IF 10.7

MedComm Pub Date : 2025-09-03 DOI: 10.1002/mco2.70349

Guangyi Shen, Jiachen Liu, Yinhuai Wang, Zebin Deng, Fei Deng

{"title":"Ferroptosis in Cancer and Inflammatory Diseases: Mechanisms and Therapeutic Implications","authors":"Guangyi Shen, Jiachen Liu, Yinhuai Wang, Zebin Deng, Fei Deng","doi":"10.1002/mco2.70349","DOIUrl":"https://doi.org/10.1002/mco2.70349","url":null,"abstract":"Ferroptosis, an iron-dependent cell death pathway driven by lipid peroxidation, has emerged as a critical pathophysiological mechanism linking cancer and inflammatory diseases. The seemingly distinct pathologies exhibit shared microenvironmental hallmarks—oxidative stress, immune dysregulation, and metabolic reprogramming—that converge on ferroptosis regulation. This review synthesizes how ferroptosis operates at the intersection of these diseases, acting as both a tumor-suppressive mechanism and a driver of inflammatory tissue damage. In cancer, ferroptosis eliminates therapy-resistant cells but paradoxically facilitates metastasis through lipid peroxidation byproducts that remodel the tumor microenvironment and suppress antitumor immunity. In chronic inflammatory diseases—from atherosclerosis to rheumatoid arthritis—ferroptosis amplifies neuroinflammatory cascades while simultaneously exposing vulnerabilities for therapeutic targeting. Central to this duality are shared regulatory nodes, including nuclear factor kappa B-driven inflammation, NOD-like receptor family pyrin domain-containing 3 inflammasome activation, and GPX4 dysfunction. Therapeutically, ferroptosis induction shows promise against therapy-resistant cancers but risks exacerbating inflammatory damage, underscoring the need for precision modulation. Emerging strategies—nanoparticle-based inducers, immunotherapy combinations, and biomarker-guided patient stratification—aim to balance prodeath efficacy against off-target toxicity. By dissecting the ferroptosis–inflammation–cancer axis, this review provides a unified framework for understanding disease pathogenesis and advancing therapies for conditions resistant to conventional treatments. Future research must prioritize spatial mapping of ferroptosis dynamics, mechanistic crosstalk with immune checkpoints, and combinatorial regimens that exploit ferroptosis vulnerabilities while mitigating its inflammatory consequences.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70349","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144935267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HBV Precore G1896A Mutation Promotes Malignancy of Hepatocellular Carcinoma by Activating Endoplasmic Reticulum Stress to Enhance Aerobic Glycolysis HBV前孔G1896A突变通过激活内质网应激增强有氧糖酵解促进肝癌恶性发展

IF 10.7

MedComm Pub Date : 2025-09-03 DOI: 10.1002/mco2.70365

Baoxin Zhao, Hongxiu Qiao, Zhiyun Gao, Yan Zhao, Weijie Wang, Yan Cui, Fangxu Li, Yuping Wang, Zhanjun Guo, Xia Chuai, Sandra Chiu

{"title":"HBV Precore G1896A Mutation Promotes Malignancy of Hepatocellular Carcinoma by Activating Endoplasmic Reticulum Stress to Enhance Aerobic Glycolysis","authors":"Baoxin Zhao, Hongxiu Qiao, Zhiyun Gao, Yan Zhao, Weijie Wang, Yan Cui, Fangxu Li, Yuping Wang, Zhanjun Guo, Xia Chuai, Sandra Chiu","doi":"10.1002/mco2.70365","DOIUrl":"https://doi.org/10.1002/mco2.70365","url":null,"abstract":"Hepatitis B virus (HBV) precore G1896A mutation is closely associated with poor prognosis of liver disease. We previously revealed that the G1896A mutation could enhance HBV replication and promote hepatocellular carcinoma (HCC) cell growth both in vitro and in vivo. However, the in-depth mechanisms by which this mutation promotes the malignancy of HCC still need to be explored. Here, we examined the activation of endoplasmic reticulum (ER) stress and glycolysis in HBV G1896A mutation–associated HCC. Bioinformatics, chromatin immunoprecipitation assay and dual-luciferase assay were performed to give insight into the underlying molecular interaction between ER stress and glycolysis. Here, we observed that HBV G1896A mutation also promoted HCC cell invasion and migration. Furthermore, HBV G1896A mutation induced ER stress, and specifically, PERK-ATF4 pathway was responsible for the HCC cell malignancy. Mechanistically, PERK-ATF4 signaling induced transcriptional activation of PFKFB3, a key gene in the process of glycolysis. Finally, in vitro rescue experiments and in vivo efficacy studies revealed that the ATF4-PFKFB3 axis is necessary for the HCC tumor growth and metastasis. These results highlight that the ER stress and glycolysis are involved in the HCC-promotion function of HBV G1896A mutation, providing new insights into HBV-related HCC.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70365","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144935268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prevalence of Adverse Childhood Experiences and Long-Term Associations With Mental Health Among Adults: A Nationwide Cross-Sectional Study in China 儿童期不良经历的患病率及其与成人心理健康的长期关系：一项中国全国性的横断面研究

IF 10.7

MedComm Pub Date : 2025-09-01 DOI: 10.1002/mco2.70366

Yi Guo, Yibo Wu, Siyuan Fan, Haibo Wang

{"title":"Prevalence of Adverse Childhood Experiences and Long-Term Associations With Mental Health Among Adults: A Nationwide Cross-Sectional Study in China","authors":"Yi Guo, Yibo Wu, Siyuan Fan, Haibo Wang","doi":"10.1002/mco2.70366","DOIUrl":"https://doi.org/10.1002/mco2.70366","url":null,"abstract":"This study aimed to estimate the prevalence of adverse childhood experiences (ACEs) and explore their associations with mental health among Chinese adults. This population-based, cross-sectional survey was conducted in China in 2023. Data on participants' ACEs, depressive symptoms, anxiety symptoms, suicidal ideation, and other information were collected among participants who were selected using multi-stage stratified quota random sampling. Of 30,054 participants, 26.0% (7809/30,054) reported at least one ACE. The prevalence of major depression symptoms, moderate or severe anxiety symptoms, and suicidal ideation were 19.5%, 12.7%, and 21.7%, respectively. There was a dose‒response relationship between the cumulative number of ACEs and mental health among Chinese adults. Compared to those with no ACEs, the adjusted odds ratios (ORs) and 95% confidence interval for major depression symptoms were 1 ACE: 1.340 (1.226‒1.465), 2 ACEs: 1.769 (1.588‒1.971), 3 ACEs: 2.172 (1.909‒2.472), and ≥4 ACEs: 3.084 (2.712‒3.507). The ORs for anxiety symptoms of 1, 2, 3, and ≥4 ACEs were 1.262 (1.135‒1.403), 1.714 (1.513‒1.942), 2.119 (1.831‒2.452), and 2.890 (2.512‒3.325). The ORs for suicidal ideation were 1.056 (0.966‒1.154), 1.324 (1.188‒1.477), 1.470 (1.287‒1.679), and 3.134 (2.761‒3.557). Sexual abuse survivors were at great risk for mental health problems. Comprehensive measures are needed to support populations affected by ACEs.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70366","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144927563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Preconditioning With TGF-β Inhibitors Enhances Therapeutic Efficacy of Endothelial Progenitor Cells for Wound Healing in Diabetic Mice TGF-β抑制剂预处理增强内皮祖细胞对糖尿病小鼠创面愈合的治疗作用

IF 10.7

MedComm Pub Date : 2025-09-01 DOI: 10.1002/mco2.70364

Dongsheng Su, Fuyi Cheng, Qingyuan Jiang, Yong Zhang, Fei Du, Cheng Pan, Yixin Ye, Lin Zhang, Pusong Zhao, Huilin Wang, Qi Xiong, Xiaolan Su, Hongxin Deng

{"title":"Preconditioning With TGF-β Inhibitors Enhances Therapeutic Efficacy of Endothelial Progenitor Cells for Wound Healing in Diabetic Mice","authors":"Dongsheng Su, Fuyi Cheng, Qingyuan Jiang, Yong Zhang, Fei Du, Cheng Pan, Yixin Ye, Lin Zhang, Pusong Zhao, Huilin Wang, Qi Xiong, Xiaolan Su, Hongxin Deng","doi":"10.1002/mco2.70364","DOIUrl":"https://doi.org/10.1002/mco2.70364","url":null,"abstract":"Diabetic wound (DW) represent a common complication of diabetes. Despite advances in regenerative repair utilizing endothelial progenitor cells (EPCs), challenges such as low survival and impaired angiogenic function of EPCs remain. Herein, we explored an effective method to induce injury-induced protection for EPCs and improves their function. This was achieved through cell preconditioning under conditions of nutrient deprivation and high glucose (NDHG), combined with sb431542, a transforming growth factor beta (TGF-β) signaling inhibitor. Specifically, after three generations of cell passage during preconditioning, umbilical cord-derived endothelial cells (ECs) exhibited characteristics resembling those of EPCs, with over 80% of the cells expressed CD34, a typical marker of EPCs. Notably, these preconditioned EPC-like cells (pEPCs) showed tolerance to pathological environment, as evidenced by robust cell viability, improved antioxidant capacity, and stable tube-forming ability under NDHG condition. The protective effect of preconditioning in pEPCs is partly achieved by activating the PI3K/AKT pathway to upregulate the expression of Nrf2 and HIF-1α. Importantly, pEPCs exhibited therapeutic potential in two diabetic mouse models-limb ischemia and skin wounds by enhancing blood vessel formation and facilitating tissue repair. Overall, this preconditioning method induced the generation of functionally enhanced pEPCs, providing an alternative source of cells for treating DWs.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70364","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144927564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PARP (Poly ADP-ribose Polymerase) Family in Health and Disease PARP（聚adp核糖聚合酶）家族与健康和疾病

IF 10.7

MedComm Pub Date : 2025-09-01 DOI: 10.1002/mco2.70314

Pengyuan Lei, Wenfeng Li, Jinhua Luo, Nanxin Xu, Yahe Wang, Dafei Xie, Hua Guan, Bo Huang, Xin Huang, Pingkun Zhou

{"title":"PARP (Poly ADP-ribose Polymerase) Family in Health and Disease","authors":"Pengyuan Lei, Wenfeng Li, Jinhua Luo, Nanxin Xu, Yahe Wang, Dafei Xie, Hua Guan, Bo Huang, Xin Huang, Pingkun Zhou","doi":"10.1002/mco2.70314","DOIUrl":"https://doi.org/10.1002/mco2.70314","url":null,"abstract":"The poly(ADP-ribose) polymerase (PARP) family consists of 17 members of nicotinamide adenine dinucleotide (NAD⁺)-dependent enzymes that regulate key biological processes by catalyzing adenosine diphosphate (ADP)-ribosylation, either poly(ADP-ribosyl)ation (PARylation) or mono(ADP-ribosyl)ation (MARylation). These biological processes encompass DNA repair, metabolism, telomere maintenance, and immune responses. Based on structural and functional features, the PARP family is classified into subcategories, such as DNA-dependent PARPs, Tankyrase, CCCH-type PARPs, MacroPARPs, and atypical PARPs. These enzymes dynamically maintain genome stability through mechanisms, including base excision repair and homologous recombination, while also regulating telomere dynamics and metabolic pathways. Dysregulation of PARP activity is implicated in the pathogenesis of diverse human diseases. Though PARP inhibitors have gained therapeutic interest in oncology, their wider roles in nononcological conditions, such as neurodegenerative diseases, cardiovascular disorders, and viral infections, remain poorly defined. This review elucidates the unique structural features of PARP family members and describes their multiple roles under physiological and pathological conditions, thus providing insights into treatment strategies. Additionally, it summarizes the advances and challenges in PARP-targeted therapies and explores future directions for innovative therapeutic approaches. The findings may serve as a valuable resource for informing both clinical research and drug development.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70314","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144927569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetic Regulation of Aging and its Rejuvenation 衰老及其返老还衰的表观遗传调控

IF 10.7

MedComm Pub Date : 2025-09-01 DOI: 10.1002/mco2.70369

Yongpan An, Qian Wang, Ke Gao, Chi Zhang, Yanan Ouyang, Ruixiao Li, Zhou Ma, Tong Wu, Lifan Zhou, Zhengwei Xie, Rui Zhang, Guojun Wu

{"title":"Epigenetic Regulation of Aging and its Rejuvenation","authors":"Yongpan An, Qian Wang, Ke Gao, Chi Zhang, Yanan Ouyang, Ruixiao Li, Zhou Ma, Tong Wu, Lifan Zhou, Zhengwei Xie, Rui Zhang, Guojun Wu","doi":"10.1002/mco2.70369","DOIUrl":"https://doi.org/10.1002/mco2.70369","url":null,"abstract":"Aging increases the global burden of disease, yet its molecular basis remains incompletely understood. Recent studies indicate that reversible epigenetic drift—spanning DNA methylation clocks, histone codes, three-dimensional chromatin, and noncoding RNA networks—constitutes a central regulator of organismal decline and age-related diseases. How these epigenetic layers interact across different tissues—and how best to translate them into therapeutic strategies—are still open questions. This review outlines the specific mechanisms by which epigenetic changes influence aging, highlighting their impact on genomic instability, stem-cell exhaustion, and mitochondrial dysfunction. We critically evaluate emerging rejuvenation strategies—partial OSKM reprogramming, CRISPR–dCas9 epigenome editing, NAD⁺/sirtuin boosters, HDAC inhibitors, microbiota transfer, and precision lifestyle interventions—detailing their efficacy in resetting epigenetic age and restoring tissue homeostasis. Integrating single-cell multiomics and second-generation epigenetic clocks, we propose a roadmap for translating these insights into safe, personalized antiaging medicine.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70369","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144927565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Repurposing Mercaptopurine Through Collateral Lethality to Treat Cancers with Somatic RB1–NUDT15 Loss 巯基嘌呤通过侧枝致死性治疗躯体RB1-NUDT15缺失的癌症

IF 10.7

MedComm Pub Date : 2025-09-01 DOI: 10.1002/mco2.70361

Tao Zhou, Huayun Yan, Dandan Yin, Yun Deng, Huancheng Fu, Zichen Zhao, Shuang Li, Xiaoxi Lu, Yiqi Deng, Hai-Ning Chen, Wei-Han Zhang, Yunying Shi, Yangjuan Bai, Bei Cai, Lanlan Wang, Zhaoqian Liu, Wei Zhang, Lili Jiang, Yang Shu, Bo Liu, Yan Zhang, Heng Xu

{"title":"Repurposing Mercaptopurine Through Collateral Lethality to Treat Cancers with Somatic RB1–NUDT15 Loss","authors":"Tao Zhou, Huayun Yan, Dandan Yin, Yun Deng, Huancheng Fu, Zichen Zhao, Shuang Li, Xiaoxi Lu, Yiqi Deng, Hai-Ning Chen, Wei-Han Zhang, Yunying Shi, Yangjuan Bai, Bei Cai, Lanlan Wang, Zhaoqian Liu, Wei Zhang, Lili Jiang, Yang Shu, Bo Liu, Yan Zhang, Heng Xu","doi":"10.1002/mco2.70361","DOIUrl":"https://doi.org/10.1002/mco2.70361","url":null,"abstract":"Somatic retinoblastoma 1 (RB1) loss is prevalent across different cancer types and is enriched in treatment-refractory tumors, such as castration-resistant prostate cancer (CRPC) and small-cell lung cancer, but cannot be considered as a direct druggable target. In this study, we revealed that the close proximity of nudix hydrolase 15 (NUDT15) and RB1 may result in their common somatic codeletion or epigenomic cosilencing in different cancer types and subsequent significant positive correlations of their expressions at the bulk transcriptional and single-cell levels. With clinical CRPC samples, co-loss of RB1 and NUDT15 were commonly observed (14 out of 21). Due to the contribution of NUDT15 deficiency to thiopurine-induced toxicity, exploiting a vulnerability conferred by RB1–NUDT15 loss raised the possibility of repurposing thiopurine (e.g., mercaptopurine) for precise therapeutics. A positive relationship between RB1/NUDT15 ploidy score and mercaptopurine drug sensitivity was found in 543 cancer cell lines. Experimentally, knocking-down NUDT15 sensitizes the cancer cell lines to mercaptopurine treatment by inhibiting cell cycle progression and increasing apoptosis, but does not induce mercaptopurine-related leucopenia in xenograft model. Our study elucidates the molecular basis for precise mercaptopurine therapy in RB1-deficient tumors and demonstrates how leveraging collateral lethality alongside drug repurposing uncovers targetable vulnerabilities in stratified patient cohorts.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70361","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144927568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Polarization of Tumor Cells and Tumor-Associated Macrophages: Molecular Mechanisms and Therapeutic Targets 肿瘤细胞和肿瘤相关巨噬细胞的极化：分子机制和治疗靶点

IF 10.7

MedComm Pub Date : 2025-09-01 DOI: 10.1002/mco2.70372

Guohao Wei, Bin Li, Mengyang Huang, Mengyao Lv, Zihui Liang, Chuandong Zhu, Lilin Ge, Jing Chen

{"title":"Polarization of Tumor Cells and Tumor-Associated Macrophages: Molecular Mechanisms and Therapeutic Targets","authors":"Guohao Wei, Bin Li, Mengyang Huang, Mengyao Lv, Zihui Liang, Chuandong Zhu, Lilin Ge, Jing Chen","doi":"10.1002/mco2.70372","DOIUrl":"https://doi.org/10.1002/mco2.70372","url":null,"abstract":"Tumor-associated macrophages (TAMs) are prominent constituents of solid tumors, and their prevalence is often associated with poor clinical outcomes. These highly adaptable immune cells undergo dynamic functional changes within the immunosuppressive tumor microenvironment (TME), engaging in reciprocal interactions with malignant cells. This bidirectional communication facilitates concurrent phenotypic transformation: tumor cells shift toward invasive mesenchymal states, whereas TAMs develop immunosuppressive, pro-tumorigenic traits. Increasing evidence highlights metabolic reprogramming, characterized by dysregulation of lipid metabolism, amino acid utilization, and glycolytic activity, as the fundamental molecular basis orchestrating this pathological symbiosis. However, a comprehensive understanding of how metabolic reprogramming specifically coordinates the mutual polarization of tumor cells and TAMs is lacking. This review thoroughly examines the molecular mechanisms governing this co-polarization process, detailing critical transcriptional regulators, essential signaling pathways, and the maintenance of adaptive phenotypes within the TME. Furthermore, this review critically assesses promising therapeutic strategies aimed at disrupting this alliance, including the use of metabolically targeted agents, engineered chimeric antigen receptor macrophages, and TAM-selective nanoparticle delivery systems. These insights provide a crucial foundation for the development of next-generation cancer immunotherapies focused on reprogramming pathological polarization dynamics to overcome treatment resistance and improve clinical outcomes.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70372","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144927310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pleural Mesothelioma: Pathogenesis, Diagnosis, Treatment, Prognosis, and Survival 胸膜间皮瘤：发病、诊断、治疗、预后和生存

IF 10.7

MedComm Pub Date : 2025-09-01 DOI: 10.1002/mco2.70327

Libo Zhang, Meijuan Huang

{"title":"Pleural Mesothelioma: Pathogenesis, Diagnosis, Treatment, Prognosis, and Survival","authors":"Libo Zhang, Meijuan Huang","doi":"10.1002/mco2.70327","DOIUrl":"https://doi.org/10.1002/mco2.70327","url":null,"abstract":"Pleural mesothelioma (PM) presents significant challenges in clinical management, with current treatment options such as chemotherapy, anti-angiogenic therapies, and immunotherapies only modestly extending progression-free survival (PFS) and overall survival (OS). Another relevant reason is the absence of subsequent-line therapy strategies following progression of PM after approved therapy. Despite extensive research efforts, the development of effective targeted therapies has proven difficult, as most identified mutations in PM tend to be tumor suppressors rather than the driving mutations seen in other cancers. This review aims to provide an in-depth analysis of the biological mechanisms of PM, focusing on genetic alterations, the tumor's immune microenvironment, and dysregulated signaling pathways that contribute to tumorigenesis and resistance to treatment. Additionally, we discuss the growing importance of biomarkers for patient stratification and the development of personalized therapeutic approaches tailored to individual molecular profiles. We also explore promising avenues for novel therapeutic strategies, such as combination therapies and immunotherapeutic interventions. By integrating insights from both basic and clinical research, this review seeks to present a comprehensive framework for understanding PM and advancing its therapeutic management, ultimately aiming to improve patient outcomes through more effective and targeted treatment approaches.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70327","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144927566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cancer Immunotherapy in Combination with Radiotherapy and/or Chemotherapy: Mechanisms and Clinical Therapy 癌症免疫治疗联合放疗和/或化疗：机制和临床治疗

IF 10.7

MedComm Pub Date : 2025-08-31 DOI: 10.1002/mco2.70346

Xinmin Wang, Jing Jing

{"title":"Cancer Immunotherapy in Combination with Radiotherapy and/or Chemotherapy: Mechanisms and Clinical Therapy","authors":"Xinmin Wang, Jing Jing","doi":"10.1002/mco2.70346","DOIUrl":"https://doi.org/10.1002/mco2.70346","url":null,"abstract":"Since the United States Food and Drug Administration approved the first immune checkpoint inhibitor ipilimumab for metastatic melanoma in 2011, ICIs have been approved for a range of cancers and significantly improving treatment outcomes. However, the objective response rate of ICI monotherapy remains modest (10–40%), with clinical benefit observed in only 15–20% of patients. The limited efficacy of ICIs in many patients is often attributed to poorly immunogenic (“cold”) tumors. Radiotherapy and chemotherapy exhibit immunomodulatory properties that can enhance tumor immunogenicity. These effects provide a rationale for combining ICIs with conventional therapies. Current research lacks systematic synthesis and consistent clinical evidence on the immunomodulatory effects of radio/chemotherapy, and the optimal selection and sequencing of radio/chemotherapy with immunotherapy remain unclear, limiting the optimization of combination strategies with immunotherapy. This review outlines the current landscape of cancer immunotherapy and elucidates the immunomodulatory effects of radiotherapy and chemotherapy that form the basis for combination strategies. It further summarizes clinical advances in combined modalities and discusses associated toxicities, management approaches, and potential predictive biomarkers. This review provides a comprehensive framework for understanding and optimizing radio/chemo-immunotherapy by integrating mechanistic insights with clinical evidence to guide future personalized cancer treatment strategies.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 9","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70346","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144923381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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