Medical Oncology最新文献

{"title":"A20 promotes OPN ubiquitination and degradation to inhibit cell growth and invasion in human hepatocellular carcinoma.","authors":"Xiangqian Zhang, Zhi Li, Jianyan Qin, Dandan Zhu, Shuhong Zhang, Ye Zhang, Ying Fu, Xiaojin Liu, Qigang Shao","doi":"10.1007/s12032-026-03423-2","DOIUrl":"10.1007/s12032-026-03423-2","url":null,"abstract":"<p><p>Abnormal osteopontin (OPN) expression has been implicated in hepatocellular carcinoma (HCC) progression. In this study, we assessed the prognostic value and biological functions of OPN in HCC. We also identified that A20 interacts with OPN and promotes OPN ubiquitination and protein degradation through the ubiquitin-proteasome system. The reduction in OPN levels induced by A20 attenuates OPN-associated proliferative and migratory phenotypes in HCC cells. Notably, advanced HCC tissues exhibited elevated OPN levels, while A20 expression showed variable patterns in clinical samples. In the clinical cohort, high OPN expression was associated with poorer overall survival, while high A20 expression was also unexpectedly associated with unfavorable prognosis. Combined analysis of OPN and A20 expression provided complementary prognostic stratification for HCC patients. Consequently, our results reveal a mechanism involving OPN ubiquitination and suggest that the OPN/A20 expression profile may provide prognostic stratification for patients after HCC resection. Considering the significance of OPN expression in HCC, our research also provides insights into potential therapeutic strategies for HCC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer-associated mitochondrial homeostasis disrupted and retrograde signaling activated.","authors":"Pinya Liu, Zihan Wang, Shuhua Xi, Yue Wang","doi":"10.1007/s12032-026-03405-4","DOIUrl":"10.1007/s12032-026-03405-4","url":null,"abstract":"<p><p>This review discusses mitochondrial homeostasis disrupted and retrograde signaling activated in oncogenesis and cancer progression. We summarize mitochondrial alterations and dysfunction in cancer, including mitochondrial DNA mutations, copy number alterations, dynamics changes and abnormalities of mitochondria enzymes in cancer. Furthermore, we discuss the findings on the main molecular mechanisms and roles of mitochondrial retrograde signaling pathways networks, such as reactive oxygen species (ROS), unfolded protein response (mtUPR), calcium and other retrograde signaling on cancer progression. Dysfunctional mitochondria induced retrograde signaling can lead to changes in gene expression. Tumor cells intimidate mitochondrial regulatory pathways to support tumor growth. Looking forward, we highlight critical knowledge gaps, including the need to decipher the spatiotemporal dynamics of retrograde signals, the context‑dependent dual roles of mitochondrial stress responses, and the integration of multi‑omics data to identify predictive biomarkers. We also discuss emerging therapeutic strategies that target mitochondrial retrograde signaling, such as small‑molecule modulators of mitochondrial calcium uniporter, ROS‑scavenging nanomedicines, and combination regimens with immune checkpoint inhibitors. Mitochondrial retrograde signaling might be served as a potential target for new therapeutic interventions in cancers, and future research should focus on translating these mechanistic insights into clinically actionable approaches.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ablation-immunotherapy synergy in cancer: mechanisms of the abscopal effect, emerging clinical applications, and translational roadmaps for next-generation onco-immunology.","authors":"Mohammed Ali Hama, Mohammed Adnan Madhat, Farhang Hameed Awlqadr, Awa Hama Amin Mahmood, Rawa Abdalrahim Abdalla, Rahand Kamal Ali, Sivar Hama Tahir Kareem, Nihad Ebrahim Hama, Shnya Rahman Hamalaw, Ammar Mohammed Al-Farga","doi":"10.1007/s12032-026-03396-2","DOIUrl":"10.1007/s12032-026-03396-2","url":null,"abstract":"<p><p>Tumor ablation is rapidly being appreciated as not only a locoregional cytoreductive tool but also an important modulator of antitumor immunity. Many ablative methods (including, but not limited to, radiofrequency ablation, microwave ablation, cryoablation, high-intensity focused ultrasound, and photothermal and photodynamic methods) have been shown to induce immunogenic cell death, release tumor-associated antigens, and produce danger-associated molecular signals that can remodel the tumor microenvironment. While such effects can trigger innate and adaptive immune responses, they are usually not sufficient to confer durable systemic tumor control. One such example is the abscopal effect, a rare and unpredictable occurrence in which local therapy induces shrinkage of both primary and distant metastases. Combining ablation with immunotherapy represents a powerful strategy to overcome these limitations of immunotherapy. While ablation can function as an in situ vaccine by increasing tumor antigen availability and inflammatory signaling, immunotherapeutic agents, particularly immune checkpoint inhibitors, can enhance and prolong T-cell-mediated responses by alleviating immune exhaustion and disrupting suppressive pathways. Preclinical and early clinical studies on several solid tumors have indicated that this synergy can promote immune priming, enhance the infiltration of cytotoxic lymphocytes, and result in global disease control. Despite this, therapeutic responses continue to vary, indicating persisting obstacles related to optimal modality choice, treatment timing, tumor immune contexture, and biomarker-driven patient stratification. This review brings together mechanistic insights and clinical evidence to define the biological foundations of ablation-immunotherapy synergy, with a particular focus on the abscopal effect as a model system for systemic immune activation. It further defines the critical translational hurdles and strategic imperatives that need to be addressed to convert rare immune-mediated responses into replicable and clinically meaningful outcomes.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nutritional inflammatory hematological risk index predicts clinical outcomes in patients with advanced NSCLC receiving immunotherapy.","authors":"Yiqing Hu, Zhigang Chen, Mengxian Yao, Lei Gan","doi":"10.1007/s12032-026-03440-1","DOIUrl":"10.1007/s12032-026-03440-1","url":null,"abstract":"<p><p>In real-world clinical settings, patients with advanced non-small cell lung cancer (NSCLC) receiving immune checkpoint inhibitors (ICIs) display significant heterogeneity, highlighting the need to identify key prognostic biomarkers and clinical factors. This retrospective study included 340 advanced NSCLC patients treated with ICIs. Cox regression analyses identified factors associated with progression-free survival (PFS). A Nutritional Inflammatory Hematological Risk Index (NIHRI) was constructed using these factors, and a prognostic nomogram was developed. Performance was assessed using the C-index, calibration plots, and decision curve analysis (DCA), with internal validation via bootstrapping. Hemoglobin and the albumin-to-alkaline phosphatase ratio (AAPR) were independent prognostic factors. The NIHRI, combining dichotomized hemoglobin (< 120 g/L vs. ≥120 g/L) and AAPR (< 0.56 vs. ≥0.56), stratified patients into low- (0 points), intermediate- (1 point), and high-risk (2 points) groups, with significantly different PFS (P<0.001). The nomogram, incorporating NIHRI, tumor stage, PD-L1, and ECOG-PS, demonstrated a C-index of 0.70 (optimism-corrected: 0.69) and predictive accuracy for 1-, 2-, and 3-year PFS (AUCs: 0.81, 0.85, and 0.88, respectively). DCA confirmed its acceptable clinical net benefit. We developed and validated a novel prognostic tool, the NIHRI, based on a combination of hemoglobin and AAPR. This integrated nomogram provides a non-invasive and clinically accessible quantitative method for predicting prognosis in patients with NSCLC undergoing immunotherapy, thereby aiding in personalized clinical decision-making.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RBM protein family: Focusing on the occurrence, progression and treatment of cancer.","authors":"Huhu Zhang, Wenxin Zheng, Lingxi Li, Chenhui Geng, Yuxiang Wang, Jianyu Zhang, Yulan Sun, Xuanyu Zhang, Bing Li","doi":"10.1007/s12032-026-03439-8","DOIUrl":"10.1007/s12032-026-03439-8","url":null,"abstract":"<p><p>The RNA-binding motif (RBM) protein family plays a crucial role in regulating RNA metabolism, including transcription, splicing, stability, and translation. Dysregulation of RBM proteins has been increasingly implicated in the initiation, progression, and therapeutic resistance of various cancers. This review summarizes current knowledge on the RBM protein family, with a focus on their involvement in alternative splicing and m6A RNA methylation-two key post-transcriptional mechanisms that influence cancer biology. Members such as RBM5 and RBM10 function as tumor suppressors by modulating apoptosis, cell cycle, and splicing of oncogenic transcripts, while others like RBM15 and RBM15B contribute to tumorigenesis through m6A modification and downstream signaling pathways. The dual roles of certain RBM proteins in different cancer contexts highlight their complexity and potential as both biomarkers and therapeutic targets. Further investigation into the molecular mechanisms of RBM proteins may provide new insights for cancer diagnosis and treatment strategies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Engineered mesenchymal stem cell-derived small extracellular vesicles delivering miR-124 suppress colorectal cancer progression through EZH2 downregulation and attenuation of STAT3 signaling.","authors":"Roudabeh Behzadi Andouhjerdi, Fatemeh Hosseini, Niki Hosseinzadeh, Sakineh Zivari, Shokoufeh Salkhordeh, Marzieh Mohammadi, Maryam Rahmani, Parmida Hatami, Shima Sadat Naji, Mohammad Pourtahmasebi, Mina Khanabadi, Mahtab Golbahar, Arezoo Hajesmaeili, Parisa Eftekhari, Mohadeseh Asbaghi, Ali Norouz-Nejad, Parastoo Akbarabadi, Mohammad H Ghazimoradi, Sadegh Babashah, Zeinab Piravar","doi":"10.1007/s12032-026-03418-z","DOIUrl":"10.1007/s12032-026-03418-z","url":null,"abstract":"<p><p>Colorectal cancer (CRC) progression is driven by dysregulated molecular pathways and epigenetic alterations, including enhancer of zeste homolog 2 (EZH2)-mediated histone methylation and STAT3 hyperactivation. While microRNA-124 (miR-124) acts as a tumor suppressor by targeting EZH2, its clinical translation is hindered by delivery challenges. Here, we engineered mesenchymal stem cell-derived small extracellular vesicles (MSC-sEVs) to deliver miR-124, exploiting their tumor-homing capacity and biocompatibility to suppress CRC progression. Bioinformatic analysis of clinical datasets revealed miR-124 downregulation in CRC tissues, correlating with advanced stages and poor prognosis. Lentiviral transduction enabled efficient miR-124 packaging into MSC-sEVs, which were internalized by CRC cells, restoring functional miR-124 levels. Mechanistically, miR-124 directly silenced EZH2, thereby suppressing its oncogenic activity. This led to attenuated STAT3 phosphorylation-a dual effect that inhibited proliferation, migration, and epithelial-mesenchymal transition (EMT) in CRC cells. In vitro, MSC-sEV-miR-124 induced apoptosis, sensitized cells to 5-fluorouracil, and reversed chemoresistance via EZH2 downregulation. In vivo, MSC-sEV-miR-124 significantly reduced tumor growth in BALB/c mice, downregulated EZH2/STAT3 signaling, and suppressed Ki-67 and EMT markers in xenografts. This study provides proof-of-concept that engineered MSC-sEVs can serve as a delivery platform for miR-124 in murine CRC models, offering a dual-targeting strategy against EZH2 and STAT3 to disrupt CRC progression. Our findings suggest that EV-based miRNA delivery warrants further investigation as a strategy to modulate the tumor microenvironment, providing a foundation for development aimed at overcoming epigenetic and oncogenic signaling barriers in CRC therapy.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal circ55033 promotes cigarette smoke-induced bladder cancer by modulating EMT and stem cell properties.","authors":"Hao Geng, Yu Wu, Jiaxing Ma, Wei Zhang, Zhaofeng Liang, Tao Zhang","doi":"10.1007/s12032-026-03444-x","DOIUrl":"10.1007/s12032-026-03444-x","url":null,"abstract":"<p><p>Bladder cancer has high morbidity and mortality, and cigarette smoke is a major risk factor for this disease. Exosomal circRNAs are widely involved in tumor progression, while their roles in smoke-related bladder cancer remain unclear. In the present study, we identified and validated circ55033, a highly expressed circRNA in clinical samples from smoking patients. Functional experiments demonstrated that cigarette smoke induced EMT and cancer stemness in bladder cancer cells via exosome-transported circ55033. Mechanistically, circ55033 acts as a molecular sponge for miR-1286 to exert its oncogenic effects. Notably, exosomal circ55033 exhibits preliminary diagnostic capacity in patient serum and represents a promising translational candidate for non-invasive liquid biopsy biomarkers and targeted therapeutic interventions against smoking-related bladder cancer. These findings provide novel insights into the mechanisms underlying cigarette smoke-induced bladder cancer and highlight the potential of exosomal circ55033 as a preliminary candidate diagnostic and therapy biomarker.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GLIS3 promotes the malignant biological behavior of gastric cancer cells by transcriptionally regulating PNPO to influence autophagy.","authors":"Yuejin Li, Yiming Ouyang, Yu Zhu, Dezhi Hou, Xing Li, Xiaodong Guo, Ping Sheng, Hailong Wu, Yingzhong Liao, Kunmei Gong, Linhai Li","doi":"10.1007/s12032-026-03433-0","DOIUrl":"10.1007/s12032-026-03433-0","url":null,"abstract":"<p><p>Gastric cancer (GC) is among the most common malignant tumors worldwide and is a major contributor to increasing cancer incidence and mortality. GLIS family zinc finger 3 (GLIS3) is involved in GC progression, but its specific regulatory mechanisms remain incompletely understood. A GC tumor-bearing model was established by subcutaneously injecting MKN-45 cells into nude mice. RT‒qPCR and Western blotting were employed to detect the expression of key genes and proteins. CCK-8, colony formation, and Transwell assays were utilized to assess cell proliferation, migration, and invasion capabilities. Immunofluorescence and MDC staining were performed to examine autophagy-related indicators, and chromatin immunoprecipitation (ChIP) was performed to validate the binding of GLIS3 to the PNPO promoter. GLIS3 expression was upregulated in patients with GC and was significantly associated with shortened patient survival. GLIS3 knockdown inhibited the proliferation, migration, and invasion of MKN-45 cells in vitro and suppressed tumor growth in nude mice. Further studies revealed that GLIS3 knockdown inhibited the malignant biological behaviors of MKN-45 cells by suppressing autophagy. Additionally, GLIS3 bound to the PNPO promoter and promoted its transcription. Overexpression of PNPO increased the viability, proliferation, migration, invasion, and autophagy of MKN-45 cells in the context of GLIS3 knockdown, whereas further treatment with the autophagy inhibitor 3-MA weakened these effects. GLIS3 activates autophagy by transcriptionally regulating PNPO expression, thereby promoting the malignant biological behaviors of GC cells.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mdivi-1 augments chlorpromazine's anticancer effect via modulation of mitochondrial dynamics, hallmarks of cancer-related cellular behavior, and oxidative stress.","authors":"Thoria Donia, Doha F Ismail, Samar S Alkafaas, Eiman Adly, Ashraf A Tabll, Mohamed Hessien","doi":"10.1007/s12032-026-03364-w","DOIUrl":"10.1007/s12032-026-03364-w","url":null,"abstract":"<p><p>The multifaceted therapeutic potential of phenothiazines was previously documented. This study investigated the anticancer effect of chlorpromazine (CPZ) in hepatoma and breast cancer cell lines and further explored the implications of mitochondrial dynamics. To establish this aim, the cytotoxic and antimitotic effects of CPZ combined with the mitochondrial fission inhibitor (mdivi-1) were assessed in HepG2 and MDA-MB-231 cells using MTT and clonogenic assays, respectively. Apoptosis and nuclear changes were evaluated with Annexin V/PI, acridine orange/ethidium bromide, and DAPI staining. Moreover, cell migration was examined using a wound-healing assay and the expression of epithelial-mesenchymal transition (EMT) markers. Additionally, 2',7'-dichlorodihydrofluorescein diacetate staining was used to assess cellular ROS, whereas the expression of mitochondrial fusion- and fission-related genes was assessed by RT-PCR. The results addressed CPZ's cytotoxic effect in both cancer cell types. The IC₅₀ decreased when cells were concomitantly treated with CPZ and mdivi-1, where HepG2 cells were more responsive than MDA-MB-231 cells. Additionally, dual treatment impaired cell membrane integrity, caused chromatin condensation, increased apoptosis, reduced colony count, restricted cell migration, and downregulated the expression of the mesenchymal markers (vimentin and DDR2 genes). Although mdivi-1 alone upregulated mitochondrial fusion genes (MFN1/MFN2/OPA), combined treatment with CPZ, however, dysregulated both fusion and fission-related genes. The mechanisms underlying the anticancer activity of CPZ and the enhancing potential of mdivi-1 involved chromatin condensation, reduction of the antioxidant capacity, overproduction of cellular ROS, downregulation of Nrf2, and subsequent apoptosis. In conclusion, this work emphasizes the anticancer effect of CPZ and highlights the involvement of mdivi-1 in promoting the anticancer potential against liver and breast cancers.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stable isotopes from Earth science to bedside medicine: beyond tracers and toward mechanistic biomarkers in medical oncology.","authors":"Emma U Hammarlund, Per Malmberg, Julhash U Kazi, Nicole R Posth, Kenneth J Pienta","doi":"10.1007/s12032-026-03436-x","DOIUrl":"10.1007/s12032-026-03436-x","url":null,"abstract":"<p><p>Stable isotopes are non-radioactive variants of the same element whose small mass differences produce predictable effects in chemical and biological systems. While medicine has mainly used the administration of enriched stable isotopes as tracers of physiological function, the natural sciences developed stable-isotope ratios into robust measures of source, transformation, and underlying mechanism across Earth and life history. This analytical power - that often goes beyond conventional concentration-based assays - emerged through advances in isotope theory, mass spectrometry, but perhaps most importantly also globally shared reference systematics. Here, we review that trajectory and argue that medicine is positioned for a similar shift, as new computational and analytical tools make isotope analysis increasingly compatible with clinical throughput. In this shift, some natural isotope variation may serve as mechanistic biomarkers of physiology and disease. Integrated with multiomics and machine learning, stable isotopes could support earlier detection, improved risk stratification, and personalized care, particularly in cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 11","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}