MedCommPub Date : 2025-10-03DOI: 10.1002/mco2.70391
Zhaoyun Liu, Jiao Lai, Ziyu Ma, Jianhua Pan, Chun Yang, Rong Fu
{"title":"Targeting the Ubiquitin–Proteasome System for Cancer","authors":"Zhaoyun Liu, Jiao Lai, Ziyu Ma, Jianhua Pan, Chun Yang, Rong Fu","doi":"10.1002/mco2.70391","DOIUrl":"https://doi.org/10.1002/mco2.70391","url":null,"abstract":"<p>Ubiquitin is a highly conserved small molecule that exists in large quantities in eukaryotic cells and plays a crucial role in protein quality control by phagocytosis and degradation of ubiquitin-modified proteins. The abnormal expression of the ubiquitin–proteasome system (UPS) in cancer leads to the abnormal expression of ubiquitin ligases and ubiquitin-binding enzymes, resulting in the abnormal accumulation of ubiquitinated proteins. Consequently, UPS dysregulation can contribute to tumor initiation, progression, and resistance to therapy. While proteasome inhibitors have shown clinical success, comprehensive reviews integrating upstream UPS components and their therapeutic potential are lacking. This paper reviews the composition of the UPS, its tumor-promoting mechanisms, as well as the small molecule inhibitors and proteasome inhibitors based on this system, including their mechanisms of action and adverse effects, and explores their clinical advances in the treatment of cancer. This review provides a valuable framework for developing next-generation anti-cancer therapies and establishes the UPS as a critical therapeutic target for precision oncology.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70391","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224073","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}
MedCommPub Date : 2025-09-30DOI: 10.1002/mco2.70397
{"title":"Correction to “RNA Modifications in Cancer”","authors":"","doi":"10.1002/mco2.70397","DOIUrl":"10.1002/mco2.70397","url":null,"abstract":"<p>Han Wu, Shi Chen, Xiang Li, Yuyang Li, Yiwen Qin, Bohe Shi, Yifei Tang, Zhuoyi Yan, Yang Hao, Dongxu Wang, Weiwei Liu.</p><p><i>RNA modifications in cancer</i>. MedComm. 2024; [doi: http://doi.org/10.1002/mco2.70042].</p><p>In the published version of this article, the name of the fifth author was incorrectly listed as <b>“Yiwen Qing”</b>. The correct spelling of the author's name is <b>“Yiwen Qin”</b>.</p><p>The author order and affiliations remain unchanged. All authors have approved this correction.</p><p>We apologize for this error.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12483941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145214923","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}
MedCommPub Date : 2025-09-29DOI: 10.1002/mco2.70403
Xiaowen Liang, Yue Yin, Yuanlong Lin, Shiman Chen, Qi Qian, Jing Yuan, Liuqing Yang, Yang Yang
{"title":"Molecular and Cellular Mechanisms of Respiratory Syncytial Viral Infection: Its Implications for Prophylactic and Therapeutic Pharmaceuticals","authors":"Xiaowen Liang, Yue Yin, Yuanlong Lin, Shiman Chen, Qi Qian, Jing Yuan, Liuqing Yang, Yang Yang","doi":"10.1002/mco2.70403","DOIUrl":"10.1002/mco2.70403","url":null,"abstract":"<p>Respiratory syncytial virus (RSV) is a notorious pathogen that serves as the leading cause of lower respiratory tract infections (LRTI) among infants, the elderly, and immunocompromised individuals. Its widespread prevalence exerts a considerable burden on global healthcare systems and economies, owing to the high rates of hospitalization and the potential for long-term health complications. Significant progress has been achieved in RSV prevention strategies during recent years, with three vaccines currently approved worldwide for active immunization in adults aged 60 years and older, as well as pregnant women. Furthermore, the monoclonal antibody nirsevimab has been approved for the prevention of RSV infections in infants. However, effective antiviral treatments for postinfection cases remain an unmet clinical need. This review comprehensively elaborates the molecular and cellular mechanisms of RSV infection, including viral structure, replication cycle, and pathogenic mechanisms. Meanwhile, we systematically summarize the latest advances in preventive and therapeutic agents and analyze the practical applications and existing limitations of current immunization strategies. Furthermore, we discuss and propose the challenges and future directions in drug development. The review provide insights for developing novel and effective prevention and treatment strategies against RSV infection.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145202567","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}
MedCommPub Date : 2025-09-29DOI: 10.1002/mco2.70406
Renyuan Wang, Song Gu, Young Hwa Kim, Aejin Lee, Haodong Lin, Dongsheng Jiang
{"title":"Diabetic Wound Repair: From Mechanism to Therapeutic Opportunities","authors":"Renyuan Wang, Song Gu, Young Hwa Kim, Aejin Lee, Haodong Lin, Dongsheng Jiang","doi":"10.1002/mco2.70406","DOIUrl":"10.1002/mco2.70406","url":null,"abstract":"<p>Diabetic wound healing, characterized by persistent inflammation, impaired angiogenesis, and dysfunctional cellular responses, remains a major clinical challenge due to its complex pathophysiology. This challenge is most evident in diabetic foot ulcers (DFUs), which carry high risks of infection, recurrence, and amputation, contributing substantially to patient morbidity, mortality, and healthcare costs. Despite multidisciplinary care, debridement, and advanced dressings, healing outcomes are often suboptimal, highlighting an urgent need for deeper pathophysiological insights and more effective therapeutic strategies. This review synthesizes current understanding of DFU pathogenesis, emphasizing how sustained metabolic dysfunction disrupts fibroblast and immune cell function, thereby perpetuating chronic wounds. We also critically examine commonly used animal models and their limitations in replicating the complexity of human DFUs and discuss emerging therapeutic approaches with translational promise. Advancing our understanding of these mechanisms and validating innovative interventions may ultimately reduce DFU-related amputations and mortality, improve healing outcomes, and enhance patient quality of life. This review aims to catalyze future research and therapeutic innovation in diabetic wound care.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12477442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145202591","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}
MedCommPub Date : 2025-09-27DOI: 10.1002/mco2.70411
Dongqin Zhou, Yu Chen, Xudong Liu, Juan He, Luyao Shen, Yongpeng He, Jiangang Zhang, Yu Zhou, Nan Zhang, Yanquan Xu, Juan Lei, Ran Ren, Huakan Zhao, Xianghua Zeng, Yongsheng Li
{"title":"Cholesterol 25-Hydroxylase Enhances Myeloid-Derived Suppressor Cell (MDSC) Immunosuppression via the Stimulator of Interferon Genes (STING)-Tank-Binding Kinase 1 (TBK1)-Receptor-Interacting Protein Kinase 3 (RIPK3) Pathway in Colorectal Cancer","authors":"Dongqin Zhou, Yu Chen, Xudong Liu, Juan He, Luyao Shen, Yongpeng He, Jiangang Zhang, Yu Zhou, Nan Zhang, Yanquan Xu, Juan Lei, Ran Ren, Huakan Zhao, Xianghua Zeng, Yongsheng Li","doi":"10.1002/mco2.70411","DOIUrl":"https://doi.org/10.1002/mco2.70411","url":null,"abstract":"<p>Myeloid-derived suppressor cells (MDSCs) represent a significant immunosuppressive population within the tumor microenvironment of colorectal cancer (CRC). Their activity has been strongly associated with the reprogramming of cholesterol metabolism, although the underlying mechanisms remain unclear. To investigate this, we generated myeloid-specific cholesterol 25-hydroxylase (CH25H) knockdown mice and differentiated bone marrow cells from wild-type (WT) or <i>Ch25h</i><sup>f/f</sup> Lyz2<sup>Cre</sup> mice into MDSCs, subsequently treating them with 25-hydroxycholesterol (25HC). Immune function was evaluated using flow cytometry, Western blotting, and real-time polymerase chain reaction (PCR). Our findings indicated that CH25H and its metabolite 25HC were significantly upregulated in CRC-associated MDSCs. The loss of CH25H impaired their immunosuppressive capacity by reducing arginase-1 (ARG1) expression, an effect that was restored by 25HC supplementation. Mechanistically, 25HC suppressed the activation of the cyclic guanosine monophosphate–adenosine monophosphate synthase–stimulator of interferon genes (cGAS–STING) pathway and the downstream tank-binding kinase 1 (TBK1). TBK1 formed a complex with receptor-interacting protein kinase 3 (RIPK3), thereby repressing ARG1 expression through phosphorylation-dependent signaling. Collectively, these findings reveal a previously unrecognized CH25H–25HC–STING axis in MDSC-mediated immune regulation and suggest that targeting cholesterol metabolism may provide a promising therapeutic strategy for CRC immunotherapy.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70411","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146879","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}
MedCommPub Date : 2025-09-27DOI: 10.1002/mco2.70373
Andrea Nicolini, Paola Ferrari, Roberto Silvestri, Dario A. Bini
{"title":"Targeted Therapies in the Most Common Advanced Solid Tumors, Drug Resistance, and Counteracting Progressive Micrometastatic Disease: The Next Frontier of Research","authors":"Andrea Nicolini, Paola Ferrari, Roberto Silvestri, Dario A. Bini","doi":"10.1002/mco2.70373","DOIUrl":"https://doi.org/10.1002/mco2.70373","url":null,"abstract":"<p>The era of targeted therapies has significantly advanced our understanding of cancer growth and metastasis. Intrinsic or acquired drug resistance remains a major challenge, rendering clinically overt metastatic disease incurable in most patients. This review first examines key clinical trials and their primary outcomes involving targeted therapies in the most common advanced solid tumors, along with the main mechanisms underlying drug resistance. Recently, micrometastatic disease has emerged as a novel focus of investigation aimed at definitively curing advanced solid tumors. Accordingly, this review explores the biology of micrometastases, current challenges in their detection and monitoring, and the main strategies proposed to prevent their progression. The potential roles of nanotechnology and artificial intelligence-driven predictive models are also discussed. Furthermore, we highlight specific characteristics of micrometastatic disease that favor immune modulation, and we evaluate the effectiveness of an immunotherapy regimen that inhibits immune suppression. The lead time provided by serum tumor markers, used experimentally to better track the progression of otherwise undetectable micrometastatic disease, also forms the mechanistic basis for a novel protocol we propose to prevent relapse in high-risk cancer patients. This innovative protocol holds scientific relevance being supported by an appropriate mathematical model and ready for immediate application in clinical practice.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70373","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146877","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}
{"title":"Guanine Nucleotide Exchange Factors and Small GTPases: Their Regulation and Functions, Diseases, and Therapeutic Targets","authors":"Zexing Lin, Chujun Ni, Haiyang Jiang, Huan Yang, Liting Deng, Peizhao Liu, Xuanheng Li, Yilong Yu, Weijie Li, Runnan Wang, Bo Liao, Jiaqi Kang, Juanhan Liu, Xiuwen Wu, Jianan Ren, Yun Zhao","doi":"10.1002/mco2.70362","DOIUrl":"https://doi.org/10.1002/mco2.70362","url":null,"abstract":"<p>Guanine nucleotide exchange factors (GEFs) and their small GTPase substrates constitute a fundamental regulatory system that governs diverse cellular processes, including cytoskeletal dynamics, membrane trafficking, and transcriptional regulation. Since their discovery, GEFs have been recognized as molecular switches that activate small GTPases by catalyzing GDP-to-GTP exchange, thereby playing pivotal roles in cellular signaling and homeostasis. Despite extensive research, key gaps remain in understanding the spatiotemporal regulation of GEF isoforms, their functional redundancy in disease, and the development of isoform-specific drugs. This review examines the regulatory mechanisms and physiological roles of GEFs, highlighting their growing potential as therapeutic targets. We explore the phylogenetic classification of GEFs into major families (Ras, Rho, Rab, and ArfGEFs) and their regulatory networks, which encompass subcellular localization, posttranslational modifications, and scaffolding interactions. Special emphasis is placed on GEF–H1, a microtubule-regulated RhoGEF, and its roles in cytoskeletal remodeling, cancer metastasis, and immune responses. We also examine GEF dysregulation in diseases like cancer, neurodegeneration, and cardiovascular disorders, and assess current therapies, such as small-molecule inhibitors and emerging PROTAC technology. This review connects GEF biology with clinical applications by combining basic research with translational insights, providing guidance for precision medicine and novel therapeutic strategies targeting GEF-related diseases.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70362","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146878","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}
MedCommPub Date : 2025-09-23DOI: 10.1002/mco2.70320
Sachin Kadian, Shubhangi Shukla, Amit K. Yadav, Brahamdutt Arya, Sushant Sethi, Vishal Chaudhary, Roger Narayan
{"title":"Recent Advancements in Graphene Quantum Dot-Based Bioimaging and Drug Delivery Systems","authors":"Sachin Kadian, Shubhangi Shukla, Amit K. Yadav, Brahamdutt Arya, Sushant Sethi, Vishal Chaudhary, Roger Narayan","doi":"10.1002/mco2.70320","DOIUrl":"https://doi.org/10.1002/mco2.70320","url":null,"abstract":"<p>Due to their unique physicochemical, optical, and electronic properties, traditional quantum dots (QDs) have been used for various optoelectronic applications, including semiconductor lasers, photodetectors, transistors, and solar cells. However, unlike other traditional QDs, graphene quantum dots (GQDs), nanosized graphene sheets that possess edge effects and quantum confinement along with a collective structural feature of graphene, have shown less toxicity and desirable biocompatibility, making them an appropriate part of the carbon family for use in biomedical applications. This review article highlights the recent advances and roles of GQDs in healthcare, with a particular focus on their applications involving bioimaging and drug delivery. Furthermore, we provide an overview of the different synthesis methods for GQDs, including the top-down and bottom-up approaches, and discuss the modifications that enhance their functionality, such as the incorporation of heteroatoms (e.g., nitrogen, sulfur, and phosphorus) to improve their properties. This review further considers the biological, optical, and toxicological attributes of GQDs, followed by recent developments involving the use of GQDs for drug delivery and bioimaging applications. Last, we describe the challenges, future prospects, and potential directions for advancing the real-time bioimaging and drug delivery applications of GQDs, including platforms for therapeutic agent release and medical diagnosis.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70320","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146403","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}
MedCommPub Date : 2025-09-23DOI: 10.1002/mco2.70410
Shu Chen, Kai Yu, Zhengming Deng, Xiaopei Hao, Ping Shi, Zhengzheng Wang, Jiali Xu, Jingjing Dai
{"title":"Hypomethylation-Enhanced F-Box Protein 32 Promotes Hepatocellular Carcinogenesis via Ubiquitin-Mediated PHLPP2 Degradation","authors":"Shu Chen, Kai Yu, Zhengming Deng, Xiaopei Hao, Ping Shi, Zhengzheng Wang, Jiali Xu, Jingjing Dai","doi":"10.1002/mco2.70410","DOIUrl":"https://doi.org/10.1002/mco2.70410","url":null,"abstract":"<p>F-Box Protein 32 (FBXO32), a F-box protein family member, exhibits oncogenic and tumor-suppressive roles in various carcinomas. However, its function and underlying molecular mechanisms in hepatocellular carcinoma (HCC) are still unknown. We observed that FBXO32 was overexpressed in HCC tissues than normal tissues, which is pertaining to poor prognosis in HCC patients. Functional tests demonstrated that FBXO32 enhanced HCC cell proliferation, invasion, and metastasis, which was confirmed in vivo using mouse models. Proteomics-based approaches and computational analyses reported a positive correlation between FBXO32 and PI3K–AKT pathway, identifying pleckstrin homology domain leucine-rich repeat protein phosphatase 2 (PHLPP2) as an interacting protein. Mechanistically, DNA promoter hypomethylation elevated FBXO32 expression in HCC cells, promoting K48-linked PHLPP2 polyubiquitination at the K592 and K942 sites through direct interactions. Notably, targeting FBXO32 significantly inhibited tumor growth in both an orthotopic HCC model and an organoid model derived from HCC patients. To sum up, this work emphasizes the part of FBXO32 in propelling HCC progression via facilitating PI3K–AKT pathway activation via PHLPP2 degradation.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70410","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145146391","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}
MedCommPub Date : 2025-09-21DOI: 10.1002/mco2.70398
Bingxin Gong, Yusheng Guo, Qi Wan, Jie Lou, Yi Li, Tingjie Xiong, Peng Mo, Yiqun Chen, Xiaowen Liu, Zilong Wu, Zhaokai Wang, Dongxuan Wei, Xi Zhang, Hongxiang Zeng, Xiaofei Zhang, Hui Wang, Lian Yang
{"title":"A Combined Model Based on Bone Mineral Density for Noninvasive Prediction of Prognosis in Non-Small Cell Lung Cancer Patients Receiving Immune Checkpoint Inhibitors: A Multicenter Retrospective Study","authors":"Bingxin Gong, Yusheng Guo, Qi Wan, Jie Lou, Yi Li, Tingjie Xiong, Peng Mo, Yiqun Chen, Xiaowen Liu, Zilong Wu, Zhaokai Wang, Dongxuan Wei, Xi Zhang, Hongxiang Zeng, Xiaofei Zhang, Hui Wang, Lian Yang","doi":"10.1002/mco2.70398","DOIUrl":"https://doi.org/10.1002/mco2.70398","url":null,"abstract":"<p>The prognostic value of baseline bone mineral density (BMD) and posttreatment BMD decrease (BMDD) in non-small cell lung cancer (NSCLC) patients receiving immune checkpoint inhibitor (ICI) treatment remains unclear. We assembled data of 2096 patients with advanced NSCLC from five institutions to develop a combined model incorporating BMD/BMDD and clinical characteristics for noninvasive prognosis prediction. BMD was automatically assessed using a deep learning-based method. Compared with the physiological BMD group and the non-severe BMDD group, the pathological BMD group and the severe BMDD group had shorter progression-free survival (PFS) (hazard ratio [HR]: 1.19, <i>p</i> = 0.003; and HR: 1.19, <i>p</i> = 0.002, respectively) and overall survival (OS) (HR: 1.31, <i>p</i> < 0.001; and HR: 1.30, <i>p</i> < 0.001). Compared with the single BMD/BMDD model, the combined model had higher Harrell's concordance indexes (<i>c</i>-indexes) (PFS: 0.580 and OS: 0.654). Transcriptomic analysis of 130 patients from the NSCLC radiogenomic cohort revealed upregulation of epithelial–mesenchymal transition, inflammatory, and hypoxia pathways, and increased macrophage infiltration in tumors of patients with pathological BMD. This study showed that lower baseline BMD and more severe BMDD are associated with poorer prognosis. BMD in combination with clinical characteristics can help to improve risk stratification and prognosis prediction.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 10","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70398","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111237","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}