MedComm最新文献

{"title":"Carbonaceous particle exposure triggered accumulation of Osteopontin/SPP1+ macrophages contributes to emphysema development","authors":"Lianyong Han, Verena Haefner, Ali Önder Yildirim, Heiko Adler, Tobias Stoeger","doi":"10.1002/mco2.70061","DOIUrl":"10.1002/mco2.70061","url":null,"abstract":"<p>Dear Editor,</p><p>Chronic obstructive pulmonary disease (COPD) is an inflammatory disease characterized by airway obstruction and loss of alveolar surface, together resulting in progressive and irreversible airflow limitations and shortage of breath. Chronic bronchitis and emphysema are two major phenotypes of the disease. Cigarette smoke (CS) is a long-known cause of COPD, and it accounts for more than 70% of COPD cases, as reported by WHO,<span><sup>1</sup></span> but the contribution of indoor and outdoor air pollution is increasingly acknowledged.<span><sup>2</sup></span> As one of the major air pollutants, ambient particle inhalation has been widely reported to contribute to several chronic lung diseases, in particular COPD. Typically, animal studies revealed that the inhalation of soot-like carbonaceous nanoparticles (CNPs) can cause both local inflammation in the lung as well as systemic inflammation, allowing the application of CNP as a representative environmental and combustion-derived particle to investigate its potential toxicological effects as well as the association with chronic lung diseases. Our previous study showed that repeated exposure of mice to CNP, mimicking a human urban exposure scenario under the condition of latent gammaherpesvirus infection (particles as a second hit on top of latent virus infection), caused interstitial inflammation, alveolar injury and cell death leading to progressive alveolar air space enlargement, thereby demonstrating a crucial contribution of environmental particle exposure to lung emphysema development.<span><sup>3, 4</sup></span> Several mechanisms have been suggested to contribute to epithelial cell damage by air pollutants and inhaled particles.</p><p>Secreted phosphoprotein 1 (SPP1), also known as Osteopontin (OPN), is a matricellular protein expressed by many cell types, exhibiting an important role in various inflammatory responses. For instance, it has been shown that inhalation of CNP or CS caused OPN release in the airways of a murine COPD model.<span><sup>5</sup></span> Furthermore, in many observational studies, OPN release is also increased in various body fluids including sputum and plasma from COPD patients compared to healthy individuals.<span><sup>6, 7</sup></span> While plasma OPN levels have been associated with exposure to air pollution, which in turn was linked to worsening emphysema, the mechanistic link between particle exposure triggered SPP1 and COPD development has so far only been drawn for CS.</p><p>To study the expression of SPP1 during COPD development, we analyzed <i>SPP1</i> messenger RNA (mRNA) levels from either emphysema or COPD patients across four different cohorts. Consistently, we found that <i>SPP1</i> is significantly elevated in lung tissue of either emphysema or COPD patients compared to controls (Figure 1A), supporting the clinical relevance of SPP1 induction during COPD development. Experimentally, in a CS-induced mouse COPD model, <i>Spp1</i> wa","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061391","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":"Dimethyl fumarate alleviate hepatic ischemia–reperfusion injury through suppressing cGAS-STING signaling","authors":"Yi Xiong,&nbsp;Jiawen Chen,&nbsp;Kun Li,&nbsp;Wei Liang,&nbsp;Jinwen Song,&nbsp;Xiusheng Qiu,&nbsp;Baoyu Zhang,&nbsp;Dongbo Qiu,&nbsp;Yunfei Qin","doi":"10.1002/mco2.70077","DOIUrl":"10.1002/mco2.70077","url":null,"abstract":"<p>Hepatic ischemia–reperfusion (I/R) injury frequently occurs during the perioperative phase of liver surgery. Inappropriate activation of STING signaling can trigger excessive inflammation response to aggravate hepatic I/R injury. Dimethyl fumarate (DMF) is an FDA-approved immunomodulatory drug used to treat multiple sclerosis and psoriasis due to its notable anti-inflammation properties. However, the mechanism and targets of DMF in immunomodulation remain unclear. Here, we found that DMF suppresses cGAS-STING activation induced by HSV-1, hering testis DNA, and mitochondrial DNA in a variety of cells. DMF significantly reduces hepatic I/R injury and inhibits cGAS-STING pathway activation in mice. The alleviating effect of DMF on hepatic I/R injury was negligible in STING-knockout mice. Mechanistically, DMF directly inhibits STING activation via an autophagy-independent pathway, and the immunocoprecipitation experiment showed that DMF inhibited STING recruitment of downstream TBK1 and IRF3. Our study found that DMF protects liver I/R injury by inhibiting the STING pathway and may be a potential target of this disease.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143061343","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":"Acute respiratory distress syndrome (ARDS): from mechanistic insights to therapeutic strategies","authors":"Rongli Xie,&nbsp;Dan Tan,&nbsp;Boke Liu,&nbsp;Guohui Xiao,&nbsp;Fangchen Gong,&nbsp;Qiyao Zhang,&nbsp;Lei Qi,&nbsp;Sisi Zheng,&nbsp;Yuanyang Yuan,&nbsp;Zhitao Yang,&nbsp;Ying Chen,&nbsp;Jian Fei,&nbsp;Dan Xu","doi":"10.1002/mco2.70074","DOIUrl":"10.1002/mco2.70074","url":null,"abstract":"<p>Acute respiratory distress syndrome (ARDS) is a clinical syndrome of acute hypoxic respiratory failure caused by diffuse lung inflammation and edema. ARDS can be precipitated by intrapulmonary factors or extrapulmonary factors, which can lead to severe hypoxemia. Patients suffering from ARDS have high mortality rates, including a 28-day mortality rate of 34.8% and an overall in-hospital mortality rate of 40.0%. The pathophysiology of ARDS is complex and involves the activation and dysregulation of multiple overlapping and interacting pathways of systemic inflammation and coagulation, including the respiratory system, circulatory system, and immune system. In general, the treatment of inflammatory injuries is a coordinated process that involves the downregulation of proinflammatory pathways and the upregulation of anti-inflammatory pathways. Given the complexity of the underlying disease, treatment needs to be tailored to the problem. Hence, we discuss the pathogenesis and treatment methods of affected organs, including 2019 coronavirus disease (COVID-19)-related pneumonia, drowning, trauma, blood transfusion, severe acute pancreatitis, and sepsis. This review is intended to provide a new perspective concerning ARDS and offer novel insight into future therapeutic interventions.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049264","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":"Airway stenosis: classification, pathogenesis, and clinical management","authors":"Pengwei Zhao,&nbsp;Zheng Jiang,&nbsp;Xuexin Li,&nbsp;Mailudan Ainiwaer,&nbsp;Leyu Li,&nbsp;Dejuan Wang,&nbsp;Lixiao Fan,&nbsp;Fei Chen,&nbsp;Jun Liu","doi":"10.1002/mco2.70076","DOIUrl":"10.1002/mco2.70076","url":null,"abstract":"<p>Airway stenosis (AS) is a fibroinflammatory disease characterized by abnormal activation of fibroblasts and excessive synthesis of extracellular matrix, which has puzzled many doctors despite its relatively low prevalence. Traditional treatment such as endoscopic surgery, open surgery, and adjuvant therapy have many disadvantages and are limited in the treatment of patients with recurrent AS. Therefore, it is urgent to reveal the pathogenesis of AS and accelerate its clinical transformation. Based on the discovered pathogenesis, including fibrosis, inflammation, epithelial–mesenchymal transition, metabolic reprogramming, microbiome, genetic susceptibility, and other mechanisms, researchers have developed a series of treatments, such as drug therapy, gene therapy, stem cell therapy, growth factor therapy, protein therapy, and photodynamic therapy. This review introduces the classification of AS, explores the existing pathogenesis and preclinical treatments developed based on the pathogenesis, and finally summarizes the current clinical management. In addition, the prospect of exploring the interaction between different types of cells and between microorganisms and cells to identify the intersection of multiple mechanisms based on single-cell RNA sequencing, 16S rRNA gene sequencing and shotgun metagenomic sequencing is worth looking forward to.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11769711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049273","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":"At the nucleus of cancer: how the nuclear envelope controls tumor progression","authors":"Francesca Paganelli,&nbsp;Alessandro Poli,&nbsp;Serena Truocchio,&nbsp;Alberto M. Martelli,&nbsp;Carla Palumbo,&nbsp;Giovanna Lattanzi,&nbsp;Francesca Chiarini","doi":"10.1002/mco2.70073","DOIUrl":"10.1002/mco2.70073","url":null,"abstract":"<p>Historically considered downstream effects of tumorigenesis—arising from changes in DNA content or chromatin organization—nuclear alterations have long been seen as mere prognostic markers within a genome-centric model of cancer. However, recent findings have placed the nuclear envelope (NE) at the forefront of tumor progression, highlighting its active role in mediating cellular responses to mechanical forces. Despite significant progress, the precise interplay between NE components and cancer progression remains under debate. In this review, we provide a comprehensive and up-to-date overview of how changes in NE composition affect nuclear mechanics and facilitate malignant transformation, grounded in the latest molecular and functional studies. We also review recent research that uses advanced technologies, including artificial intelligence, to predict malignancy risk and treatment outcomes by analyzing nuclear morphology. Finally, we discuss how progress in understanding nuclear mechanics has paved the way for mechanotherapy—a promising cancer treatment approach that exploits the mechanical differences between cancerous and healthy cells. Shifting the perspective on NE alterations from mere diagnostic markers to potential therapeutic targets, this review calls for further investigation into the evolving role of the NE in cancer, highlighting the potential for innovative strategies to transform conventional cancer therapies.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049278","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":"WSB2 inhibits apoptosis and autophagy by targeting NOXA for degradation","authors":"Shengpeng Shao,&nbsp;Danrui Cui,&nbsp;Chutian Zheng,&nbsp;Xiufang Xiong,&nbsp;Yongchao Zhao","doi":"10.1002/mco2.70071","DOIUrl":"10.1002/mco2.70071","url":null,"abstract":"&lt;p&gt;NOXA protein, a pro-apoptotic member of the BCL2 (B-cell lymphoma 2) protein family, exhibits a high affinity for binding to MCL1 (myeloid cell leukemia 1) and interacts with BCL2A1 (B-cell lymphoma 2-related protein A1). These interactions release BIM (BCL2 like protein 11), triggering apoptosis. Furthermore, NOXA facilitates proteasome-mediated MCL1 degradation, a critical response to various anti-cancer drugs and extracellular stimuli, including UV (ultraviolet) irradiation. Additionally, during oncogenic RAS activation, NOXA induces autophagic cell death by displacing MCL1 from Beclin-1, a key component of the class III PI3K (phosphoinositide 3-kinase) complex required for autophagosome biogenesis.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; Therefore, NOXA plays an essential role in regulating apoptotic and autophagic cell death, and its induction is a promising therapeutic target for anti-cancer treatments.&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt;&lt;/p&gt;&lt;p&gt;NOXA level regulation is tightly controlled at both transcriptional and post-translational levels. Previous studies have demonstrated that CRL5 (Cullin-RING Ligase 5) mediates NOXA ubiquitylation and degradation.&lt;span&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/span&gt; The CRL5 complex comprises four components: a scaffold protein (CUL5), adaptor proteins (Elongin B/C), a substrate receptor SOCS (suppressor of cytokine signaling) protein, and a RING protein (RBX2/SAG). The SOCS protein specifically recognizes and binds to substrates.&lt;span&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/span&gt; In mammalian cells, there are 37 SOCS substrate receptor proteins.&lt;span&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/span&gt; However, the specific receptors for NOXA recognition remain unidentified, posing a challenge to the development of inhibitors targeting NOXA degradation. In this study, we demonstrate that the substrate receptor protein WSB2 (WD repeat and SOCS box containing 2) targets NOXA for degradation.&lt;/p&gt;&lt;p&gt;To identify the receptor in the CRL5 complex responsible for recognizing and binding NOXA, we performed an siRNA-based screening targeting all known CRL5 receptor proteins and HSP90A/B in Huh7 cells. HSP90A/B client proteins undergo degradation by the CRL5 ligase following treatment with HSP90 inhibitors. Subsequently, NOXA accumulation was assessed via immunoblotting. WSB2 emerged as a candidate due to the highest accumulation of NOXA observed upon its knockdown (Figure S1A). Next, we observed a significant increase in NOXA protein levels upon WSB2 silencing across various cancer cell lines, including Huh7, H1299, and A549 (Figure 1A). Interestingly, WSB2 knockdown did not alter NOXA mRNA levels in Huh7 and H1299 cells but moderately increased them in A549 cells (Figure 1A). The observed increase in NOXA mRNA levels in A549 cells, which harbor wild-type p53, is likely due to transcriptional activation of p53. Since p53 is a known substrate of WSB2,&lt;span&gt;&lt;sup&gt;4&lt;/sup&gt;&lt;/span&gt; its accumulation following WSB2 knockdown could explain this transcriptional effect. These findings suggest that WSB2 primarily regulates NOXA le","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049295","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":"The design of retroviral vectors used in the CAR-T products, risk management, and future perspective","authors":"Huifang Yin,&nbsp;Xuejing Wei","doi":"10.1002/mco2.70067","DOIUrl":"10.1002/mco2.70067","url":null,"abstract":"<p>Chimeric antigen receptor T-cell (CAR-T) therapy is a revolutionary approach in cancer treatment. More than 10 CAR-T products have already approved on market worldly wide, and they use either gamma retroviral vectors or lentiviral vectors to deliver the CAR gene. Both vectors have the ability to effectively and persistently integrate the CAR gene into T cells. Despite the advancements in CAR-T therapy, the potential risks associated with the vectors, particularly the risks of the secondary malignancies, still remain as a concern. This article compares the characteristics of gamma retroviral and lentiviral vectors, discusses the development of vector packaging systems, and examines the design of self-inactivating (SIN) vectors. It also addresses the risks of secondary malignancies that might possibly be associated with the retroviral vectors, and the strategies to decrease the risks and increase the safer clinical use of the vectors. This article also discusses the current regulatory landscape and management approaches aiming to mitigate these risks through stringent safety measures and ongoing monitoring. Future perspectives focus on improving the safety profiles of the vectors and broadening their scope of use. The article provides a thorough overview of the most recent research discoveries and regulatory updates in the field of CAR-T therapy, highlighting the significance of a balanced strategy that strikes a balance between innovation and patient safety in the development and implementation of CAR-T therapy.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049242","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":"Butyrolactone I blocks the transition of acute kidney injury to chronic kidney disease in mice by targeting JAK1","authors":"Zijun Zhang,&nbsp;Ziming Zhao,&nbsp;Changxing Qi,&nbsp;Xiaotian Zhang,&nbsp;Yang Xiao,&nbsp;Chengjuan Chen,&nbsp;Yu Zou,&nbsp;Xia Chen,&nbsp;Lianghu Gu,&nbsp;Jianzheng Huang,&nbsp;Kun Huang,&nbsp;Ming Xiang,&nbsp;Tiantai Zhang,&nbsp;Qingyi Tong,&nbsp;Yonghui Zhang","doi":"10.1002/mco2.70064","DOIUrl":"10.1002/mco2.70064","url":null,"abstract":"<p>Chronic kidney disease (CKD) is a disease that affects more than 850 million people. Acute kidney injury (AKI) is a common cause of CKD, and blocking the AKI–CKD transition shows promising therapeutic potential. Herein, we found that butyrolactone I (BLI), a natural product, exerts significant nephroprotective effects, including maintenance of kidney function, inhibition of inflammatory response, and prevention of fibrosis, in both folic acid- and ureteral obstruction-induced AKI–CKD transition mouse models. Notably, BLI showed greater blood urea nitrogen reduction and anti-inflammatory effects than telmisartan. Bioinformatics analysis and target confirmation assays suggested that BLI directly binds to JAK1, and kinase inhibition assay confirmed it is a potent JAK1inhibitor with an IC₅₀ of 0.376 µM. Experiments in JAK1-knockdown mice also proved that BLI targets JAK1 to work. Furthermore, BLI demonstrated nephroprotective effects and safety comparable to ivarmacitinib, the well-known JAK1 inhibitor. Mechanistically, BLI targets JAK1 and inhibits its phosphorylation and JAK-STAT activation, subsequently regulating the downstream signaling pathways to inhibit reactive oxygen species production, inflammation, and ferroptosis, thereby preventing the occurrence of kidney fibrosis and blocking the AKI–CKD transition process. This study demonstrates for the first time that BLI is a JAK1 inhibitor and a promising candidate for delaying CKD progression, which warrants further investigation.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025891","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":"Neutrophil heterogeneity and plasticity: unveiling the multifaceted roles in health and disease","authors":"Weifeng He,&nbsp;Lingfeng Yan,&nbsp;Dongxue Hu,&nbsp;Jianlei Hao,&nbsp;Yih-Cherng Liou,&nbsp;Gaoxing Luo","doi":"10.1002/mco2.70063","DOIUrl":"10.1002/mco2.70063","url":null,"abstract":"<p>Neutrophils, the most abundant circulating leukocytes, have long been recognized as key players in innate immunity and inflammation. However, recent discoveries unveil their remarkable heterogeneity and plasticity, challenging the traditional view of neutrophils as a homogeneous population with a limited functional repertoire. Advances in single-cell technologies and functional assays have revealed distinct neutrophil subsets with diverse phenotypes and functions and their ability to adapt to microenvironmental cues. This review provides a comprehensive overview of the multidimensional landscape of neutrophil heterogeneity, discussing the various axes along which diversity manifests, including maturation state, density, surface marker expression, and functional polarization. We highlight the molecular mechanisms underpinning neutrophil plasticity, focusing on the complex interplay of signaling pathways, transcriptional regulators, and epigenetic modifications that shape neutrophil responses. Furthermore, we explore the implications of neutrophil heterogeneity and plasticity in physiological processes and pathological conditions, including host defense, inflammation, tissue repair, and cancer. By integrating insights from cutting-edge research, this review aims to provide a framework for understanding the multifaceted roles of neutrophils and their potential as therapeutic targets in a wide range of diseases.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025970","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":"Patient-derived xenograft model in cancer: establishment and applications","authors":"Ao Gu,&nbsp;Jiatong Li,&nbsp;Meng-Yao Li,&nbsp;Yingbin Liu","doi":"10.1002/mco2.70059","DOIUrl":"10.1002/mco2.70059","url":null,"abstract":"<p>The patient-derived xenograft (PDX) model is a crucial in vivo model extensively employed in cancer research that has been shown to maintain the genomic characteristics and pathological structure of patients across various subtypes, metastatic, and diverse treatment histories. Various treatment strategies utilized in PDX models can offer valuable insights into the mechanisms of tumor progression, drug resistance, and the development of novel therapies. This review provides a comprehensive overview of the establishment and applications of PDX models. We present an overview of the history and current status of PDX models, elucidate the diverse construction methodologies employed for different tumors, and conduct a comparative analysis to highlight the distinct advantages and limitations of this model in relation to other in vivo models. The applications are elucidated in the domain of comprehending the mechanisms underlying tumor development and cancer therapy, which highlights broad applications in the fields of chemotherapy, targeted therapy, delivery systems, combination therapy, antibody–drug conjugates and radiotherapy. Furthermore, the combination of the PDX model with multiomics and single-cell analyses for cancer research has also been emphasized. The application of the PDX model in clinical treatment and personalized medicine is additionally emphasized.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 2","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143018613","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}