Anti-Cancer Drugs最新文献

{"title":"Complete response with trastuzumab in heavily pretreated HER2-positive metastatic salivary duct carcinoma.","authors":"Rumeysa Çolak, Caner Kapar, Mesut Yilmaz","doi":"10.1097/CAD.0000000000001733","DOIUrl":"10.1097/CAD.0000000000001733","url":null,"abstract":"<p><p>Salivary duct carcinoma (SDC), an aggressive and relatively rare tumor, accounts for approximately 10% of all salivary gland malignancies. We report a case of a patient with a metastatic, human epidermal growth factor receptor 2 (HER2)-positive parotid SDC efficiently treated with docetaxel and trastuzumab combination after multiple series of chemotherapies. A 61-year-old man presented with SDC. After adjuvant radiotherapy, imaging revealed multiple metastatic lesions in the lungs. Systemic treatment with carboplatin and paclitaxel was initiated. After disease progression, doxorubicin, vinorelbine, and capecitabine were performed. Neurotrophic tropomyosin receptor kinase and AR (androgen receptor) were negative. Immunohistochemistry determined a HER2-positive score of 3. After multiple chemotherapy, the patient was started with combination of docetaxel and trastuzumab. A complete response was obtained after 3 months of treatment in the patient. In conclusion, SDCs are highly aggressive malignant tumors. Targeted therapy with trastuzumab targeting HER2 overexpression is a reasonable option in metastatic settings.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"675-677"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960405","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":"Denticleless homolog-mediated ubiquitin-proteasome degradation of forkhead box O1 contributes to development of carboplatin resistance in retinoblastoma.","authors":"Xian Liu, Shou-Feng Jiao, Chun-Yi Liu, Rui Luo, Han Liu, Yong Chai","doi":"10.1097/CAD.0000000000001738","DOIUrl":"10.1097/CAD.0000000000001738","url":null,"abstract":"<p><p>This study aimed to investigate the role of forkhead box O1 (FOXO1) in carboplatin-resistant retinoblastoma (RB) cells, focusing on its subcellular distribution and regulation through ubiquitin-dependent degradation mediated by denticleless homolog (DTL). The study sought to elucidate the molecular mechanisms underlying carboplatin resistance in RB and explore potential therapeutic strategies to overcome chemoresistance. Carboplatin-resistant RB cell lines (Y79/CBP and WERI-Rb-1/CBP) were established by incremental drug exposure. Bioinformatics analysis of the GSE111168 dataset identified differentially expressed genes associated with ubiquitination pathways. DTL expression was modulated using adeno-associated virus-mediated knockdown and overexpression. FOXO1 protein levels, subcellular localization, and ubiquitination were assessed via western blotting, immunofluorescence, and coimmunoprecipitation (Co-IP). The effects of DTL knockdown and LOM612 treatment on cell proliferation, apoptosis, and tumor growth were evaluated in vitro and in vivo using xenograft models. FOXO1 expression and nuclear localization were significantly reduced in carboplatin-resistant RB cells, with elevated levels of FOXO1 ubiquitination. Proteasome inhibitors preserved FOXO1 protein levels, implicating the ubiquitin-proteasome system in its degradation. DTL was identified as a significantly overexpressed gene in both resistant cells and patient-derived samples. Silencing DTL increased FOXO1 protein expression and nuclear accumulation, while Co-IP confirmed the interaction between DTL and FOXO1, mediated by the WD40 domain of DTL. Combined DTL knockdown and LOM612 treatment synergistically inhibited cell proliferation and invasion, promoted apoptosis in vitro, and significantly reduced tumor growth and induced apoptosis in vivo. DTL-mediated ubiquitination and degradation of FOXO1 play a critical role in carboplatin resistance in RB. Dual targeting of DTL and FOXO1 nuclear translocation may represent a promising therapeutic strategy to overcome chemoresistance and improve clinical outcomes in RB.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"648-663"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207469","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":"α-Asarone attenuates tumor-associated macrophages-induced gemcitabine resistance in pancreatic carcinoma via the transforming growth factor-beta 1/growth factor independent 1 axis.","authors":"Jiaqi Yu, Yuzhe Xue, Zhaofeng Gao, Lingyu Hu, Xiaorong Liu, Xuesong He, Xiaoguang Wang","doi":"10.1097/CAD.0000000000001740","DOIUrl":"10.1097/CAD.0000000000001740","url":null,"abstract":"<p><p>Pancreatic cancer is characterized by aggressiveness and poor prognosis. The development of gemcitabine resistance, especially tumor-associated macrophage (TAM) -induced resistance in the tumor microenvironment, has greatly limited its therapeutic effectiveness. This study investigates the effects and underlying mechanisms of the plant-derived bioactive compound α-asarone in reversing gemcitabine resistance induced by TAMs in pancreatic cancer, offering potential therapeutic alternatives. Flow cytometry was used to assess the cell cycle and apoptosis in pancreatic cancer cells. Transforming growth factor-beta 1 (TGF-β1) secretion was measured by ELISA, and Cell Counting Kit-8 assays to evaluate the survival of PANC-1 cells treated with gemcitabine. Western blotting and quantitative real-time PCR were used to analyze growth factor independent 1 (Gfi-1) expression and its association with gemcitabine resistance. α-Asarone effectively reversed gemcitabine resistance in pancreatic cancer cells. Treatment with α-asarone reduced TGF-β1 levels in TAM condition medium, which in turn led to the upregulation of Gfi-1 expression. Gfi-1 was found to negatively regulate the expression of drug resistance factors, including connective tissue growth factor (CTGF) and high mobility group box 1 (HMGB1), thereby reversing gemcitabine resistance in pancreatic cancer cells. Those results indicate that α-asarone enhances Gfi-1 expression, downregulates CTGF and HMGB1, and restores gemcitabine sensitivity by reducing TGF-β1 secretion from TAMs. α-Asarone can effectively reverse gemcitabine resistance in pancreatic cancer by reducing TGF-β1 secretion from TAMs, upregulating Gfi-1, and downregulating resistance factors such as CTGF and HMGB1. This restoration of gemcitabine sensitivity may improve the therapeutic efficacy of gemcitabine in pancreatic cancer treatment.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"664-674"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12329808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282231","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":"Early sensitivity and rapid resistance to drug therapy in primary pulmonary nuclear protein in testis carcinoma.","authors":"Ji Ma, Yaru Tian, Yan Zhang, Lin Song, Xue Zhen, Jing Sang, Dongfang Meng, Xin Ye","doi":"10.1097/CAD.0000000000001741","DOIUrl":"10.1097/CAD.0000000000001741","url":null,"abstract":"<p><p>Nuclear protein in testis (NUT) carcinoma is a rare disease characterized by aggressive and rapid progression. There is no standard management of primary pulmonary NUT carcinoma until now, and the median overall survival is only 4.4 months. Here, we describe a case where a 48-year-old woman presented with a dry, lasting half a month, and she was diagnosed with primary pulmonary NUT carcinoma and was given chemotherapy, immunotherapy, antiangiogenesis therapy, and palliative radiotherapy. When secondary tumor progression, she was conducted an organoid drug sensitivity test for better guide therapy. The initial two cycles of first-line and second-line treatments in our patient proved effective and improved the overall survival to more than 8 months. This is the first report of the use of an organoid drug sensitivity test for primary pulmonary NUT carcinoma. It provides a new approach for selecting drugs, particularly when multiple lines of treatment have proven ineffective and the next steps are unclear.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"698-701"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172449","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":"Enhanced plasma and brain concentrations and medulloblastoma cytotoxicity of asciminib and nilotinib by P-glycoprotein inhibition with tariquidar.","authors":"Eric M Thompson, Lin Cheng, Ivan Spasojevic","doi":"10.1097/CAD.0000000000001728","DOIUrl":"10.1097/CAD.0000000000001728","url":null,"abstract":"<p><p>ABL1 and ABL2 are putative drivers of medulloblastoma leptomeningeal dissemination. ABL1/ABL2 inhibitors, nilotinib and asciminib, are P-glycoprotein substrates. The purpose of this work is to elucidate P-glycoprotein expression in the brain/brain tumors and to determine if P-glycoprotein inhibition increases plasma and brain concentrations and medulloblastoma cytotoxicity of nilotinib and asciminib. ABCB1 (P-glycoprotein) mRNA expression was analyzed from multiple datasets of brain and brain tumor specimens. Cytotoxicity assays of medulloblastoma cells were conducted. In a mouse model, the pharmacokinetics of asciminib and nilotinib, with and without tariquidar, were determined using LC/MS. ABCB1 mRNA expression varied by brain region and was significantly lower in the cerebellum ( P  < 0.05). There was a bimodal increase in brain ABCB1 expression at ages 0-3 and 21-23 ( P  < 0.05). ABCB1 expression in pediatric brain tumors was similar to normal brain. The addition of tariquidar significantly reduced medulloblastoma cell viability compared to asciminib alone ( P  < 0.01). Tariquidar increased asciminib plasma and brain concentrations at 24 h ( P  = 0.0005 and P  = 0.0002, respectively) and nilotinib brain concentrations at 3 h ( P  = 0.0009). Tariquidar increased the area under the curve (AUC) brain : plasma ratio of asciminib from 0.33 to 10.16% and of nilotinib from 1.16 to 9.61%. Tariquidar prolonged the plasma half-life of asciminib from 2.21 to 10.49 h and nilotinib from 7.63 to 14.64 h. P-glycoprotein inhibition increased the brain concentrations, AUC, and half-life of asciminib and nilotinib and increased cytotoxicity in medulloblastoma cells.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"622-628"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12331432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960422","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":"First-line treatment with a combination of immunotherapy, anti-EGFR monoclonal antibodies, and chemotherapeutics for unresectable left KRAS/BRAF wild-type microsatellite-stable colorectal cancer: a case report.","authors":"Yaoyi Zhang, Dongfeng Wang, Ke Zhang, Sheng Li, Chen Yu","doi":"10.1097/CAD.0000000000001736","DOIUrl":"10.1097/CAD.0000000000001736","url":null,"abstract":"<p><p>Immunotherapy shows limited efficacy in microsatellite-stable (MSS) colorectal cancer. This case report describes a 40-year-old male with left-sided kirsten rat sarcoma viral oncogene homolog (KRAS)/v-raf murine sarcoma viral oncogene homolog B (BRAF) wild-type, MSS colorectal cancer and liver metastases who achieved complete regression of metastases following first-line treatment with toripalimab, cetuximab, and FOLFIRI (irinotecan + fluorouracil + leucovorin), enabling curative-intent surgical resection. The patient achieved a progression-free survival of 16 months and an overall survival exceeding 20 months. The regimen demonstrated excellent tolerability without severe adverse events, suggesting that this triple combination represents a promising strategy for conversion therapy in advanced MSS colorectal cancer.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"686-690"},"PeriodicalIF":2.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144214663","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":"Identification of uridine phosphatase 1 as a potential therapeutic target in gastric cancer by integrated bioinformatics analysis and experimental validation.","authors":"Yongfeng Wang, Yichen Feng, Chengzhang Zhu, Ling Guan, Shengfeng Wang, Anqi Zou, Miao Yu, Yuan Yuan, Hui Cai","doi":"10.1097/CAD.0000000000001745","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001745","url":null,"abstract":"<p><p>Gastric cancer remains a major global health challenge, and its early diagnosis and prognosis prediction pose significant challenges to the current clinical treatment of gastric cancer. Finding gastric cancer biomarkers is essential to comprehending its pathophysiology and creating novel targeted treatments. Following the acquisition and processing of the gastric cancer sample, the single-cell RNA sequencing data, monocyte subpopulation characterization, and cell type identification were performed. Key gene modules linked to gastric-cancer-related monocytes were identified using high-dimensional weighted gene co-expression network analysis. Machine-learning diagnostic models were created utilizing the discovered gastric-cancer-related monocyte-related genes (GCRMORGs). A prognostic model was developed with the uridine phosphatase 1 (UPP1)-related risk scores and verified in separate cohorts, and multiple immunological analyses were performed. Finally, using various experimental assays, we thoroughly investigated the function of the UPP1 gene in gastric cancer. Gastric cancer samples showed a distinct immune milieu topography with an abundance of monocytes. Eventually, 32 GCRMORGs were identified. Diagnostic models demonstrated a high degree of efficacy in differentiating between patients with gastric cancer and the control group. The prognostic model showed significant predictive value for gastric cancer patients' survival. At the same time, we have confirmed from experimental perspectives that a poor prognosis for patients is indicated by a high expression of UPP1 in gastric cancer tissue. Important monocyte subpopulations associated with gastric cancer samples were detected in our investigation. The prognosis of patients with gastric cancer can be predicted using a predictive model based on 32 GCRMORGs. In addition, focusing on UPP1 in gastric cancer may yield novel therapeutic targets and approaches.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939603","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":"https://doi.org/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: PIK3CA-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":""},"PeriodicalIF":2.2,"publicationDate":"2025-08-08","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":"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":"https://doi.org/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":""},"PeriodicalIF":2.2,"publicationDate":"2025-08-05","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":"9-Hexadecenoic acid inhibits the aggressiveness of gastric cancer via targeting PTPN1/FTH1 signaling.","authors":"Xin Wang, Haiyan Peng","doi":"10.1097/CAD.0000000000001724","DOIUrl":"10.1097/CAD.0000000000001724","url":null,"abstract":"<p><p>9-Hexadecenoic acid (9-HA) possesses anti-tumor properties. However, the effects of 9-HA on gastric cancer are scarcely reported. The present study aimed to investigate the effects of 9-HA on gastric cancer. mRNA levels were detected by reverse transcription quantitative PCR. Protein expression was detected by western blot. Cell behaviors were analyzed using Cell Counting Kit-8, colony formation, transwell, and propidium iodide staining assays. Co-localization of PTPN1 and FTH1 was determined using fluorescence in situ hybridization assay. In vivo assay was conducted to further verify the effects of 9-HA on gastric cancer. 9-HA suppressed the malignant behavior of gastric cancer. Moreover, 9-HA promoted iron-overload-dependent ferroptosis of gastric cancer in vivo and in vitro. Traditional Chinese medicine systems pharmacology predicted that 9-HA could target PTPN1, which was upregulated in gastric cancer cells. PTPN1-mediated phosphorylation of FTH1 contributed to the latter degradation. Overexpressed PTPN1 alleviated the effects of 9-HA, promoting the aggressiveness of gastric cancer and suppressing tumor cell ferroptosis. Interestingly, overexpressed PTPN1 antagonized the effects of 9-HA, promoted tumor growth, and inhibited the ferroptosis of gastric cancer. In summary, 9-HA-mediated downregulation of PTPN1 drives ferroptosis and inhibit the aggressiveness of gastric cancer. Thence, 9-HA may be an alternative strategy for gastric cancer.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"549-559"},"PeriodicalIF":2.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963184","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}