Journal of Hematology & Oncology最新文献

{"title":"Cytokine fusion proteins for solid tumor therapy: mechanistic insights and clinical advances","authors":"Yufang Wang,Jing Zheng,Zhen Li,Jingjing Qu,Yuqing Ren,Ziwan Cai,Yuekang Li,Wenjia Sun,Nan Jiang,Cuihong Cai,Kexin Ruan,Jiahe Shi,Zheya Zhang,Jianya Zhou","doi":"10.1186/s13045-026-01842-2","DOIUrl":"https://doi.org/10.1186/s13045-026-01842-2","url":null,"abstract":"","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"53 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148893676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutathione reductase deficiency potentiates the immunogenicity of ferroptosis and cuproptosis via amplified reactive oxygen species accumulation and cGAS-STING pathway activation.","authors":"Xiaoyi Deng, Zaidong Deng, Bin Zhu, Ruiqi Hu, Jing Ma, Changheng Li, Pu Zhang, Lei Li, Hui Yang, Yu Liu, Yanxun V Yu, Youngnam N Jin","doi":"10.1186/s13045-026-01840-4","DOIUrl":"10.1186/s13045-026-01840-4","url":null,"abstract":"<p><strong>Background: </strong>Cancer remains a major therapeutic challenge due to drug resistance and metastasis, processes driven by oxidative stress and redox imbalance. Targeting this vulnerability through ferroptosis (iron-dependent lipid peroxidation) and cuproptosis (copper-driven mitochondrial dysfunction), two ROS-mediated cell death pathways, offers a promising therapeutic strategy. However, clinical translation is hindered by incomplete understanding of their redox regulation and limited immunogenicity.</p><p><strong>Methods: </strong>A genome-wide CRISPR knockout screen was performed to identify key regulators of ferroptosis. Genetic depletion or pharmacological inhibition of candidate genes was evaluated across multiple cancer cell lines for sensitivity to ferroptosis inducer RSL3 and the cuproptosis inducer elesclomol (Es). Antitumor efficacy was assessed in xenograft, orthotopic, metastatic, and syngeneic mouse models, alone or combined with immune checkpoint inhibitors. Mechanistic studies also examined ROS production, mitochondrial stress, mitochondrial DNA release, cGAS-STING activation, and immune responses within the tumor microenvironment.</p><p><strong>Results: </strong>Glutathione reductase (GSR), a central enzyme maintaining reduced glutathione (GSH) homeostasis, was identified as the top suppressor of ferroptosis. GSR knockout or pharmacological inhibition markedly sensitized diverse cancer cell lines to RSL3-induced ferroptosis, while GSR overexpression conferred resistance. Strikingly, GSR depletion also enhanced sensitivity to cuproptosis triggered by the copper ionophore Es. In multiple in vivo tumor models, GSR inhibition synergizes with RSL3 or Es to suppress tumor growth, inhibit lung metastasis, and prolong survival. Mechanistically, GSR deficiency amplified ROS production, induced mitochondrial stress, and triggered the cytosolic mitochondrial DNA release under ferroptotic or cuproptotic stress, activating the cGAS-STING pathway in vitro and in vivo. This increased inflammatory cytokine production, promoted immunogenic cell death, and enhanced the release of damage-associated molecular patterns (DAMPs), including HMGB1. Together, GSR inhibition combined with a ferroptosis or cuproptosis inducer transformed the tumor microenvironment into a highly immune stimulatory state, thereby enhancing the efficacy of immune checkpoint blockade through increased dendritic cell activation and T-cell infiltration and activation.</p><p><strong>Conclusions: </strong>GSR represents a key molecular node connecting and modulating ferroptosis and cuproptosis through redox regulation. Targeting GSR amplifies ROS-mediated immunogenic cell death, triggers cGAS-STING activation in cancer cells, and enhances the efficacy of cancer immunotherapy, providing a promising redox-based therapeutic strategy.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-definition spatial transcriptomics visualizes the cellular and molecular architecture underlying perineural invasion in localized prostate cancer.","authors":"Paul Vinu Salachan, Line Raaby, Jacob Fredsøe, Benedicte Ulhøi, Michael Borre, Karina D Sørensen","doi":"10.1186/s13045-026-01841-3","DOIUrl":"10.1186/s13045-026-01841-3","url":null,"abstract":"<p><p>Distinguishing indolent from aggressive tumors remains a key challenge in the clinical management of prostate cancer (PC), highlighting the need for better tools for accurate risk stratification. A defining feature of aggressive PC is its propensity for perineural invasion (PNI), a pathological finding that is associated with poor prognosis. Despite its clinical significance, very little is known about the spatial and molecular determinants of PNI in PC. To address this, we used high-definition spatial transcriptomics (Visium HD) to profile the PNI-associated tumor microenvironment (TME) of a representative PC patient at near single-cell resolution. Spatial mapping of the expressed genes and inferred cell types revealed transcriptionally divergent malignant cell states spatially linked to PNI within this patient. Nerve-invasive PC cells were organized within a distinct spatially localized niche that exhibited altered TME characteristics, including increased proportions of macrophages, CD4 T-cells, and endothelial cells, suggesting coordinated changes in the tumor- and immune microenvironments. The PNI-associated niche in this patient further displayed enrichment of pathways involved in immune regulation and extracellular matrix remodeling, consistent with PNI-associated niche remodeling. APP-CD74 was identified as a potential signaling axis associated with tumor-nerve, nerve-macrophage, and nerve-endothelial cell interactions, suggesting PNI in this patient may be associated with distinct microenvironmental signaling programs. We further revealed a PNI-associated PC signature that held biomarker potential at the early-localized and advanced-metastatic disease stages. Although based on a single patient, these results contribute to our understanding of the spatial and molecular features of PNI in PC and may help guide personalized treatment choices for PC patients in the future.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mucosal immunity: mechanism and application in cancer immunotherapy.","authors":"Maosen Xu, Ruolan Xia, Yuquan Wei, Xingchen Peng, Xiawei Wei","doi":"10.1186/s13045-026-01829-z","DOIUrl":"10.1186/s13045-026-01829-z","url":null,"abstract":"<p><p>Recent advances in immunotherapy have significantly revolutionized cancer treatment landscape and prompted extensive research into novel vaccine-based anti-tumor therapy. As the primary defense against external infections, the mucosal immune response plays a pivotal role in maintaining normal physiological functions and preventing pathogen invasion. Mucosal tissues are among the most common sites of tumor initiation, and therefore harnessing mucosal immune to fight against malignant cells represents a feasible option for optimizing and improving current antitumor therapies. Over the past few decades, numerous efforts have been devoted to designing ideal and effective mucosal vaccine. Some clinical trials using mucosal vaccine for cancer therapy have been also launched continually. In this review, we introduce the mechanisms of mucosal immunity, with a focus on the respiratory, gastrointestinal, and urogenital tracts. We also summarize recent research and clinical trials on the application of mucosal vaccines in anti-tumor therapy, aiming to provide new perspectives and directions for future studies.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current and future therapies for triple-negative breast cancer.","authors":"Zi-Xun Wang, Xi-Yu Liu, Yu-Xiao Wu, Yu-Ling Xiao, Li-Ping Ge, Song-Yang Wu, Yi-Zhou Jiang, Zhi-Ming Shao","doi":"10.1186/s13045-026-01839-x","DOIUrl":"10.1186/s13045-026-01839-x","url":null,"abstract":"<p><p>Triple-negative breast cancer remains an aggressive and biologically heterogeneous breast cancer subtype. Although the therapeutic landscape has expanded, durable disease control remains clinically challenging in many settings. Existing reviews often organize TNBC therapy by drug class or molecular subtype, which can obscure how treatment response is shaped by interacting biological layers. Here, we review current and emerging therapeutic strategies through a three-layer framework: tumor-cell-intrinsic vulnerabilities, the local immune and stromal microenvironment, and host-level systemic modifiers. We summarize established approaches, including chemotherapy, immune checkpoint blockade, antibody-drug conjugates and PARP inhibition in biomarker-defined settings, and distinguish them from maturing or exploratory strategies such as pathway-directed therapy, epigenetic modulation, anti-vascular combinations, regulated cell-death induction, cellular therapy, vaccines, microbiome-related interventions, liquid biopsy, AI-supported multiomics and adaptive trial designs. This framework integrates evidence level, disease stage, biomarker reliability and patient tolerance into treatment selection for TNBC precision therapy.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma biomarkers predicting development of lung cancer 5 years before diagnosis.","authors":"Kostas A Papavassiliou, Athanasios G Papavassiliou","doi":"10.1186/s13045-026-01838-y","DOIUrl":"https://doi.org/10.1186/s13045-026-01838-y","url":null,"abstract":"","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13474877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148760052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: First in human phase 1 study of DT2216, a selective BCL-xL degrader, in patients with relapsed/refractory solid malignancies.","authors":"Daruka Mahadevan, Minal Barve, Devalingam Mahalingam, Jay Parekh, Michael Kurman, James Strauss, Larry Tremaine, Robert Hromas, Joshua Sills, John McCulloch, John Harkey, Stacy Suberg, Lisa Zimmerman, Guangrong Zheng, Daohong Zhou","doi":"10.1186/s13045-026-01837-z","DOIUrl":"10.1186/s13045-026-01837-z","url":null,"abstract":"","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13459379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The KRAS targeting revolution in metastatic pancreatic cancer: insights from the landmark RASolute-302 trial and emerging allele-specific strategies at ASCO 2026.","authors":"Serena Pillozzi, Elisa Giommoni, Giulia Petroni, Daniele Rossini, Daniele Lavacchi, Marco Brugia, Andrea Galli, Lorenzo Antonuzzo","doi":"10.1186/s13045-026-01834-2","DOIUrl":"10.1186/s13045-026-01834-2","url":null,"abstract":"<p><p>Survival in metastatic pancreatic ductal adenocarcinoma (mPDAC) has long been limited by a dismal second-line therapeutic ceiling dictated by conventional chemotherapy. However, breakthrough data from the ASCO 2026 Annual Meeting and the publication of the phase III RASolute-302 trial mark a definitive shift toward targeted KRAS inhibition. This correspondence highlights how the first-in-class pan-RAS (ON) inhibitor daraxonrasib (RMC-6236) virtually doubled median overall survival (13.2 vs. 6.6 months) and progression-free survival compared to chemotherapy in second-line mPDAC, establishing a new standard of care. Concurrently, we evaluate emerging allele-specific strategies from ASCO 2026 designed to optimize target engagement and safety. These include the selective KRAS G12D inhibitor DN022150 and promising horizontal combinations pairing the G12D inhibitor HRS-4642 with either the anti-PD-L1 antibody adebrelimab or a Nectin-4-targeted antibody-drug conjugate (ADC). Furthermore, we address the KRAS G12C cohort where farnesyl transferase co-inhibition (darlifarnib plus adagrasib) successfully bypasses adaptive resistance. Ultimately, the therapeutic landscape of mPDAC is transitioning toward tailored genomic frameworks. Future success will rely on optimizing the clinical sequencing or combination of pan-RAS and allele-specific agents, guided by real-time liquid biopsies, to permanently dismantle resistance and transform mPDAC into a manageable molecular entity.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13453085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148697681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A phase 1 trial of CD123-directed chimeric antigen receptor T-cell therapy in adults with relapsed/refractory acute myeloid leukemia or blastic plasmacytoid dendritic cell neoplasm.","authors":"Lihua E Budde, Marissa M Del Real, Joo Song, Tracey Stiller, Yan Wang, Ahmed Aribi, Karamjeet Sandhu, Ryotaro Nakamura, Emanuela C Marcucci, Jian J Wu, Kenneth Ng, Mary C Clark, Brent Wood, Jamie R Wagner, Jinny Paul, Christine E Brown, Anthony Stein, Guido Marcucci, M Suzette Blanchard, Joycelynne Palmer, Stephen J Forman","doi":"10.1186/s13045-026-01833-3","DOIUrl":"10.1186/s13045-026-01833-3","url":null,"abstract":"<p><strong>Background: </strong>Patients with relapsed acute myeloid leukemia (AML), particularly following allogeneic stem cell transplant (alloHCT), have extremely limited therapeutic options. CD123 is an AML-associated antigen and represents an attractive target for immunotherapy. We report outcomes of a phase 1 trial evaluating CD123-targeting chimeric antigen receptor (CAR) T cells in patients with relapsed/refractory (r/r) AML or blastic plasmacytoid dendritic cell neoplasm (BPDCN).</p><p><strong>Methods: </strong>This was a single center, open-label, phase 1 dose escalation study enrolling patients with either CD123-positive r/r AML (Arm 1) or BPDCN (Arm 2). Patients received autologous or donor-derived allogeneic CD123 CAR T cells following lymphodepletion. The co-primary objectives were to examine safety and anti-tumor activity using an activity-constrained for toxicity design and to determine the recommended phase 2 dose. Secondary objectives included assessments of progression-free and overall survival.</p><p><strong>Results: </strong>We enrolled 41 patients, of whom 21 patients (n = 19 on Arm 1 and n = 2 on Arm 2) received CD123 CAR T-cell infusion. The median age of treated AML patients was 45 years (range: 20-71); the two BPDCN patients were aged 24 and 75 years. Among AML patients, 17 (89%) had undergone prior alloHCT. AML patients received 50 × 10⁶ (n = 2), 200 × 10⁶ (n = 6), or 500 × 10⁶ (n = 11) CAR T cells; BPDCN patients received 100 × 10⁶ CAR T cells. There was no dose-limiting toxicity, prolonged myelosuppression, or graft-versus-host disease. Fourteen (74%) AML patients developed grade ≤ 3 cytokine release syndrome (CRS) and 11 (58%) experienced grade ≤ 2 neurotoxicity. Fifteen of 19 treated AML patients were evaluable for disease response for overall best response, of whom 4 (26.7%) had best response of complete remission, including 2 with incomplete count recovery. Neither patient with BPDCN developed CRS but both experienced grade 1 neurotoxicity. One of 2 BPDCN patients achieved CR and relapsed at 3 months. CAR T cell expansion was dose-dependent, but persistence was limited.</p><p><strong>Conclusions: </strong>CD123-directed CAR T-cell therapy is feasible and demonstrates a favorable safety profile in patients with r/r AML and BPDCN, including those with prior alloHCT. Although the estimated overall complete remission rate was modest, these findings provide a foundation for further optimization of CD123 CAR T-cell design, patient selection, and combination strategies.</p><p><strong>Trial registration: </strong>This trial was registered at ClinicalTrials.gov as NCT02159495.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13536854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A modular γδ TCR-T platform combining KRAS pMHC targeting with re-dosable mRNA engager redirection.","authors":"Ángel Ramírez-Fernández, Adham S Bear, Elahe Kamali, Robert Bartoszek, Matthew Ho, Gregory M Chen, Devin Dersh, Laura Córdoba-Espejo, Jiageng Liu, Mosha Deng, Miriam Velasco-Sidro, Ankita Jain, Julia Han Noll, Caitlin R Hopkins, Owen Koucky, Janna Minehart, Alexander J Dimitri, Erik Williams, Maya Lavorando, Alejandro Segura-Tudela, John Scholler, Julie Barber-Rotenberg, Julie K Jadlowsky, Daniel J Powell, Anne Chew, Vanessa E Gonzalez, Donald L Siegel, Bruce L Levine, Michael T Lotze, Carl H June, James L Riley, Robert H Vonderheide, Friederike Herbst, Joseph A Fraietta","doi":"10.1186/s13045-026-01836-0","DOIUrl":"10.1186/s13045-026-01836-0","url":null,"abstract":"<p><p>Solid tumors often evade TCR-engineered αβ T cells when antigen expression varies or when the restricting Human Leukocyte Antigen (HLA) allele is lost. γδ T cells, in contrast, detect cellular dysregulation through non-peptide/Major Histocompatibility Complex (MHC) cues, including phosphoantigens and stress ligands, and can be developed as allogeneic therapies. Although intratumoral γδ T cell signatures are associated with improved outcome across cancers, γδ recognition itself is broad and still selected within the thymus just as αβ T cell receptors (TCRs) are. It does not, however, anchor specificity to a defined driver-mutation pMHC epitope. We therefore asked whether a high-affinity, co-receptor-independent αβ TCR could graft oncogenic-driver specificity onto γδ T cells while leaving the endogenous γδ TCR intact. We knocked the KRASG12V/HLA-A*11:01 TCR A11v into primary human γδ T cells. Engineered cells co-expressed the transgenic αβ TCR and the endogenous γδ TCR and lysed KRASG12V/HLA-A*11:01⁺ tumor cells in vitro and in vivo. To cover potential resistance through loss of HLA-A*11:01, we delivered an mRNA lipid nanoparticle (LNP) encoding a secreted mesothelin×CD3 (M5) bispecific T cell engager (TCE). LNP-M5 produced circulating TCE that redirected γδ A11v T cells and polyclonal bystander T cells to kill mesothelin⁺ targets, accompanied by development of higher γδ A11v T cell counts in vivo. In humanized mice bearing mixed HLA-A*11:01⁺ and HLA-A*11:01 - KRASG12V tumors, γδ A11v T cells produced transient control, whereas adding LNP-M5 yielded complete responses and prolonged survival. Thus, this two-part therapy couples invariant driver targeting to tunable redirection and addresses loss of the restricting HLA allele, a central escape route for TCR-based therapy. It provides an off-the-shelf reagent to enable KRAS-anchored treatment with the ability to redeliver the reagent.</p>","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"19 1","pages":""},"PeriodicalIF":47.8,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13536626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}