FGFR1 and suppressing integrin β1/TGFβ signaling. 新型蒽醌化合物Kanglexin通过激活FGFR1和抑制整合素β1/TGFβ信号传导，防止动脉粥样硬化中的内皮细胞向间质转化。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2024-12-01 Epub Date: 2024-10-21 DOI: 10.1007/s11684-024-1077-3

Yixiu Zhao, Zhiqi Wang, Jing Ren, Huan Chen, Jia Zhu, Yue Zhang, Jiangfei Zheng, Shifeng Cao, Yanxi Li, Xue Liu, Na An, Tao Ban, Baofeng Yang, Yan Zhang

{"title":"The novel anthraquinone compound Kanglexin prevents endothelial-to-mesenchymal transition in atherosclerosis by activating FGFR1 and suppressing integrin β1/TGFβ signaling.","authors":"Yixiu Zhao, Zhiqi Wang, Jing Ren, Huan Chen, Jia Zhu, Yue Zhang, Jiangfei Zheng, Shifeng Cao, Yanxi Li, Xue Liu, Na An, Tao Ban, Baofeng Yang, Yan Zhang","doi":"10.1007/s11684-024-1077-3","DOIUrl":"10.1007/s11684-024-1077-3","url":null,"abstract":"Endothelial-mesenchymal transition (EndMT) disrupts vascular endothelial integrity and induces atherosclerosis. Active integrin β1 plays a pivotal role in promoting EndMT by facilitating TGFβ/Smad signaling in endothelial cells. Here, we report a novel anthraquinone compound, Kanglexin (KLX), which prevented EndMT and atherosclerosis by activating MAP4K4 and suppressing integrin β1/TGFβ signaling. First, KLX effectively counteracted the EndMT phenotype and mitigated the dysregulation of endothelial and mesenchymal markers induced by TGFβ1. Second, KLX suppressed TGFβ/Smad signaling by inactivating integrin β1 and inhibiting the polymerization of TGFβR1/2. The underlying mechanism involved the activation of FGFR1 by KLX, resulting in the phosphorylation of MAP4K4 and Moesin, which led to integrin β1 inactivation by displacing Talin from its β-tail. Oral administration of KLX effectively stimulated endothelial FGFR1 and inhibited integrin β1, thereby preventing vascular EndMT and attenuating plaque formation and progression in the aorta of atherosclerotic Apoe-/- mice. Notably, KLX (20 mg/kg) exhibited superior efficacy compared with atorvastatin, a clinically approved lipid-regulating drug. In conclusion, KLX exhibited potential in ameliorating EndMT and retarding the formation and progression of atherosclerosis through direct activation of FGFR1. Therefore, KLX is a promising candidate for the treatment of atherosclerosis to mitigate vascular endothelial injury.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"1068-1086"},"PeriodicalIF":3.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142462768","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}

引用次数: 0

Novel perspectives on the link between obesity and cancer risk: from mechanisms to clinical implications. 肥胖与癌症风险之间联系的新视角：从机制到临床影响。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2024-12-01 Epub Date: 2024-11-14 DOI: 10.1007/s11684-024-1094-2

Xiaoye Shi, Aimin Jiang, Zhengang Qiu, Anqi Lin, Zaoqu Liu, Lingxuan Zhu, Weiming Mou, Quan Cheng, Jian Zhang, Kai Miao, Peng Luo

{"title":"Novel perspectives on the link between obesity and cancer risk: from mechanisms to clinical implications.","authors":"Xiaoye Shi, Aimin Jiang, Zhengang Qiu, Anqi Lin, Zaoqu Liu, Lingxuan Zhu, Weiming Mou, Quan Cheng, Jian Zhang, Kai Miao, Peng Luo","doi":"10.1007/s11684-024-1094-2","DOIUrl":"10.1007/s11684-024-1094-2","url":null,"abstract":"Existing epidemiologic and clinical studies have demonstrated that obesity is associated with the risk of a variety of cancers. In recent years, an increasing number of experimental and clinical studies have unraveled the complex relationship between obesity and cancer risk and the underlying mechanisms. Obesity-induced abnormalities in immunity and biochemical metabolism, including chronic inflammation, hormonal disorders, dysregulation of adipokines, and microbial dysbiosis, may be important contributors to cancer development and progression. These contributors play different roles in cancer development and progression at different sites. Lifestyle changes, weight loss medications, and bariatric surgery are key approaches for weight-centered, obesity-related cancer prevention. Treatment of obesity-related inflammation and hormonal or metabolic dysregulation with medications has also shown promise in preventing obesity-related cancers. In this review, we summarize the mechanisms through which obesity affects the risk of cancer at different sites and explore intervention strategies for the prevention of obesity-associated cancers, concluding with unresolved questions and future directions regarding the link between obesity and cancer. The aim is to provide valuable theoretical foundations and insights for the in-depth exploration of the complex relationship between obesity and cancer risk and its clinical applications.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"945-968"},"PeriodicalIF":3.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618183","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}

引用次数: 0