Medical Oncology最新文献

{"title":"FBXO32 ubiquitination of SUFU promotes progression and lenvatinib resistance in hepatocellular carcinoma via hedgehog signaling.","authors":"Shunyi Wang, Rui Peng, Chen Chen, Daoyuan Tu, Jun Cao, Bingbing Su, Songsong Fan, Yangyang Miao, Chi Zhang, Guoqing Jiang, Shengjie Jin, Dousheng Bai","doi":"10.1007/s12032-025-02644-1","DOIUrl":"10.1007/s12032-025-02644-1","url":null,"abstract":"<p><p>Lenvatinib is a prevalent treatment for hepatocellular carcinoma (HCC), yet resistance to the drug significantly limits its effectiveness. This study investigates the role of FBXO32 (F-Box Protein 32) in HCC progression and lenvatinib resistance. Methods: We utilized the GSE211850 and GSE46408 datasets to identify an E3 ubiquitin ligase that is highly expressed in both lenvatinib-resistant HCC cells and HCC tissues. The expression and clinical relevance of this E3 ubiquitin ligase were further validated using lenvatinib-resistant HCC cells, online databases, and HCC clinical tissue samples. The phenotype was verified by cell and animal experiments. Techniques such as RNA sequencing, western blotting, immunofluorescence, Co-immunoprecipitation (Co‑IP), Ubiquitination, and cycloheximide (CHX) chase assay reveal the mechanism. FBXO32 is highly expressed in both lenvatinib-resistant HCC cells and HCC tissues. High FBXO32 expression correlated with increased ALT, AFP levels, larger tumors, and advanced TNM stages, serving as an independent risk factor for overall survival (OS) and recurrence-free survival (RFS). Functional assays demonstrated that FBXO32 overexpression enhanced cell proliferation, stemness, apoptosis resistance, and lenvatinib resistance, while knockdown had opposing effects. KEGG enrichment analysis indicated a link between FBXO32 and the Hedgehog signaling pathway. FBXO32-mediated degradation of SUFU, a Hedgehog pathway inhibitor, activated this pathway. Inhibiting Hedgehog signaling counteracted FBXO32's impact on HCC growth and resistance. Conclusion: FBXO32 is a critical marker for lenvatinib efficacy and HCC prognosis, suggesting that targeting FBXO32 or the Hedgehog pathway could provide innovative strategies for overcoming lenvatinib resistance in HCC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"98"},"PeriodicalIF":2.8,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605569","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":"Targeting EGFR and PI3K/mTOR pathways in glioblastoma: innovative therapeutic approaches.","authors":"Gursimran Singh, Rohit, Pankaj Kumar, Khadga Raj Aran","doi":"10.1007/s12032-025-02652-1","DOIUrl":"10.1007/s12032-025-02652-1","url":null,"abstract":"<p><p>Glioblastoma (GBM) stands as the most aggressive form of primary brain cancer in adults, characterized by its rapid growth, invasive nature, and a robust propensity to induce angiogenesis, forming new blood vessels to sustain its expansion. GBM arises from astrocytes, star-shaped glial cells, and despite significant progress in understanding its molecular mechanisms, its prognosis remains grim. It is frequently associated with mutations or overexpression of the epidermal growth factor receptor (EGFR), which initiates several downstream signaling pathways. Dysregulation of key signaling pathways, such as EGFR/PTEN/AKT/mTOR, drives tumorigenesis, promotes metastasis and leads to treatment resistance. The modest survival benefits of the conventional treatment of surgical resection followed by radiation and chemotherapy underscore the pressing need for innovative therapeutic approaches. In most the tumor, overexpression of EGFR is found associated with GBM and mutations in its several variants are important for promoting ongoing mitogenic signaling and tumor growth. This receptor inhibits apoptosis and promotes cell survival and proliferation by activating downstream PI3K/AKT/mTOR pathways. This route is typically blocked by PTEN, a crucial tumor suppressor, however, GBM frequently results in abnormalities in this protein. The aim of this review is to explore the molecular foundations of GBM, with a focus on the EGFR and PI3K/mTOR pathways and their impact on tumor behavior. Additionally, this review highlights EGFR and PI3K/AKT/mTOR inhibitors currently in clinical and preclinical trials, addressing treatment resistance, challenges, and future directions.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"97"},"PeriodicalIF":2.8,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597316","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 miR-92a-3p modulates M2 macrophage polarization in colorectal cancer: implications for tumor migration and angiogenesis.","authors":"Wei Zhao, Yudan Wu, Yixiao Wang, Tongyi Li, Qiuyan Liu, Zhiping Hou","doi":"10.1007/s12032-025-02635-2","DOIUrl":"10.1007/s12032-025-02635-2","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most prevalent malignant neoplasms globally. Its development and metastasis are closely associated with the polarization of macrophages within the tumor microenvironment (TME). In particular, the polarization of M2-type macrophages has been demonstrated to be related to the promotion of tumor growth, migration, and angiogenesis. This study aims to investigate the role of miR-92a-3p in colon cancer-derived exosomes in regulating M2-type macrophage polarization by targeting EID2B and to elucidate the impact of this process on tumor migration and angiogenesis. MicroRNAs that were differentially expressed in plasma exosomes from CRC patients were initially identified through a search of the GEO database. The results were then verified by RT-qPCR using miR-92a-3p. The uptake of exosomes was observed via laser confocal microscopy, and the impact of miR-92a-3p on the polarization of exosomes and macrophages was examined through the use of RT-qPCR and WB. A bioinformatics analysis and a dual-luciferase reporter assay were employed to identify the downstream target of miR-92a-3p and to investigate its effect on the MAPK/ERK pathway. miR-92a-3p was upregulated in plasma exosomes of colon cancer patients and exhibited a positive correlation with lymph node metastasis. The results demonstrated that miR-92a-3p was capable of promoting M0 macrophage polarization toward the M2 phenotype, and of enhancing the migratory and invasive capacities of CRC cells, as well as their angiogenic potential in vitro. Bioinformatic analysis and experimental validation demonstrated that miR-92a-3p targeted EID2B and that this target gene was negatively correlated with M2-type macrophage polarization. The results demonstrated that miR-92a-3p promotes macrophage M2 polarization by activating the MAPK/ERK pathway. miR-92a-3p activates the MAPK/ERK pathway and induces macrophage M2 polarization by targeting EID2B, thereby promoting migration and angiogenesis in CRC. These findings offer new potential targets for the treatment of colon cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"96"},"PeriodicalIF":2.8,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584901","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":"Young-onset metastatic colorectal cancer: an opportunity and a vision for progress in cancer.","authors":"Prasad D Cooray, Nicole Jane Cooper","doi":"10.1007/s12032-025-02640-5","DOIUrl":"10.1007/s12032-025-02640-5","url":null,"abstract":"<p><p>Metastatic young-onset colorectal cancer (yo-CRC) is a distinct and aggressive disease subtype that is becoming increasingly prevalent worldwide with Australia leading the world in this trend. This article provides an evidence-based perspective, through the prism of authors' personal experience, to craft an effective pathway not only to deliver improved outcomes for the patients but also to reduce disparities and foster collaboration amongst the cancer-treating community and indeed patients. It highlights an opportunity to re-define, re-design, and create a model that is rewarding to patients and cancer-treating community. Although our focus is on the high unmet needs group of yo-CRC, this model has the potential to expand to other cancer types and care models. We analyse the unique epidemiological trends, challenges, and burdens, emphasising the need for tailored treatment approaches for younger patients with colorectal cancer especially in the metastatic setting. We identify current gaps in clinical practice and research. To improve real-world outcomes, we propose a conceptual framework to enhance clinician-patient communication and treatment planning. Central to our approach is the integration of a Registry of Incidence, Intervention, and Outcomes (RIIO), which enables real-time data collection and analysis, improving treatment personalisation and efficacy. This registry could revolutionise patient care and drive research innovation through enhanced data sharing and collaboration. We advocate for a patient-centric integrated care model that utilises all available therapies to maximise survival and quality of life. Our perspective underscores the urgent need for a paradigm shift in how yo-CRC is viewed, researched and managed, proposing a pathway to significantly enhanced outcomes. Whilst it is feasible to expand the concepts discussed here for all colorectal cancer and indeed all cancer types, we believe this approach is most relevant and acutely needed in yo-CRC setting for reasons detailed in the manuscript.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"95"},"PeriodicalIF":2.8,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582323","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":"Selinexor in the treatment of liposarcoma: from preclinical evidence to clinical practice.","authors":"Piotr Remiszewski, Wiktor Gaik, Aleksandra Skora, Julia Wąż, Kinga Filipek, Agata Pisklak, Monika Dudzisz-Śledź, Piotr Rutkowski, Anna Czarnecka","doi":"10.1007/s12032-025-02651-2","DOIUrl":"10.1007/s12032-025-02651-2","url":null,"abstract":"<p><p>Selinexor is a new compound studied for the treatment of liposarcoma, particularly dedifferentiated liposarcoma (DDLPS), where treatment options remain limited. As a first-in-class oral exportin-1 (XPO1) inhibitor, selinexor has shown anti-tumour activity in preclinical models, particularly in MDM2- and CDK4-amplified DDLPS, where it induces apoptosis, inhibits tumour growth and promotes nuclear retention of p53. Preclinical studies have also suggested potential synergy with doxorubicin and eribulin, although these findings have yet to be validated in randomised clinical trials. The phase II/III SEAL trial (NCT02606461) evaluated selinexor versus placebo in patients with advanced, previously treated DDLPS. While the study demonstrated a statistically significant, albeit modest, improvement in median progression-free survival (PFS) from 2.1 to 2.8 months, no overall survival benefit was observed. In addition, selinexor was associated with significant toxicity, including fatigue, nausea and weight loss. Similarly, a phase Ib/II study (NCT03042819) evaluating selinexor in combination with doxorubicin reported a 21% response rate and a median PFS of 5.5 months, although this regimen was also associated with high rates of neutropenia and fatigue. Despite these results, selinexor is not currently approved for the treatment of liposarcoma and its clinical utility remains under investigation. Ongoing studies, such as the SeliSarc trial (NCT04595994) evaluating selinexor in combination with gemcitabine and the NRSTS2021 trial (NCT06239272) evaluating selinexor in paediatric soft tissue sarcoma, aim to further define its role. The results of these studies will be critical in determining whether selinexor can be incorporated into standard sarcoma treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"94"},"PeriodicalIF":2.8,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582322","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":"Prodelphinidin from purple sweet potato induces apoptosis in human triple-negative breast cancer cells via ROS-mediated ER stress activation.","authors":"Jiluan Zhang, Zihan Chen, Shibo Wang, Lingxue Kong, Jinjuan Liu","doi":"10.1007/s12032-025-02642-3","DOIUrl":"10.1007/s12032-025-02642-3","url":null,"abstract":"<p><p>Triple negative breast cancer (TNBC), a highly aggressive and heterogeneous subtype of breast cancer, lacks an effective targeted therapy. Conventional medication has limited efficacy in treating TNBC, which highlights the potential of developing therapeutic agents from natural bioactive compounds. This study aimed to investigate the cytotoxicity of prodelphinidin (PD), an anthocyanin found in purple sweet potato, in human MDA-MB-231 and MDA-MB-436 cells. The results showed that PD selectively inhibited human breast cancer, particularly TNBC. Furthermore, PD demonstrated significant dose- and time-dependent inhibition of MDA-MB-231 and MDA-MB-436 cell activity. Flow cytometry and western blot analysis revealed that PD induced cell apoptosis by down-regulating Bcl-2, activating caspase-3/9, and cleaving PARP. Additionally, PD treatment upregulated the expression of p-elF2α, GRP78, and CHOP, indicating the involvement of endoplasmic reticulum stress (ERS). PD treatment also increased the production of reactive oxygen species (ROS) and decreased superoxide dismutase (SOD) activity in TNBC cells. The cytotoxicity of PD reduced significantly by pre-treatment with caspase inhibitors (Ac-DEVD-CHO and Z-LEHD-FMK). In conclusion, PD effectively inhibited the proliferation and induced apoptosis in TNBC cells through the activation of ROS and endoplasmic reticulum stress.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"92"},"PeriodicalIF":2.8,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567517","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":"Macrophage-derived lncRNAs in cancer: regulators of tumor progression and therapeutic targets.","authors":"Muath Suliman, Raed Obaid Saleh, Muktesh Chandra, Khetam Habeeb Rasool, Majid Jabir, Sabrean F Jawad, Thikra F Hasan, Mithilesh Singh, Manmeet Singh, Abhayveer Singh","doi":"10.1007/s12032-025-02643-2","DOIUrl":"10.1007/s12032-025-02643-2","url":null,"abstract":"<p><p>Macrophages are key tumor microenvironment (TME) regulators, exhibiting remarkable plasticity that enables them to either suppress or promote cancer progression. Emerging evidence highlights the critical role of macrophage-derived long non-coding RNAs (lncRNAs) in shaping tumor immunity, influencing macrophage polarization, immune evasion, angiogenesis, metastasis, and therapy resistance. This review comprehensively elucidates the functional roles of M1- and M2-associated lncRNAs, detailing their molecular mechanisms and impact on cancer pathogenesis. In summary, elucidating the roles of lncRNAs derived from macrophages in cancer progression offers new avenues for therapeutic strategies, significantly improving patient outcomes in the fight against the disease. Further research into the functional significance of these lncRNAs and the development of targeted therapies is essential to harness their potential fully in clinical applications. We further explore their potential as biomarkers for cancer prognosis and therapeutic targets for modulating macrophage activity to enhance anti-cancer immunity. Targeting macrophage-derived lncRNAs represents a promising avenue for precision oncology, offering novel strategies to reshape the TME and improve cancer treatment outcomes.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"91"},"PeriodicalIF":2.8,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567516","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":"Nanomaterials in gastric cancer: pioneering precision medicine for diagnosis, therapy, and prevention.","authors":"Tiantian Liu, Yanmei Gu, Yang Zhao, Yumin Li","doi":"10.1007/s12032-025-02650-3","DOIUrl":"10.1007/s12032-025-02650-3","url":null,"abstract":"<p><p>Gastric cancer (GC) continues to be a major health issue globally due to its high rates of both occurrence and mortality. Despite advancements in treatment, the outlook for those affected remains poor, highlighting the critical need for new diagnostic and treatment methods. Nanotechnology, especially nanoparticles, is emerging as a crucial innovation in cancer care by improving imaging, targeting drug delivery, and enhancing early detection. These nanoparticles are also enhancing the effectiveness of treatments like phototherapy, chemotherapy, and immunotherapy. Notably, they show potential in addressing infections like Helicobacter pylori (H. pylori), which is known to increase the risk of developing GC. This review underscores the pivotal role of nanotechnology in enhancing the integrated management of GC, offering a basis for future advancements in the field.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"93"},"PeriodicalIF":2.8,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573439","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":"Bone marrow mesenchymal stem cells enrich breast cancer stem cell population via targeting metabolic pathways.","authors":"Zahra Ghanbari Movahed, Kamran Mansouri, Ali Hamrahi Mohsen, Maryam M Matin","doi":"10.1007/s12032-025-02632-5","DOIUrl":"10.1007/s12032-025-02632-5","url":null,"abstract":"<p><p>The role of cancer cell metabolic reprogramming in the formation and maintenance of cancer stem cells (CSCs) has been well established. This reprogramming involves alterations in the metabolic pathways of cancer cells, leading to the acquisition of stem cell-like properties such as self-renewal and differentiation. This study aimed to investigate the potential effects of bone marrow mesenchymal stem cells (BM-MSCs) on the enrichment of breast CSCs. Exosomes (Exo) and conditioned media (CM) were isolated from BM-MSCs for use in this experimental study. The impact of BM-MSCs-Exo and BM-MSCs-CM on the expression of stemness genes NANOG and OCT-4, as well as CD24 and CD44 markers, was assessed in MCF-7 and MDA-MB-231 cell cultures to identify CSCs. Furthermore, the effects of BM-MSCs-Exo and BM-MSCs-CM on cancer cell metabolism were evaluated by examining changes in glycolysis, the pentose phosphate pathway (PPP), and amino acid profiles. Additionally, the influence of BM-MSCs-Exo and BM-MSCs-CM on tumor growth in vivo was also investigated. The analysis of stemness marker expression in cells treated with BM-MSCs-Exo and BM-MSCs-CM revealed an increase in stemness characteristics compared to the control group. Furthermore, the examination of changes in cell metabolism following these treatments showed alterations in glycolysis, PPP, and amino acid metabolism pathways. Additionally, it was demonstrated that BM-MSCs-Exo and BM-MSCs-CM can promote tumor growth in mice following transplantation of 4T1 cells. These findings suggest that BM-MSCs-Exo and BM-MSCs-CM can enrich the population of CSCs in MCF-7 and MDA-MB-231 cells by targeting metabolic pathways, however, further studies are required to elicit the exact mechanisms of these phenomena.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"90"},"PeriodicalIF":2.8,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567515","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":"Effects of royal jelly on ovary cancer cells proliferation and apoptosis.","authors":"Ender Deniz Asmaz, Sabire Güler, Berrin Zık","doi":"10.1007/s12032-025-02638-z","DOIUrl":"10.1007/s12032-025-02638-z","url":null,"abstract":"<p><p>The aim of the present study is to investigate the proliferative or apoptotic effects of different doses and durations of Royal jelly (RJ) on serous type epithelial ovarian cancer, which is the most common epithelial ovarian cancer. For this purpose, cells of the Skov-3 human ovarian adenocarcinoma cell line were grown in McCoy medium and seeded in 6-well plates. RJ was prepared as a stock solution (1000 mg RJ/10 ml dH₂O) and 1, 5, 10, 20, and 50 mg/ml RJ doses from the prepared stock solution were added to the medium for 24, 48, and 72 h incubated. After the treatment of RJ, the cell viability test (Tripan Blue), Ki-67 to determine the proliferative effect, cleaved-Caspase-3 and cleaved PARP expressions to determine its apoptotic effect were examined by immunocytochemical and immunofluorescence methods. In addition, findings were supported by the TUNEL method. As a result of the experiments, it was determined that 1 mg/ml and 24 h treatment of RJ did not affect cell proliferation and apoptosis, but generally, 50 mg/ml of RJ for 72 h inhibited proliferation in cancer cells and induced apoptosis. The use of royal jelly both monotherapeutically and in combination as an alternative treatment for ovarian cancer may provide the basis for new experimental protocols.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"89"},"PeriodicalIF":2.8,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557240","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}