Anti-Cancer Drugs最新文献

{"title":"FV-429 suppresses cancer cell migration and invasion by EMT via the Hippo/YAP1 pathway in pancreatic cancer cells.","authors":"Zhiying Wang, Xingxing Pan, Xinyue Ma, Yilu Zhang, Yuan Gao, Yongjian Guo, Yuxin Zhou","doi":"10.1097/CAD.0000000000001718","DOIUrl":"10.1097/CAD.0000000000001718","url":null,"abstract":"<p><p>Pancreatic cancer is one of the most common malignant tumors of the digestive system, with the majority of patients not succumbing to the primary tumor but rather to metastasis. Epithelial-mesenchymal transition (EMT) is abnormally activated in numerous cancers, whereby it promotes tumor cell migration and invasion. Yes-associated protein 1 (YAP1) is commonly overexpressed in various cancer types and plays an oncogenic role. We demonstrated that FV-429, a derivative of the natural flavonoid wogonin, inhibited the invasion and metastasis of pancreatic cancer cells by modulating EMT-related proteins. FV-429 enhances the expression of p-LATS1, thereby promoting the conversion of YAP1 to p-YAP1. Meanwhile, it suppresses the nuclear translocation of YAP1, thereby affecting the expression of E-cadherin and snail1, which, in turn, impacts the EMT. The Hippo-signaling pathway inhibitor TDI-011536 was used to validate these results. In vivo , a mouse model of pancreatic cancer lung metastasis was established using PANC02 cells to validate the antimetastatic effect of FV-429, which confirmed its action through the Hippo/YAP1 pathway. In addition, FV-429 demonstrated high safety and low toxicity. In conclusion, we demonstrated that FV-429 inhibits migration, invasion, and metastasis of human pancreatic cancer cells by affecting the Hippo/YAP1 pathway, suggesting that FV-429 has the potential to be a novel therapeutic agent for pancreatic cancer.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"527-538"},"PeriodicalIF":2.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603574","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":"A fatty acid metabolism-related gene signature can predict poor prognosis in glioma.","authors":"Chuanyu Li, Xinran Xue, Jiahui Kong, Jianjun Zhang","doi":"10.1097/CAD.0000000000001719","DOIUrl":"10.1097/CAD.0000000000001719","url":null,"abstract":"<p><p>Gliomas, arising from supportive glial cells in the central nervous system, present significant challenges in oncology due to their varying aggressiveness and poor prognosis, particularly in high-grade forms. Understanding the molecular pathways involved in glioma progression is essential for developing effective treatment strategies. This study aimed to develop a fatty acid metabolism (FAM)-related gene signature to better predict poor prognosis in glioma patients, thereby facilitating more targeted therapeutic approaches. We employed the Least Absolute Shrinkage and Selection Operator regression analysis to identify a gene signature associated with FAM from The Cancer Genome Atlas and Chinese Glioma Genome Atlas RNA-seq datasets. Survival analyses, including Kaplan-Meier and Cox regression analyses, were conducted to assess the prognostic value of the identified genes. A total of seven FAM-related genes were associated with survival outcomes in isocitrate dehydrogenase-1 wild-type glioblastoma. The constructed gene signature effectively stratified patients into high-risk and low-risk groups, with high-risk patients demonstrating significantly poorer survival. PTGR1 emerged as the core gene, closely linked to malignant progression and poor prognosis. The FAM-related gene signature developed in this study provides a reliable tool for predicting poor outcomes in glioma patients. PTGR1, identified as a pivotal gene within this signature, may serve as a potential target for future therapeutic interventions, offering promising avenues for enhancing patient survival.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"567-574"},"PeriodicalIF":2.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974314","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":"Nivolumab- and ipilimumab-induced myositis, myasthenia gravis, and myocarditis in a patient with metastatic melanoma.","authors":"Berin Inan, Ulkuhan Duzgun, Zeynep Ergul-Ulger, Can Ebru Bekircan-Kurt, Busra Nur Ceylan, Omer Karadas, Zeki Odabasi","doi":"10.1097/CAD.0000000000001727","DOIUrl":"10.1097/CAD.0000000000001727","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have revolutionized advanced cancer treatment and prolonged survival; however, they are associated with several immune-related adverse events in up to 60% of patients, affecting various organ systems. A 73-year-old male patient with metastatic melanoma was admitted with left-sided ptosis, diplopia, head drop, and proximal muscle weakness. The patient had been undergoing treatment with nivolumab and ipilimumab, and his symptoms emerged 4 days after receiving the second cycle of the immunotherapy regimen. He was diagnosed as having ICI-related myositis, myasthenia gravis (MG), and myocarditis based on electromyography, muscle biopsy, antibody status, troponin level, and cardiac evaluation. ICIs were withdrawn and the patient was treated with intravenous methylprednisolone, intravenous immunoglobulin, and plasma exchange; however, the patient was treatment-refractory, necessitating long-term immunosuppression with rituximab. Subsequently, he responded well, and nivolumab monotherapy was resumed. The patient has been neurologically stable for 4 months without any recurrence of ICI-related adverse effects. ICI-related myositis, MG, and myocarditis are rare but can be severe and potentially life-threatening. Therefore, early recognition and immediate treatment are crucial for improving prognosis. To the best of our knowledge, this is the only case with nivolumab- and ipilimumab-induced triple overlap syndrome successfully treated with rituximab.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"600-605"},"PeriodicalIF":2.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061917","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":"Deubiquitinating enzyme UCHL1 stabilizes CAV1 to inhibit ferroptosis and enhance docetaxel resistance in nasopharyngeal carcinoma.","authors":"Yixian Ye, Peng Wang, Daquan Wu, Fengrong Tang, Na Shen, Guanghui Hou","doi":"10.1097/CAD.0000000000001721","DOIUrl":"10.1097/CAD.0000000000001721","url":null,"abstract":"<p><p>The overexpression of CAV1 in many cancers is linked to chemotherapy resistance, but the exact mechanisms by which CAV1 contributes to resistance in nasopharyngeal carcinoma (NPC) are not fully known. Our research aims to elucidate the potential pathways by which CAV1 contributes to chemotherapy resistance in NPC, providing a basis for developing strategies to overcome resistance. A docetaxel-resistant NPC cell line was established, and CAV1 expression was analyzed in the cell line and the resistant variant using western blot. The sensitivity of the resistant cell line to docetaxel was assessed via cell counting kit-8, colony formation assays, and flow cytometry. Flow cytometry was used to measure lipid reactive oxygen species levels, while kits were employed to determine Fe 2+ and malondialdehyde concentrations. The Ubibrowser database helped identify ubiquitination enzymes that interact with CAV1. The binding relationship between UCHL1 and CAV1 was studied using co-immunoprecipitation and immunofluorescence, which also evaluated the deubiquitination activity of UCHL1 on CAV1. CAV1 is overexpressed in NPC tissues and cells, correlating with adverse patient prognoses. In docetaxel-resistant cells, CAV1 expression is elevated compared to standard NPC cells. Silencing CAV1 increased the sensitivity of these resistant cells to docetaxel. Additionally, treatment with the ferroptosis inducer erastin could counteract the effects of CAV1 overexpression on drug resistance. UCHL1 interacted with CAV1 and inhibited its ubiquitin-mediated degradation pathway. By deubiquitinating CAV1, UCHL1 stabilizes and increases its expression, which inhibits ferroptosis and enhances the resistance of NPC cells to docetaxel.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"539-548"},"PeriodicalIF":2.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965157","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":"Distribution of side effects of anti-EGFR treatments in patients with metastatic colorectal cancer and evaluation of their relationship with survival.","authors":"Mert Erciyestepe, Okan Aydin, Sermin Dinc Sonusen, Ahmet Emin Ozturk, Emir Celik, Muhammed Mustafa Atci, Kayhan Erturk","doi":"10.1097/CAD.0000000000001755","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001755","url":null,"abstract":"<p><p>Many previous studies have investigated cetuximab and panitumumab's efficacy, safety, and side effects. Only a few studies have evaluated the relationship between toxicity and survival. Therefore, we conducted this study to examine the relationship between the side effects of anti-EGFR agents and survival in metastatic colorectal cancer patients. Our study is a single-center retrospective analysis of the medical records of 100 metastatic colorectal cancer patients between September 2014 and September 2023. Overall survival (OS) was found to be statistically significantly longer in patients who developed skin toxicity during anti-EGFR treatment (26.0 vs. 70.0 months) (P < 0.001). Similarly, OS was significantly better in patients with hypomagnesemia (P < 0.001) and constipation (P < 0.001) side effects. In contrast, OS was significantly worse in patients with lung toxicity (P = 0.016). Ocular side effects during anti-EGFR treatment did not affect OS statistically significantly (P = 0.268). The median PFS of patients with skin toxicity with anti-EGFR agents and hypomagnesemia in first-line treatment was 22.0 months (19.4-24.5) and 21.0 months (18.2-23.8), respectively (P = 0.002, P = 0.022). In the second line, the median PFS of patients with skin toxicity and patients with hypomagnesemia who received anti-EGFR therapy was 19.0 months (6.2-31.8) and 17.0 months (8.4-25.6), respectively (P = 0.013, P = 0.037). In our study, it was found that skin toxicity and hypomagnesemia positively affected both OS and PFS. OS was longer in patients with constipation, and OS was shorter in patients with lung toxicity. We suggest that survival might be predicted by monitoring side effects of these therapeutics; therefore, studies with larger cohorts are required.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144582873","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":"First-line lorlatinib treatment in a 19-year-old patient with ALK-rearranged pulmonary large-cell neuroendocrine carcinoma: a case report and literature review.","authors":"Fatih Kemik, Pinar Bulutay, Cevat İlteriş Kikili, Bahadir Köylü, Nazan Demir, Elif Değirmenci, Kadir Burak Özer, Çisel Aydin Meriçöz, Serhan Tanju, Fatih Selçukbiricik","doi":"10.1097/CAD.0000000000001754","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001754","url":null,"abstract":"<p><p>Pulmonary large-cell neuroendocrine carcinoma (LCNEC) is a rare and aggressive subtype of nonsmall cell lung cancer, typically occurring in elderly male smokers. Its occurrence in the adolescent population is exceptionally uncommon, with only a handful of cases reported in the literature. Even more rarely, LCNEC harbors ALK fusions, an unusual molecular alteration with important therapeutic relevance. We report a 19-year-old female patient who presented with bone pain and was found to have widespread skeletal and mediastinal lymph node involvement. Initial workup revealed elevated serum calcitonin and carcinoembryonic antigen (CEA) levels, and histopathology showed high-grade neuroendocrine carcinoma with immunoreactivity for chromogranin, synaptophysin, CD56, as well as calcitonin and CEA. Due to the neuroendocrine phenotype and calcitonin positivity, metastatic medullary thyroid carcinoma was initially suspected. However, thyroid fine needle aspiration from the suspicious thyroid nodule did not provide any evidence in this direction, and the RET mutation testing was also negative. Further molecular analysis revealed an EML4-ALK fusion and a TP53 mutation in tumor tissue. The patient was diagnosed with ALK-positive LCNEC and treated with lorlatinib and denosumab combination. A marked clinical and metabolic response was achieved within 3 months of treatment initiation. To our knowledge, this is the first reported case of ALK-rearranged pulmonary LCNEC in an adolescent patient treated with a tyrosine kinase inhibitor. This case underscores the extreme rarity of LCNEC in adolescents, highlighting that ALK rearrangements, although exceptionally rare in this histological subtype, can have significant therapeutic implications. It further emphasizes the importance of routine molecular profiling in atypical clinical scenarios and supports the utility of targeted therapies in rare tumor subsets.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144582874","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":"Thrombospondin-2 induces M2 macrophage polarization through fatty acid metabolism to drive lung adenocarcinoma proliferation.","authors":"Meiling Weng, Xiaoping Zhu","doi":"10.1097/CAD.0000000000001713","DOIUrl":"10.1097/CAD.0000000000001713","url":null,"abstract":"<p><p>Tumor-associated macrophages play a critical role in regulating the progression of lung adenocarcinoma (LUAD). Platelet-derived protein thrombospondin-2 (THBS2) has been identified as a tumor marker and is known to be overexpressed in LUAD. However, the specific role of THBS2 in M2 macrophage polarization within LUAD remains unclear. We conducted bioinformatics analyses to assess the clinical significance of THBS2 expression in LUAD, which was subsequently validated using quantitative PCR. We examined the relationship between THBS2 expression and M2 macrophage infiltration. A coculture system of LUAD cells and M0 macrophages was established to investigate the influence of THBS2 on macrophage infiltration and polarization through immunofluorescence and ELISA. We explored the impact of THBS2 on fatty acid metabolism (FAM) using oil red O staining and relevant kits and elucidated the role of THBS2 in regulating M2 macrophage polarization and LUAD proliferation through cell counting kit-8 (CCK-8) and colony formation assays. Western blot was employed to assess expression changes of Bax and Bcl-2. THBS2 was highly expressed in LUAD and was associated with poor prognosis in patients. In-vitro experiments demonstrated that silencing THBS2 significantly inhibited macrophage infiltration and polarization. THBS2 primarily activated FAM pathways, inducing M2 macrophage polarization and promoting LUAD cell proliferation. THBS2 enhanced LUAD proliferation by regulating FAM to induce M2 macrophage polarization. These findings provide a theoretical basis for targeting THBS2 as a novel therapeutic strategy in LUAD.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"459-467"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143575681","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":"Response to PARP inhibitor in EGFR-tyrosine kinase inhibitor-resistant metastatic lung adenocarcinoma with germline PALB2 mutation.","authors":"Chao Zhu, Peng Xu, Lantao Li, Hongmei Wei","doi":"10.1097/CAD.0000000000001712","DOIUrl":"10.1097/CAD.0000000000001712","url":null,"abstract":"<p><p>Tumors with homologous recombination deficiency (HRD) can benefit from treatment with poly ADP-ribose polymerase inhibitors (PARPi). However, the methods for identifying HRD vary and are controversial. Several DNA repair genes in the homologous recombination repair pathway may be linked to PARPi susceptibility, and studies are underway to identify biomarkers that can predict the response to PARPi. We present a case of EGFR-tyrosine kinase inhibitor-resistant metastatic lung adenocarcinoma with a germline PALB2 mutation that was treated with fluzoparib (an orally administered PARPi). The treatment achieved surprising results and lasted for more than 4.5 months. Our study provided evidence that metastatic lung adenocarcinoma with germline PALB2 could benefit from PARPi, which improves patient outcomes.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"518-520"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539949","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":"Correlative analysis of immune-related thyroid dysfunction and prognosis in patients with advanced esophageal squamous cell carcinoma.","authors":"Liangshan Da, Ziting Qu, Yiyin Zhang, Jie Da, Kangsheng Gu","doi":"10.1097/CAD.0000000000001716","DOIUrl":"10.1097/CAD.0000000000001716","url":null,"abstract":"<p><p>To explore the clinical characteristics of immune-related thyroid dysfunction (TD) and its correlation with prognosis. By collecting the clinical data of 116 patients with advanced esophageal squamous cell carcinoma (ESCC) who received programmed death receptor-1 (PD-1) inhibitor treatment, we analyzed the clinical characteristics of immune-related TD and its influencing factors and compared the prognostic differences among patients in different groups. Immune-related TD occurred in 45 (38.8%) patients after PD-1 inhibitor treatment, and the median time to its occurrence was 11.3 weeks. The toxicity of immune-related TD was grade 1 or grade 2 and only required symptomatic treatment. Female patients, as well as those with an Eastern Cooperative Oncology Group Performance Status less than equal to 1, no lymph node metastasis, no history of drinking, and high baseline thyroid-stimulating hormone levels, were likely to develop immune-related TD. Compared with the patients in the group without immune-related TD [TD(-)], the median progression-free survival (mPFS) and median overall survival (mOS) of the patients in the immune-related TD [TD(+)] group were significantly prolonged (mPFS: 12.6 vs. 6.5 months, P  = 0.001; mOS: 20.2 vs. 11.2 months, P  < 0.001). Further subgroup analysis showed that compared with the patients in the group without immune-related overt TD (Overt_TD), the patients in the Overt_TD group had a longer PFS (mPFS: 12.4 vs. 7.3 months, P  = 0.015) and OS (mOS: 20.2 vs. 12.2 months, P  = 0.001). The 60-, 90-, and 120-day landmark analysis further confirmed that immune-related TD was significantly associated with the improvement of PFS and OS. Multivariate Cox regression analysis indicated that immune-related TD was an independent prognostic factor for PFS ( P  = 0.015) and OS ( P  = 0.004). Immune-related TD is a very common immune-related adverse event. It is safe and manageable and has potential prognostic value for patients with advanced ESCC treated with PD-1 inhibitors.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"501-508"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668781","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":"Transformation from acquired EGFR 19del/C797S to EGFR 19del/T790M in an advanced non-small cell lung cancer patient: a case report and literature review.","authors":"Xianhuai Jin, Yaping Quan, Jiao Liu, Yong Hu, Hao Li","doi":"10.1097/CAD.0000000000001707","DOIUrl":"10.1097/CAD.0000000000001707","url":null,"abstract":"<p><p>Third-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are the first-line treatment of choice for patients with EGFR-mutant advanced non-small cell lung cancer (NSCLC). However, patients treated with these inhibitors eventually develop resistance. One of the most common mechanisms is the emergence of the EGFR C797S mutation. Whether first-generation EGFR inhibitors (e.g. icotinib or gefitinib) can sustainably control EGFR-sensitive mutations/C797S NSCLC following third-generation EGFR inhibitor treatment remains insufficiently reported. Our case report discusses a female patient with advanced lung adenocarcinoma carrying an EGFR exon 19 E746_A750delELREA mutation who received almonertinib as first-line treatment and developed C797S resistance during therapy. The patient was subsequently treated with a double dose of icotinib for 8 months until disease progression occurred, along with the development of an EGFR exon 20 T790M point mutation and TP53 mutation. This case provides clinical evidence suggesting that first-generation EGFR-TKIs may be an effective treatment strategy for patients with acquired EGFR 19del/C797S resistance following EGFR TKI therapy.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"513-517"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12061377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439845","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}