Journal of Translational Medicine最新文献

{"title":"Chimeric antigen receptors discriminate between tau and distinct amyloid-beta species.","authors":"Cynthia J Siebrand, Nicholas J Bergo, Suckwon Lee, Julie K Andersen, Chaska C Walton","doi":"10.1186/s12967-025-06572-6","DOIUrl":"https://doi.org/10.1186/s12967-025-06572-6","url":null,"abstract":"<p><strong>Background: </strong>The lack of a definitive cure for Alzheimer's disease (AD) is fueling the search for innovative therapeutic strategies. Having revolutionized cancer immunotherapy, immune cell engineering with chimeric antigen receptors (CAR) is being explored to target AD. Whether CARs can recognize distinct amyloid-β (Aβ) species and tau neurofibrillary tangles (NFTs)-hallmark pathologies of AD-remains unclear.</p><p><strong>Methods: </strong>To investigate this, we engineered a series of CARs using single-chain fragment variable (scFv) derived from the variable light and heavy chains of antibodies tested in AD clinical trials. These included E2814 (E2814-CAR), targeting tau; Lecanemab (Lec-CAR) and Aducanumab (Adu-CAR), targeting Aβ; and Donanemab (Don-CAR) and Remternetug (Rem-CAR), targeting the truncated pyroglutamated Aβ species Aβp3-42. To evaluate CAR function, we utilized the murine DO11.10 CD4⁺ T-cell hybridoma line as a scalable and reproducible platform. CAR activation was assessed in response to tau preformed fibrils (PFFs), Aβ_1-42 oligomer-enriched aggregates, and Aβp3-42 aggregates, using flow cytometry for CD69 expression and ELISA for IL-2 secretion. To validate this platform, we tested Adu-CAR in primary mouse CD4⁺ T cells treated with Aβ_1-42 aggregates and assessed activation via flow cytometry for CD69 and CD25 expression.</p><p><strong>Results: </strong>DO11.10 cells expressing E2814-CAR-but not Lec-CAR-responded to tau PFFs. In contrast, cells expressing Adu-CAR, and to a lesser extent Lec-CAR-but not E2814-CAR-responded to Aβ_1-42 aggregates. For Aβp3-42 aggregates, Rem-CAR elicited the strongest response, followed by Adu-CAR, while E2814-CAR and Don-CAR showed no activation. The activation of Adu-CAR by Aβ_1-42 aggregates was recapitulated in primary CD4⁺ T cells, as measured by CD69 expression.</p><p><strong>Conclusions: </strong>Our findings demonstrate that CARs can detect and discriminate between tau PFFs, Aβ1-42, and Aβp3-42 aggregates. This highlights the potential of repurposing AD antibodies for CAR-based therapies to selectively target tau NFTs and distinct forms of Aβ senile plaques.</p>","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"605"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interpenetrating network hydrogel-loaded embryonic stem cell-derived endocardial cells improves cardiac function after myocardial infarction.","authors":"Boshi Liu, Laiping Zhang, Xiao Guan, Jie Liu, Weinian Shou, Xin Chen, Xiaohui Li, Dayan Cao","doi":"10.1186/s12967-025-06603-2","DOIUrl":"https://doi.org/10.1186/s12967-025-06603-2","url":null,"abstract":"<p><strong>Background: </strong>With an in-depth understanding of cardiac cell differentiation, cell therapy derived from stem cells has shown promising therapeutic effects in the treatment of myocardial infarction (MI). Although many types of cardiac or noncardiac cells have been found to play protective roles in MI, the specific role of endocardial cells (ECCs) in MI has not been reported.</p><p><strong>Methods: </strong>The current study was designed to determine whether human embryonic stem cell (hESC)-derived endocardial cells (hESC-ECCs) could be protective against MI. We first developed a cell delivery system by constructing a photosensitive interpenetrating network hydrogel consisting of gelatin methacryloyl (GelMA) and silk fibroin methacryloyl (SilMA). The sorted hESC-ECCs were loaded into the delivery system and then injected into the pericardium cavity of the MI rats.</p><p><strong>Results: </strong>These results show that the cell delivery system has good biocompatibility. Moreover, the delivered endocardial cells improved cardiac function and delayed capillary atrophy after MI. Further mechanistic analysis revealed that hESC-ECCs protect the mitochondria of cardiomyocytes from damage under oxidative stress and potentially promote the angiogenesis of cardiac endothelial cells.</p><p><strong>Conclusion: </strong>Our results demonstrated that hESC-ECCs have the potential to serve as a cell therapy strategy for MI treatment by maintaining cardiomyocyte survival and facilitating angiogenesis.</p>","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"603"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiplex imaging reveals novel patterns of MRTFA/B activation in the breast cancer microenvironment.","authors":"Stephanie M Wilk, Kihak Lee, Caitlyn C Castillo, Mohamed Haloul, Alexa M Gajda, Virgilia Macias, Elizabeth L Wiley, Zhengjia Chen, Xinyi Liu, Xiaowei Wang, Maria Sverdlov, Kent F Hoskins, Ekrem Emrah Er","doi":"10.1186/s12967-025-06559-3","DOIUrl":"https://doi.org/10.1186/s12967-025-06559-3","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Breast cancer progression and metastasis involve the action of multiple transcription factors in tumors and in the cells of the tumor microenvironment (TME) and understanding how these transcription factors are coordinated can guide novel therapeutic strategies. Myocardin-related transcription factors A and B (MRTFA/B also known as MKL1/2) are two related transcription factors that redundantly control cancer cell invasion and metastasis in mouse models of breast cancer, but their roles in human cancer are incompletely understood. Here, we investigated the expression and activation of these transcription factors to better assess their tumorigenic and metastatic impact on breast cancer and cells of the tumor microenvironment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We used a multiplexed immunofluorescence approach to label MRTFA, MRTFB, tumor cells by using pan Cytokeratin, endothelial cells by using CD31, and antigen presenting cells (APCs) by using HLA-DRA on two different breast cancer tissue microarrays (TMA): The breast cancer progression TMA provided by the Cooperative Human Tissue Network (CHTN_BrCaProg3) and the University of Illinois Breast Cancer Working Group (TMA BCWG UIC-001-TMA) that included primary tumor and lymph node metastases from patients residing in the West Side and South Side of Chicago. We also used bioinformatics analyses of the TCGA and METABRIC databases and the Broad Institute's single-cell RNA sequencing portal to investigate MRTFA/B expression patterns in the cells of the tumor microenvironment (TME).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;We found that in human tumors, MRTFA/B are concurrently activated in cancer cells, but they show distinct patterns of expression across different histological subtypes and in the cells of the TME. Importantly, MRTFA expression was elevated in metastatic tumors of African American patients, who disproportionately die from breast cancer. Interestingly, in contrast to publicly available mRNA expression data, MRTFA was similarly expressed across estrogen receptor (ER) positive and negative breast tumors, while MRTFB expression was highest in ER+ breast tumors. Furthermore, MRTFA was specifically expressed in the perivascular antigen-presenting cells (APCs), which has been previously associated with immune suppression and breast cancer progression. We also found that MRTFA expression correlated with the expression of the immune checkpoint protein V-set immunoregulatory receptor (VSIR) in the TCGA data and found that MRTFA activity promotes VSIR expression in THP-1 monocytes and cultured HEK293 cells.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Our results provide unique insights into how MRTFA and MRTFB promote metastasis in human cancer, the differences of their expression patterns, and their immune suppressive function within the breast cancer TME. Our results will guide future studies on targeting MRTFA/B transcriptional activity and the resulting immune suppression in breast","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"599"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YTHDF3 regulates IL32 mRNA stability to promote osteogenic differentiation of bone mesenchymal stem cells in ankylosing spondylitis.","authors":"Bole Zhou, Xinzhe Feng, Changhao Han, Yang Wu, Junjie Qiao, Wenwen Tong, Weidong Xu","doi":"10.1186/s12967-025-06607-y","DOIUrl":"https://doi.org/10.1186/s12967-025-06607-y","url":null,"abstract":"<p><strong>Background: </strong>As a member of the family of the YTH domain and a an m6A reader, YTHDF3 is implicated in cancer and inflammatory diseases. However, its function in ankylosing spondylitis (AS)-a chronic inflammatory disease marked by aberrant bone formation-is still mysterious. The research set out to study how YTHDF3 may promote osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) in AS and delineate the underlying mechanism.</p><p><strong>Methods: </strong>BMSCs were separated from AS and healthy controls patients. YTHDF3 expression was manipulated using lentiviral transduction. Alkaline phosphatase (ALP) activity and Alizarin Red staining were utilized to assess osteogenic differentiation. This work employed quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blot (WB) analysis, and enzyme-linked immunosorbent assay to determine the expression of osteogenic markers, including RUNX2, SP7, BMP2, and OCN. Furthermore, RNA sequencing (RNA-seq), m6A sequencing (m6A-seq), and RNA immunoprecipitation were performed to identify downstream targets, particularly focusing interleukin 32 (IL32). Additionally, RNA stability assays and fluorescence in situ hybridization were used to evaluate the role of YTHDF3 in stabilizing IL32.</p><p><strong>Results: </strong>YTHDF3 expression was notably increased in AS-BMSCs in comparison with the control group. YTHDF3 overexpression promoted osteogenic differentiation, as shown by the rise in ALP activities, boosted calcium deposition, and upregulation of osteogenic markers. In contrast, the YTHDF3 knockdown inhibited these processes. IL32 was identified as a key downstream target using RNA-seq and m6A-seq, whose mRNA stability was directly regulated by YTHDF3 via m6A modifications. Notably, increased IL32 expression in AS contributed to osteogenesis.</p><p><strong>Conclusion: </strong>YTHDF3 prevents IL32 mRNA degradation and promotes osteogenic differentiation of AS-BMSCs in an m6A-dependent manner. The results shed light on previous questions regarding the molecular mechanisms behind ectopic bone formation in AS, identifying YTHDF3 as a potential therapeutic target for controlling pathological bone formation.</p>","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"604"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA profiling and immunohistochemistry analyses of circRNAs in imatinib-resistant gastrointestinal stromal tumors.","authors":"Hanxing Tong, Ning Jia, Wenyang Li, Jingjing Xu, Qiuyue Li, Xiaomeng He, Huaqin Sun, Christopher Corpe, Jin Wang","doi":"10.1186/s12967-025-06598-w","DOIUrl":"https://doi.org/10.1186/s12967-025-06598-w","url":null,"abstract":"<p><strong>Background: </strong>Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal sarcomas of the upper digestive tract. Imatinib is the first-line therapy for patients with metastatic or unresectable GISTs. However, the majority of GIST patients eventually develop imatinib resistance.</p><p><strong>Methods: </strong>To identify the factors that are responsible for imatinib resistance, we investigated the differentially expressed mRNAs and circRNAs in imatinib-naïve and imatinib-resistant GISTs via ceRNA microarrays. The expression levels of circ-BRIP1, circ-EPHB4 and their host genes were validated via quantitative real-time PCR analyses and formalin-fixed and paraffin-embedded (FFPE) tissue microarrays (TMAs).</p><p><strong>Results: </strong>We found that 107 mRNAs and 521 circRNAs were differentially expressed between imatinib-resistant and imatinib-naïve GIST tissue samples. Among them, circ-BRIP1, circ-EPHB4 and their host genes were upregulated in imatinib-resistant GISTs and associated with imatinib resistance, tumor relapse and progression, and metastasis in GIST patients. The expression level of EPHB4 was significantly greater in high-grade GISTs than in low-grade GISTs and was correlated with imatinib resistance.</p><p><strong>Conclusions: </strong>Our results demonstrated that the circRNA in situ hybridization-immunohistochemistry could not only be applied to FFPE-TMAs for high-throughput analysis of circRNA expression in tumors but also suggested a possible role for circ-BRIP1, circ-EPHB4, and their host genes in the progression of GISTs.</p>","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"601"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophages in the premetastatic and metastatic niche: key functions and therapeutic directions.","authors":"Yana Qi, Dongmei Sun, Xiaoyang Zhai, Feihu Chen, Jiling Niu, Hui Zhu","doi":"10.1186/s12967-025-06556-6","DOIUrl":"https://doi.org/10.1186/s12967-025-06556-6","url":null,"abstract":"<p><p>Metastasis plays a significant role in the high mortality rates associated with cancer and is usually the endpoint of a series of sequential and dynamic events. A crucial step in metastasis development and progression is the formation of a premetastatic niche (PMN), which provides a conducive microenvironment for the settlement and colonization of disseminated tumor cells at distant metastatic sites. Extensive research has demonstrated the significance of macrophage populations within primary tumors in promoting metastatic progression. Nevertheless, the contribution of macrophages at secondary sites to the regulation of PMN formation is frequently overlooked. This review systematically explores the role of macrophages in priming the PMN to facilitate cancer metastasis. Additionally, we provide a compendium of existing strategies to target macrophages in cancer therapy.</p>","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"602"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research advancements of antibody drug conjugates in non-small cell lung cancer with HER2 alterations.","authors":"Jiang Liu, Jianhua Liu, Jianhe Yu, Qun Ren, Yin Cai, Dadong Chen, Chuanjun Song","doi":"10.1186/s12967-025-06589-x","DOIUrl":"https://doi.org/10.1186/s12967-025-06589-x","url":null,"abstract":"<p><p>The human epidermal growth factor receptor 2 (HER2) alterations are significant genetic alterations in non-small cell lung cancer (NSCLC), encompassing mutations, amplifications, and protein overexpression. Despite the substantial progress of anti-HER2 targeted therapies in breast and gastric cancers, numerous challenges persist in the treatment of NSCLC with HER2 alterations. Presently, the options for NSCLC with HER2 alterations remain limited, with inferior efficacy observed using small molecule anti-tumor targeted agents and conventional chemotherapy. Antibody drug conjugates (ADCs), an organic combination of monoclonal antibodies and cytotoxic drugs targeting specific tumor cells, have revolutionized the treatment landscape of NSCLC with HER2 alterations. Extensive exploration of ADCs has been conducted across NSCLC patients with HER2 alterations, achieving notable efficacy in some populations. This review aims to delve into the biological characteristics and current treatment landscape of NSCLC with HER2 alterations, emphasizing the transformative research advancements surrounding ADCs. By highlighting these developments, we aspire to provide essential insights to enhance clinical practice and improve management strategies for NSCLC patients with HER2 alterations.</p>","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"600"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell sequencing atlas construction for tracheobronchial adenoid cystic carcinoma.","authors":"Jun Teng, Qinyan Hong, Heng Zou, Lei Li, Hongwu Wang","doi":"10.1186/s12967-025-06622-z","DOIUrl":"https://doi.org/10.1186/s12967-025-06622-z","url":null,"abstract":"","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"606"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLIT3-mediated intratumoral crosstalk induces neuroblastoma differentiation via a spontaneous regression-like program.","authors":"Meiling Liu, Dekang Lv, Wenjing Yan, Yi Wu, Shulan Wang, Luoxuan Wang, Jie Lei, Deshun Zeng, Zifeng Wang, Fang Liu, Bing Deng, Quentin Liu, Bin He, Min Yan","doi":"10.1186/s12967-025-06621-0","DOIUrl":"https://doi.org/10.1186/s12967-025-06621-0","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Neuroblastoma, the most common pediatric extracranial solid tumor, has heterogeneous clinical outcomes ranging from malignant progression to spontaneous regression. With the highest frequency of the elusive spontaneous regression, low-risk INSS Stage 4S neuroblastoma represents an ideal model for mechanistic investigation. Spontaneous regression is often accompanied by tumor differentiation, but the mechanisms underlying this process remain largely unclear.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Single-nucleus transcriptomics (snRNA-seq) data of neuroblastoma samples were obtained from the Synapse repository to investigate the composition of heterogeneous tumor cell clusters. The feature of the Stage 4S-specific tumor cell subpopulation was revealed through differential expression analysis, pathway enrichment analysis and pseudotime analysis, followed by clinical significance validation on public cohort datasets. The biological function of secreted SLIT3 was validated using multiple in vitro models, including recombinant protein treatment, conditioned medium treatment, and cell lines coculture, to confirm the intratumoral crosstalk effect. Orthotopic and subcutaneous xenograft models were established to verify SLIT3's in vivo function. Cellular bulk RNA-seq analysis was performed with or without SLIT3 recombinant protein treatment to discover the downstream pathways activated by SLIT3, followed by validation with specific pathway inhibitors.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Analysis of snRNA-seq revealed a distinct subpopulation of tumor cells within INSS Stage 4S neuroblastoma, characterized by a spontaneous regression-like program progressing toward differentiation. Activated SLIT-ROBO signaling was found in the Stage 4S-specific tumor cell subpopulation, which strongly correlated with favorable prognosis. Further investigation into the secreted ligands in SLIT-ROBO related pathways revealed that SLIT3 displayed the most potent enrichment in Stage 4S tumors and the strongest differentiation-inducing effect. In vitro experiments using recombinant SLIT3 protein, conditioned medium, and cell lines coculture consistently demonstrated the capacity of SLIT3 to induce neuroblastoma cell differentiation via intratumoral crosstalk, as evidenced by increased neurite outgrowth and elevated expression of neuronal differentiation markers. Both orthotopic xenograft and subcutaneous xenograft models demonstrated that SLIT3 expression suppressed tumor growth, leading to in vivo tumor differentiation. Mechanistically, PLCβ/PKC signaling mediates the SLIT3-induced neuroblastoma cell differentiation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Stage 4S-specific tumor cell subpopulation exhibits a spontaneous regression-like program, from which SLIT3 mediates intratumoral crosstalk and promotes neuroblastoma differentiation via PLCβ/PKC signaling. These findings provide new insights into the mechanism of spontaneous regression in neuroblastoma and ","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"598"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Fully volumetric body composition analysis for prognostic overall survival stratification in melanoma patients.","authors":"Katarzyna Borys, Georg Lodde, Elisabeth Livingstone, Carsten Weishaupt, Christian Römer, Marc-David Künnemann, Anne Helfen, Lisa Zimmer, Wolfgang Galetzka, Johannes Haubold, Christoph M Friedrich, Lale Umutlu, Walter Heindel, Dirk Schadendorf, René Hosch, Felix Nensa","doi":"10.1186/s12967-025-06633-w","DOIUrl":"10.1186/s12967-025-06633-w","url":null,"abstract":"","PeriodicalId":17458,"journal":{"name":"Journal of Translational Medicine","volume":"23 1","pages":"596"},"PeriodicalIF":6.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}