Medical Oncology最新文献

{"title":"NEK2 promotes the progression of osteosarcoma through the AKT/p-AKT pathway and interacts with FoxM1.","authors":"Xin Tan, Xiaojing Liang, Yi Feng, Ming Xie, Kun Zhong, Wenwu Luo, Yurao Wang, Yu Yin, Yongping Cai","doi":"10.1007/s12032-025-02657-w","DOIUrl":"10.1007/s12032-025-02657-w","url":null,"abstract":"<p><p>Osteosarcoma is a highly invasive and metastatic primary malignant bone tumor, and resistance to chemotherapy remains a major therapeutic challenge. Our previous studies showed that increased Forkhead box protein M1 (FoxM1) expression promotes osteosarcoma progression. While NIMA-related kinase 2 (NEK2) has emerged as a potential oncogenic factor, its functional role and molecular mechanisms in osteosarcoma remain poorly understood. Pearson's correlation analysis was performed to assess the relationship between FoxM1 and NEK2 expression using the GSE33382 dataset from GEO. Coimmunoprecipitation (Co-IP) was employed to investigate FoxM1-NEK2 interactions. NEK2 expression was modulated in the HOS and U2OS osteosarcoma cell lines through pharmacological inhibition (MBM-55), siRNA-mediated knockdown, and plasmid-mediated overexpression. Cellular proliferation was evaluated via CCK-8 and colony formation assays. Transwell migration/invasion assays and flow cytometry were performed to assess the metastatic potential and apoptosis, respectively. The protein levels of FoxM1, NEK2, and AKT/p-AKT were analyzed by Western blotting. Western blot analyses of FoxM1-overexpressing cell lines and RCM-1-treated cells revealed a positive correlation between NEK2 and FoxM1 levels. Co-IP confirmed their interaction. NEK2 knockdown significantly suppressed proliferation, migration, and invasion; enhanced cisplatin sensitivity (reduced the IC₅₀); and promoted apoptosis. Conversely, NEK2 overexpression exacerbated malignant phenotypes and decreased chemosensitivity. Mechanistically, NEK2 activation was shown to drive osteosarcoma progression via AKT/p-AKT pathway activation. This study revealed that NEK2 promotes osteosarcoma proliferation, invasion, migration, and chemoresistance while inhibiting apoptosis, likely through AKT/p-AKT signaling. These effects may be regulated by FoxM1.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"120"},"PeriodicalIF":2.8,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663971","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":"Tumor microenvironment: recent advances in understanding and its role in modulating cancer therapies.","authors":"Disha D Shah, Mehul R Chorawala, Neha R Raghani, Rajanikant Patel, Mohammad Fareed, Vivekanand A Kashid, Bhupendra G Prajapati","doi":"10.1007/s12032-025-02641-4","DOIUrl":"10.1007/s12032-025-02641-4","url":null,"abstract":"<p><p>Tumor microenvironment (TME) denotes the non-cancerous cells and components presented in the tumor, including molecules produced and released by them. Interactions between cancer cells, immune cells, stromal cells, and the extracellular matrix within the TME create a dynamic ecosystem that can either promote or hinder tumor growth and spread. The TME plays a pivotal role in either promoting or inhibiting tumor growth and dissemination, making it a critical factor to consider in the development of effective cancer therapies. Understanding the intricate interplay within the TME is crucial for devising effective cancer therapies. Combination therapies involving inhibitors of immune checkpoint blockade (ICB), and/or chemotherapy now offer new approaches for cancer therapy. However, it remains uncertain how to best utilize these strategies in the context of the complex tumor microenvironment. Oncogene-driven changes in tumor cell metabolism can impact the TME to limit immune responses and present barriers to cancer therapy. Cellular and acellular components in tumor microenvironment can reprogram tumor initiation, growth, invasion, metastasis, and response to therapies. Components in the TME can reprogram tumor behavior and influence responses to treatments, facilitating immune evasion, nutrient deprivation, and therapeutic resistance. Moreover, the TME can influence angiogenesis, promoting the formation of blood vessels that sustain tumor growth. Notably, the TME facilitates immune evasion, establishes a nutrient-deprived milieu, and induces therapeutic resistance, hindering treatment efficacy. A paradigm shift from a cancer-centric model to a TME-centric one has revolutionized cancer research and treatment. However, effectively targeting specific cells or pathways within the TME remains a challenge, as the complexity of the TME poses hurdles in designing precise and effective therapies. This review highlights challenges in targeting the tumor microenvironment to achieve therapeutic efficacy; explore new approaches and technologies to better decipher the tumor microenvironment; and discuss strategies to intervene in the tumor microenvironment and maximize therapeutic benefits.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"117"},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657689","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":"Nanotechnology in Imatinib delivery: advancing cancer treatment through innovative nanoparticles.","authors":"Azam Ghadami, Sonia Fathi-Karkan, Bazla Siddiqui, Sonia Ashfaq Gondal, Abbas Rahdar, Negar Abbaszadeh Garousi, Zelal Kharaba, Suresh Ghotekar","doi":"10.1007/s12032-025-02660-1","DOIUrl":"10.1007/s12032-025-02660-1","url":null,"abstract":"<p><p>Nanotechnology-based drug delivery systems have improved target medicines' therapeutic efficacy and specificity in cancer therapy. Imatinib, one of the tyrosine kinase inhibitors widely used for treating chronic myeloid leukemia and gastrointestinal stromal tumors (GIST), faces many drawbacks, such as poor solubility, reduced bioavailability, and the development of resistance. The paper critically reviews advances in nanotechnology-based approaches toward the delivery of Imatinib, relating to polymeric, lipid-based, carbon-based, and stimuli-responsive nanoparticles. These methods enhance solubility, stability, and targeted distribution and are often used to facilitate the co-delivery of other anticancer drugs with considerable problems in cancer treatment. Although much potential for these technologies exists, scalability, safety, and regulatory approval, among other features, need resolution before real cost can meet clinical efficacy. Further directions would go toward bio-inspired system development, enhancing regulatory frameworks, and cost-effective manufacturing processes that bring nanotechnology into the realm of standard treatment for cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"116"},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657676","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":"EM-12, a natural sesquiterpene lactone extracted from Elephantopus mollis, promotes cancer cell apoptosis by activating ER stress.","authors":"Xiang Huang, Junzhen Zhou, Zhenhua Li, Meijun Ye, Changyan Hou, Qing Zhang, Yuanhong Chen, Qiang Li, Fengying Li, Xiaofeng Zhu, Jianwei Jiang","doi":"10.1007/s12032-025-02654-z","DOIUrl":"10.1007/s12032-025-02654-z","url":null,"abstract":"<p><p>The Elephantopus mollis H.B.K. contains various sesquiterpene lactones that have shown anti-proliferative and proapoptotic effects in various cancers, although the underlying mechanisms are partially understood. Inducing of excessive ER stress is a potential cancer therapeutic strategy. However, ER stress activator remain limited in current clinical applications. In this study, we identified that EM-12, an uncovered sesquiterpene lactone isolated from Elephantopus mollis H.B.K., as a BiP ATPase activity inhibitor through BiP ATPase activity assay in vitro. This molecule also exhibits significantly greater cytotoxicity in numerous ovarian cancer cell lines, including paclitaxel-resistance ovarian cancer cell line, compared to transformed ovarian epithelial cell lines. In addition, EM-12 exerts broad-spectrum cytotoxicity against various human cancer cell lines, including liver, nasopharyngeal, and breast cancer cell lines. Mechanically, EM-12 promotes ER stress and ER-stress-related apoptosis to against cancer cells through inhibiting BiP ATPase activity.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"115"},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657597","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":"Exosomes derived from natural killer cells: transforming immunotherapy for aggressive breast cancer.","authors":"Abdulmalik Saleh Alfawaz Altamimi, M Arockia Babu, Muhammad Afzal, Ashok Kumar Bishoyi, R Roopashree, Suman Saini, R S K Sharma, Piyus Kumar Pathak, Ashish Singh Chauhan, Kavita Goyal, Haider Ali, Nawaid Hussain Khan, Ashok Kumar Balaraman","doi":"10.1007/s12032-025-02647-y","DOIUrl":"10.1007/s12032-025-02647-y","url":null,"abstract":"<p><p>Natural killer cell-derived exosomes (NK-Exos) hold great promise as immune modulators and immunotherapeutics against cancer due to their intrinsically latent anti-tumor effects. They use these nanosized vesicles to deliver cytotoxic molecules, such as perforin, granzymes, and miRNAs, directly to cancer cells to kill them, avoiding immune suppression. NK-Exos has particular efficacy for treating aggressive breast cancer by modulating the TME to activate the immune response and suppress immunosuppressive factors. Bioengineering advances have extended the therapeutic potential of NK-Exos, which permits precise tumor cell targeting and efficient delivery of therapeutic payloads, including small RNAs and chemotherapeutic agents. In engineered NK-Exos, sensitization of cancer cells to apoptosis, reduction of tumor growth, and resistance to drugs have been demonstrated to be highly effective. When combined, NK-Exos synergizes with radiotherapy, chemotherapy, or checkpoint inhibitors, enhancing therapeutic efficacy, and minimizing systemic toxicity. This review emphasizes the critical role of NK-Exos in breast cancer treatment, their integration into combination therapies, and the need for further research to overcome existing limitations and fully realize their clinical potential.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"114"},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657598","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":"Diagnosis and treatment of cardiac tumors.","authors":"Toru Imai, Tatsunori Shimoi, Akira Kawai, Kan Yonemori","doi":"10.1007/s12032-025-02661-0","DOIUrl":"10.1007/s12032-025-02661-0","url":null,"abstract":"<p><p>Cardiac tumors, though rare, present significant diagnostic and therapeutic challenges due to their diverse nature and potential severity. These tumors, which can be primary or metastatic, are often detected incidentally through imaging modalities such as echocardiography or CT scans. Differentiating between benign and malignant forms is crucial for guiding appropriate management strategies. This review synthesizes current diagnostic approaches and treatment modalities for cardiac tumors, with a focus on the role of imaging techniques like UCG, CT, MRI, and PET in tumor characterization. Multidisciplinary treatment plans are necessary, including surgical resection for benign tumors, chemotherapy, and radiotherapy for malignant tumors, and novel targeted therapies such as MDM2 inhibitors for selected cases. While primary malignant tumors like sarcomas and mesotheliomas exhibit rapid progression and poor prognosis, recent advances in multimodal therapy offer potential improvements in survival. The incidence of primary cardiac tumors is low, with an autopsy-reported occurrence rate of 0.02%. Benign cardiac tumors, such as myxomas and fibromas, generally have favorable outcomes with surgical resection. In contrast, primary malignant tumors like sarcomas and mesotheliomas exhibit rapid progression and poor prognosis, necessitating aggressive treatment including surgery, chemotherapy, and radiotherapy. Metastatic cardiac tumors occur in approximately 10% of cancer patients at autopsy and are managed according to the treatment plan for the primary malignancy. The management of cardiac tumors requires a multidisciplinary approach tailored to tumor type, location, and systemic effects. While benign tumors often respond well to surgical management, malignant and metastatic tumors demand more complex strategies to optimize patient outcomes.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"110"},"PeriodicalIF":2.8,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649427","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}

{"title":"Cost-effective isolation of Viburnum opulus-derived nanovesicles and evaluation of their cytotoxic, anticancer, and antioxidant properties on human glioblastoma cell line U87MG.","authors":"Nazli Irmak Giritlioglu, Fatma Sayan Poyraz, Banu Mansuroglu, Semiha Erisen","doi":"10.1007/s12032-025-02669-6","DOIUrl":"10.1007/s12032-025-02669-6","url":null,"abstract":"<p><p>Glioblastoma is the most common and highly invasive glial tumor, significantly reducing patient survival. Current therapeutic approaches have limited success rates. Plant-derived nanovesicles are a rapidly developing area, recognized for their exceptional biofunctional properties, and are emerging as a promising approach in cancer treatment. The present study focuses on the isolation of nanovesicles from Viburnum opulus fruits using a cost-effective method that includes a polymer-based exosome precipitation buffer and size exclusion chromatography, followed by their characterization. Morphological analysis via Field Emission Scanning Electron Microscopy and Transmission Electron Microscopy revealed nanovesicles ranging from oval to elliptical shapes, with average diameters of 54.23 nm and 41.21 nm, respectively. Dynamic light scattering analysis determined the average size of 45.36 nm indicating the presence of nanovesicles, and the zeta potential was - 2.87 mV. Biochemical characterization showed total protein and phenolic concentrations of 1534 ± 97.78 µg/ml and 4.270 ± 0.66 mg gallic acid equivalents/L, respectively, with total antioxidant status values of 3.83 ± 0.37 mmol Trolox equivalents/L. Based on IC50 values, these nanovesicles were 7.5 times more toxic to U87MG human glioblastoma cells compared to healthy human dermal fibroblasts. Analyses including clonogenic cell survival, wound healing, apoptosis, total antioxidant status, and total oxidant status were continued on only U87MG cells, as human dermal fibroblasts showed a low response to nanovesicle treatment. Qualitative and quantitative assessments demonstrated that Viburnum opulus-derived nanovesicles effectively inhibited cancer cell proliferation and migration. Due to their non-toxic, anticancer, and antioxidant properties, these nanovesicles hold significant potential in glioblastoma management.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"112"},"PeriodicalIF":2.8,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11913919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649425","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}

{"title":"Nanomedicine innovations in colon and rectal cancer: advances in targeted drug and gene delivery systems.","authors":"Sobia Razzaq, Iqra Fatima, Zeinab Moafian, Abbas Rahdar, Sonia Fathi-Karkan, Zelal Kharaba, Maryam Shirzad, Ahmad Khan, Sadanand Pandey","doi":"10.1007/s12032-025-02670-z","DOIUrl":"10.1007/s12032-025-02670-z","url":null,"abstract":"<p><p>Nanotechnology has revolutionized cancer diagnostics and therapy, offering unprecedented possibilities to overcome the constraints of conventional treatments. This study provides a detailed overview of the current progress and difficulties in the creation of nanostructured materials, with a specific emphasis on their use in drug and gene delivery systems. The study examines tactics that attempt to improve the effectiveness and safety of chemotherapeutic drugs such as doxorubicin (Dox) by focusing on the potential of antibody-drug conjugates and functionalized nanoparticles. Moreover, it clarifies the challenges encountered in administering nanoparticles orally for gastrointestinal treatments, emphasizing the crucial physicochemical properties that affect their behavior in the gastrointestinal system. This study highlights the transformational potential of nanostructured materials in precision oncology by examining advanced breakthroughs such cell membrane-camouflaged nanoparticles and inorganic nanoparticles designed for gastrointestinal disorders. The text investigates the processes involved in the absorption of nanoparticles and their destruction in lysosomes, revealing the many methods in which enterocytes take up these particles. This study strongly supports the use of advanced nanoparticle-based methods to reduce the harmful effects on the whole body and improve the effectiveness of therapy, based on a thorough examination of current experiments on animals and humans. The main objective of this paper is to provide a fundamental comprehension that will stimulate more investigation and practical use in the field of cancer nanomedicine, advancing its boundaries.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"113"},"PeriodicalIF":2.8,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649429","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":"Role of hepatotropic viruses in promoting hepatocellular carcinoma-current knowledge and recent advances.","authors":"Piotr Starnawski, Klaudia Nowak, Zuzanna Augustyn, Dominik Malicki, Aleksandra Piąta, Dominika Lorek, Jakub Janczura","doi":"10.1007/s12032-025-02674-9","DOIUrl":"10.1007/s12032-025-02674-9","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, with chronic infections by hepatotropic viruses such as hepatitis B virus (HBV), and hepatitis C virus (HCV), being major risk factors. Chronic infections with these viruses are the leading cause of HCC worldwide, with HBV alone responsible for over 50% of cases. Despite advances in direct-acting antivirals (DAAs) for HCV and nucleos(t)ide analogues (NAs) for HBV, challenges remain in HCC prevention, early detection, and treatment. Recent research highlights the role of viral-induced metabolic alterations, such as the Warburg effect, mitochondrial dysfunction, and lipid dysregulation, in promoting HCC. Moreover, immune checkpoint inhibitors have emerged as effective treatments for advanced HCC, though responses vary between HBV- and HCV-related cancers. Additionally, novel therapeutic approaches and metabolic-targeted therapies offer promising avenues for virus-associated HCC treatment. Advancements in liquid biopsy biomarkers and artificial intelligence-driven diagnostics are improving HCC surveillance and risk stratification, potentially enabling earlier interventions. While HBV vaccination has significantly reduced HCC incidence, disparities in global vaccination coverage persist. Furthermore, antiviral therapies combined with structured surveillance programs have proven effective in reducing HCC incidence and mortality. This review highlights the complex connection between viral, genetic, and environmental factors in HCC development and underscores the importance of integrated prevention strategies to reduce its burden globally.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"111"},"PeriodicalIF":2.8,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649430","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":"LncRNA CCAT1 decreases the sensitivity to doxorubicin in lung cancer cells by regulating miR-181a/CPEB2 axis.","authors":"Qi Muge, Yu Qing, Wenshan Bao, Xiangrong Bao, Arong Gaowa, Lanying Chen","doi":"10.1007/s12032-025-02668-7","DOIUrl":"10.1007/s12032-025-02668-7","url":null,"abstract":"<p><p>Recently, long non-coding RNAs have gained an increasing amount of attention in treating lung cancer. However, a full understanding of how CCAT1 lncRNA works against proliferation is not yet available. Therefore, we assess the impact of CCAT1 on the lung cancer cell proliferation, apoptosis, and doxorubicin (DOX) sensitivity, and the involvement of miR-181a/CPEB2 pathway. For this purpose, lung cancer A549 cells were exposed to siRNA against CCAT1 and DOX and cell viability were measured by MTT assay. ELISA was used to evaluate cell apoptosis. The protein and mRNA expression levels of apoptotic markers, miR-181a and CPEB2 were measured by western blot and qRT-PCR. Knock-downing CCAT1 inhibited the cell viability of A549 cells. In addition, si-CCAT1 treatment increased apoptosis in both cell lines via modulating the anti- and pro-apoptotic markers. Si-CCAT1 increased the levels miR-181a and decreased CPEB2 in A549 cells. In conclusion, our study has provided strong evidence that lncRNA CCAT1 decreased the sensitivity to doxorubicin in lung cancer cells by regulating the miR-181a/CPEB2 axis.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"109"},"PeriodicalIF":2.8,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143639703","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}