Anti-Cancer Drugs最新文献

{"title":"Inhibition of nuclear receptor coactivator 5 overcomes acquired lenvatinib resistance driven by protein kinase B-mammalian target of rapamycin signaling in hepatocellular carcinoma.","authors":"Hongyuan Zhou, Qin Zhang, Lu Yang, Zhaolong Pan, Haijing Zheng, Zewu Zhang, Dongyang Li, Guangtao Li, Xiaomeng Liu, Xu Bao, Chen Liu, Wei Zhang","doi":"10.1097/CAD.0000000000001759","DOIUrl":"10.1097/CAD.0000000000001759","url":null,"abstract":"<p><p>Lenvatinib, a multiple-receptor tyrosine kinase inhibitor, has gained recent approval for its use as a first-line treatment of hepatocellular carcinoma (HCC). While lenvatinib demonstrates notable therapeutic efficacy, the drug resistance undermines its sustained tumor control potential. The restricted clinical utility of lenvatinib underscores the imperative necessity to elucidate the mechanisms underpinning drug resistance. We established lenvatinib-resistant cell lines and investigated the changes in their biological characteristics. Next-generation sequencing was performed to identify genes associated with lenvatinib resistance. Western blots were utilized to confirm the involvement of these genes. Using lentiviral technology, we generated cell lines with lowered nuclear receptor coactivator 5 (NCOA5), a pivotal drug resistance-related gene, to explore the underlying resistance mechanism. Moreover, we developed a subcutaneous HCC xenograft tumor model to explore strategies for reversing drug resistance. Our study showed that HCC cells acquire resistance to lenvatinib through the activation of NCOA5, thereby stimulating the NCOA5-Protein Kinase B-mammalian target of rapamycin (AKT-mTOR) axis. Furthermore, the clinical evaluation of HCC specimens established a correlation between the activation of the NCOA5 pathway and the response to lenvatinib treatment. Everolimus, an mTOR inhibitor, in combination with lenvatinib and everolimus, exerted significant synergistic effects against HCC in vivo and in vitro . HCC cells develop resistance to lenvatinib by activating the NCOA5-AKT-mTOR pathway. The combination therapy of lenvatinib with everolimus is a promising strategy to overcome acquired resistance, thereby enhancing the clinical efficacy of lenvatinib.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"779-787"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12509451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144758990","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":"Safety and efficacy of ivosidenib in the treatment of isocitrate dehydrogenase 1 mutant cholangiocarcinoma and acute myeloid leukemia: a systematic review and meta-analysis.","authors":"Rameez Qasim, Laraib Anmol, Izza Shakeel, Bakhtawar Haseeb, Hurmat Fatima Bhatti, Uzair Iqbal, Shaheer Ahmad, Muhammad Hassan, Mubashir Raza","doi":"10.1097/CAD.0000000000001757","DOIUrl":"10.1097/CAD.0000000000001757","url":null,"abstract":"<p><p>Isocitrate dehydrogenase 1 (IDH1) mutations have gained interest because of their association with malignancies, including cholangiocarcinoma and acute myeloid leukemia. Ivosidenib, an inhibitor of IDH1 mutations, inhibits the formation of the oncometabolite D-2-HG, restoring normal cellular turnover and inhibiting tumorigenesis. In July 2024, a literature search was done using these databases: PubMed, Cochrane Library, and Embase. Studies were to show the safety and efficacy of ivosidenib using 95% confidence intervals (CIs). Preferred Reporting Items for Systematic reviews and Meta-Analyses flow guidelines were followed. Four articles involving 533 patients were included. The objective response rate (ORR) and progression-free survival (PFS) were significantly improved in the control group where risk ratio was 0.79, 95% CI: 0.71-0.89, Z = 4.05, a P value less than 0.001 for PFS, and odds ratio was 0.45, 95% CI: 0.30-0.68, Z value of 3.86, and P = 0.001 for ORR. The safety profile was favorable. Overall survival (OS) did not change significantly within the groups, as indicated by a P value of 0.78, risk ratio of 0.98, 95% CI: 0.83-1.15, and Z = 0.27. Ivosidenib demonstrated a PFS advantage and improved ORR with a favorable safety profile, but no effect on the OS. Evidence is suggestive of its plausibility for clinical usage as an adjunct therapy.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"812-821"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144688617","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":"VTCN1 emerges as a biomarker of immune tolerance in osimertinib-resistant lung cancer.","authors":"Lifang Wang, Jingjie Liu, Bin Shi","doi":"10.1097/CAD.0000000000001753","DOIUrl":"10.1097/CAD.0000000000001753","url":null,"abstract":"<p><p>Osimertinib is an effective strategy for nonsmall-cell lung cancer (NSCLC). However, the acquired resistance neutralizes the efficacy of osimertinib. Herein, we investigated the potential biomarkers of osimertinib-resistant lung cancer. GSE200894 was used to analyze the differentially expressed genes in osimertinib-resistant lung cancer. Sixty-two paired surgical specimens were collected from NSCLC patients with stage I-IV. Gene expression was detected using reverse transcription (RT)-qPCR, western blot, and immunohistochemistry. V-set domain containing T cell activation inhibitor 1 (VTCN1) was overexpressed in osimertinib-resistant lung cancer. High levels of VTCN1 predicted advanced stages and distant metastasis. Moreover, VTCN1 expression was negatively correlated with the purity of CD8+ T cells in lung cancer patients. VTCN1 inhibits the infiltration of effector-memory CD8+ T cells. In addition, overexpressed VTCN1 predicted the exhaustion of CD8+ T cells. VTCN1 inhibits the tumor-killing ability of CD8+ T cells. In summary, VTCN1 is overexpressed in osimertinib-resistant lung cancer patients. High levels of VTCN1 confer to inhibition of CD8+ T cell immunity and immune tolerance in osimertinib-resistant lung cancer patients.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"797-804"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648372","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":"Applying next-generation sequencing to predict short progression-free survival in patients with advanced EGFR -mutant lung adenocarcinoma receiving epidermal growth factor receptor tyrosine kinase inhibitors.","authors":"Po-Hsin Lee, Yi-Chun Hsiao, Yen-Hsiang Huang, Kuo-Hsuan Hsu, Jeng-Sen Tseng, Ho Lin, Gee-Chen Chang, Tsung-Ying Yang","doi":"10.1097/CAD.0000000000001762","DOIUrl":"10.1097/CAD.0000000000001762","url":null,"abstract":"<p><p>For patients with advanced EGFR -mutant lung adenocarcinoma, progression-free survival (PFS) is significantly improved by epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) medications. However, a subset of patients still experiences early disease progression. In this study, we aimed to identify potential risk factors associated with shorter PFS through next-generation sequencing (NGS) analysis. This retrospective study included patients with advanced EGFR -mutant lung adenocarcinoma who received first-line EGFR-TKI treatment with upfront NGS. The genetic alterations included two types, mutations and copy number variations. Alterations involving EGFR downstream signaling pathways were classified as ' PIK3CA-AKT/RAS-RAF alterations'. Clinical and histopathological data were also collected and analyzed. We studied a total of 82 advanced lung cancer patients with sensitive EGFR mutations. Multivariable analyses showed associations with a shorter PFS for the following factors: P IK3CA-AKT/RAS-RAF alterations [hazard ratio (HR) 3.197, P  = 0.006], age ≤50 (HR 3.034, P  = 0.010), and PD-L1 ≥50% (HR 2.256, P  = 0.035). Based on the above risk factors, patients were classified into no-risk and ≥1 risk groups. In the no-risk group, third-generation EGFR-TKIs showed a numerically longer PFS compared to first/second-generation EGFR-TKIs (not reached vs. 20.0 months, P  = 0.084). However, in patients with ≥1 risk factor, third-generation EGFR-TKIs showed no PFS advantages (6.6 vs. 6.2 months, P  = 0.831). In conclusion, besides clinicopathological factors, NGS provides additional insights to predict shorter PFS after EGFR-TKI treatment. We identified three risk factors: (1) PIK3CA-AKT/RAS-RAF alterations, (2) age ≤50, and (3) PD-L1 ≥50%. Patients with these factors had poor PFS regardless of EGFR-TKI generation.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"839-845"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798023","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":"Pembrolizumab treatment in SMARCA4-deficient nonsmall cell lung cancer: high tumor mutational burden and programmed death-ligand 1(+) expression on circulating tumor cells for real-time monitoring: a case report.","authors":"Youjun Deng, Yan Huang, Songhua Cai, Chujian Huang, Wenyi Liu, Ran Jia, Zhilin Sui, Heng Zou, Zhentao Yu, Xiaotong Guo","doi":"10.1097/CAD.0000000000001758","DOIUrl":"10.1097/CAD.0000000000001758","url":null,"abstract":"<p><p>Nonsmall cell lung cancer (NSCLC) with SMARCA4 deficiency represents a rare subset of lung tumors characterized by early metastasis, poor response to chemotherapy, and unfavorable prognosis. Established therapy strategies for SMARCA4-deficient NSCLC remain elusive. While immune checkpoint inhibitors have been proposed as a potential solution, their efficacy remains uncertain. Clinical factors such as tumor mutational burden (TMB), microsatellite instability, comutations, and programmed death-ligand 1 (PD-L1) expression may influence the treatment response of SMARCA4-deficient NSCLC. Additionally, PD-L1 expression on circulating tumor cells (CTCs) provides novel insights for monitoring, and its utility in SMARCA4-deficient NSCLC remains unexplored. The present report describes the case of a 71-year-old man diagnosed with SMARCA4-deficient NSCLC who had a history of heavy smoking and chronic cough. Imaging examination revealed metastatic lymph nodes. All serum tumor markers were elevated above the normal range. Histopathological and immunohistochemical analyses of the biopsy specimen from a primary lesion in the right upper lung demonstrated irregularly arranged tumor cells, SMARCA4 deficiency, and positive PD-L1 expression. Further next-generation sequencing confirmed SMARCA4 mutation, high TMB, and microsatellite stability (MSS). The patient received pembrolizumab treatment and experienced a sustained benefit for >40 months, with persistent PD-L1 expression on CTCs observed throughout the treatment. It was revealed that pembrolizumab therapy shows promise for patients with SMARCA4-deficient NSCLC with positive PD-L1 expression, high TMB, and MSS. Dynamic monitoring of PD-L1 status on CTCs may facilitate the assessment of the immunotherapy response, and the sustained positive PD-L1 expression on CTCs may imply continued benefit from immunotherapy for patients with SMARCA4-deficient NSCLC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"822-829"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12509448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032536","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":"E26 transformation-specific transcription factor 3 tips the balance: repressing tropomyosin 2 to fuel Yes-associated protein 1-driven cisplatin resistance in ovarian cancer.","authors":"Yan Wang, Zhujing Xu, Chanfeng He, Huiling Qu, Yiting Yang, Yongzheng Lu, Xiaojuan Dong","doi":"10.1097/CAD.0000000000001761","DOIUrl":"10.1097/CAD.0000000000001761","url":null,"abstract":"<p><p>Cisplatin resistance remains a major challenge in the treatment of ovarian cancer, significantly limiting therapeutic efficacy. This study aimed to investigate the role of E26 transformation-specific transcription factor 3 (ELK3) in cisplatin resistance and elucidate the underlying molecular mechanism involving the tropomyosin 2 (TPM2)-Yes-associated protein 1 (YAP1) signaling axis. By silencing ELK3 and TPM2 in combination with cisplatin treatment, the regulatory effects of ELK3 and TPM2 on cisplatin sensitivity in ovarian cancer cells were evaluated. The interaction between ELK3 and the TPM2 promoter was verified via chromatin immunoprecipitation and dual-luciferase reporter assays. Western blotting was used to assess the expression of DNA damage marker gamma-histone H2AX and YAP1 to investigate the role of TPM2 in ELK3-mediated signaling and drug response. Cisplatin treatment markedly increased ELK3 expression. Knockdown of ELK3 enhanced cisplatin sensitivity by suppressing cell proliferation, promoting apoptosis, and increasing DNA damage. Mechanistically, ELK3 was directly bound to the promoter region of TPM2 and repressed its transcription. Downregulation of TPM2 subsequently led to increased activation of the YAP1 signaling pathway. Rescue experiments demonstrated that silencing TPM2 reversed the chemosensitizing effects of ELK3 knockdown. These findings highlight the ELK3/TPM2/YAP1 axis as a critical regulator of cisplatin resistance. By suppressing TPM2 and subsequently activating YAP1 signaling, our study identified ELK3 as a crucial transcriptional repressor that contributes to cisplatin resistance in ovarian cancer.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"788-796"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144758989","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":"Patient-derived organoid modeling predicts personalized drug responses in prostate-metastatic mantle cell lymphoma: a case report.","authors":"Xiaoting Wang, Gang Fu, Jiayi Wan, Danyan Lin, Mingyi Shui, Tingyu Zhou, Sha Zhu, Peng Jiang, Ninghan Feng","doi":"10.1097/CAD.0000000000001760","DOIUrl":"10.1097/CAD.0000000000001760","url":null,"abstract":"<p><p>Tumor heterogeneity represents a significant challenge in cancer treatment. Current therapeutic strategies frequently rely on single biopsy assessments that may not fully capture tumor complexity. In this study, we developed prostate patient-derived organoids (PDOs) from a mantle cell lymphoma (MCL) case with prostatic metastasis. Monotherapy experiments revealed that the prostate organoids were sensitive to gemcitabine but resistant to rituximab and oxaliplatin. In combination therapy experiments, the half maximal inhibitory concentration value of gemcitabine increased, indicating that the combination regimen may attenuate its efficacy. In addition, the expression of prostate cancer markers prostate-specific membrane antigen and ETS-related gene was detected in the organoids. The research findings indicate that the PDO model not only dynamically monitors changes in drug sensitivity caused by heterogeneity but also serves as a powerful tool for predicting drug responses and optimizing precision treatment strategies. This is particularly applicable to clinical decision-making for highly heterogeneous tumors like MCL.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"830-838"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783306","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":"Real-world treatment patterns and survival outcomes in patients with metastatic castration-resistant prostate cancer in France: lessons from the prospective OPALE study.","authors":"Josephine Papet, Laetitia Augusto-Pelegrin, François Christy, Justine Lequesne, Frederic Di Fiore, Florence Joly, Christian Pfister","doi":"10.1097/CAD.0000000000001756","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001756","url":null,"abstract":"<p><p>In metastatic castration-resistant prostate cancer (mCRPC), several treatments are available, including androgen-receptor pathway inhibitors (ARPis) and chemotherapy (CT). There is a lack of real-world prospective data on treatment sequences and survival. The aim of the study was to evaluate overall survival (OS) in real-world conditions for patients treated for mCRPC. The OPALE study is a French prospective observational multicentre study. We included between 2018 and 2023, 212 patients undergoing first or second-line treatment for mCRPC. The primary outcome was the median OS, defined as the time between mCRPC diagnosis and death from any cause. The key secondary endpoints included OS according to therapeutic sequences, progression-free survival, response, and toxicities. Survival analysis was estimated using the Kaplan-Meier method and compared using the log-rank test. Associations between treatments and survival were assessed using Cox models. The 212 patients received first-line treatment (L1), 130 second-line (L2), 85 third-line (L3), and 51 fourth-line (L4). Most patients received ARPis in L1 (85.8%) and then chemotherapy in L2 (56.2%) and L3 (55.3%). The mean duration of follow-up was 31.8 months. Median OS was 46.4 months [95% confidence interval (CI): 35.9-53.8]. Our data did not significantly demonstrate the superiority of one therapeutic sequence over the others. Limitations are the observational design and the lack of statistical power. The OPALE study provided valuable data on the real-life management of mCRPC, contributing to a better understanding of current practice. We did not identify any optimal regimen, reflecting the evolution of knowledge and recent recommendations.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"36 10","pages":"805-811"},"PeriodicalIF":2.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285255","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":"Combined amlexanox and anti-MCP-1 therapy suppresses tumor progression in a murine Lewis lung carcinoma model.","authors":"Xiaodan Liu, Xue Dong, Jiaona Wei, Jingxuan Tian, Yuejiao Han, Honglin Li","doi":"10.1097/CAD.0000000000001751","DOIUrl":"10.1097/CAD.0000000000001751","url":null,"abstract":"<p><p>This study aims to assess the effects of combined amlexanox and an antimonocyte chemoattractant protein-1 (MCP-1) mAb therapy in a murine Lewis lung carcinoma (LLC) model. A subcutaneous LLC model was established in mice, which were allocated to either a control group or an intervention group receiving combined amlexanox and anti-MCP-1 mAb. Tumor size was monitored regularly. Immunofluorescence staining was performed to detect MCP-1 and Ki67 expression. Western blot analysis was conducted to assess the expression of TANK-binding kinase 1 (TBK1), macrophage polarization markers (iNOS and arginase-1), and apoptosis-related proteins (MCL-1, Bcl-xL, and Bcl-2). Flow cytometry was employed to quantify macrophage phenotype distributions. TBK1 expression was significantly elevated in LLC tumor tissues. MCP-1 was found to colocalize with the M2 macrophage marker CD206. The combination therapy resulted in a significant reduction in Ki67 expression. arginase-1 expression decreased significantly, while iNOS expression indicated an upward trend, though the change was not statistically significant. Levels of the antiapoptotic proteins MCL-1 and Bcl-xL were significantly downregulated ( P  < 0.05), whereas Bcl-2 levels did not differ significantly from those in the control group ( P  > 0.05). Flow cytometric analysis indicated a significant decrease in M2 macrophages (F4/80+CD206+) in the intervention group, with no substantial change observed in the proportion of M1 macrophages (F4/80+CD86+). Combined administration of amlexanox and anti-MCP-1 mAb inhibited tumor cell proliferation, promoted apoptosis, and reduced infiltration of tumor-associated M2 macrophages, thereby contributing to suppression of tumor progression in the LLC murine model.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"742-748"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144582872","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":"Circular RNA SMARCA5 inhibits cholangiocarcinoma via microRNA-95-3p/tumor necrosis factor receptor associated factor 3 axis: Erratum.","authors":"Guangxin Wang, Xia Gao, Zhijun Sun, Tianyou He, Chaogang Huang, Shouwei Li, Haocheng Long","doi":"10.1097/CAD.0000000000001763","DOIUrl":"10.1097/CAD.0000000000001763","url":null,"abstract":"","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"36 9","pages":"777-778"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12424533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039091","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}