Anti-Cancer Drugs最新文献

Combined amlexanox and anti-MCP-1 therapy suppresses tumor progression in a murine Lewis lung carcinoma model. 氨lexanox联合抗mcp -1治疗抑制小鼠Lewis肺癌模型的肿瘤进展。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-07-07 DOI: 10.1097/CAD.0000000000001751

Xiaodan Liu, Xue Dong, Jiaona Wei, Jingxuan Tian, Yuejiao Han, Honglin Li

{"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":"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.","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}

引用次数: 0

Circular RNA SMARCA5 inhibits cholangiocarcinoma via microRNA-95-3p/tumor necrosis factor receptor associated factor 3 axis: Erratum. 环状RNA SMARCA5通过microRNA-95-3p/肿瘤坏死因子受体相关因子3轴抑制胆管癌：勘误。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-09-10 DOI: 10.1097/CAD.0000000000001763

Guangxin Wang, Xia Gao, Zhijun Sun, Tianyou He, Chaogang Huang, Shouwei Li, Haocheng Long

引用次数: 0

Effect of valproic acid and levetiracetam administration on the survival of glioma patients: a meta-analysis study. 丙戊酸和左乙拉西坦对胶质瘤患者生存的影响：一项荟萃分析研究。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-07-21 DOI: 10.1097/CAD.0000000000001746

Arya Shirani, Mobin Obeidinia, Makan Ziafati, Javad Garavand, Moazzameh Ramezani, Fatemeh Ramezani

引用次数: 0

Dysfunction of core clock genes regulates malignant phenotype and gemcitabine sensitivity of cholangiocarcinoma cells. 核心时钟基因功能障碍调节胆管癌细胞的恶性表型和吉西他滨敏感性。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-06-17 DOI: 10.1097/CAD.0000000000001744

Yin Li, Aimin Zheng, Yangang Cui, Tianbao Liu

{"title":"Dysfunction of core clock genes regulates malignant phenotype and gemcitabine sensitivity of cholangiocarcinoma cells.","authors":"Yin Li, Aimin Zheng, Yangang Cui, Tianbao Liu","doi":"10.1097/CAD.0000000000001744","DOIUrl":"10.1097/CAD.0000000000001744","url":null,"abstract":"The circadian clock governs daily rhythms in numerous physiological processes through precise regulation of gene expression and biochemical functions. Dysregulation of the circadian rhythm has been implicated in carcinogenesis and cancer progression. However, the mechanisms by which the circadian clock influences cancer phenotype and chemotherapy resistance, particularly in cholangiocarcinoma (CCA), remain poorly understood. Using cell lines established from primary CCA and metastatic ascites of two male patients, we manipulated core clock genes ( BMAL1 , PER2 , and NR1D1 ) to evaluate their effects on circadian rhythms. We analyzed alterations in circadian phenotypes at dynamic and single time points and assessed their impact on cancer-related phenotypic changes, including proliferation, apoptosis, cell cycle regulation, migration, invasion, and the expression of epithelial-to-mesenchymal transition (EMT) and cancer stem cell markers. Additionally, we examined the impact of circadian disruption on gemcitabine sensitivity. Genetic deletion of BMAL1 , PER2 , and NR1D1 disrupted circadian rhythm and significantly altered cancer phenotypes. Notably, BMAL1 and NR1D1 impairment exacerbated cell migration, invasion, and EMT activation in CCA cells. BMAL1 loss also induced gemcitabine resistance. In contrast, PER2 repression enhanced chemosensitivity and inhibited metastasis. The modulation of the circadian gene triggered phenotypic changes in CCA cells, indicating a crucial involvement of core-clock components in the pathological mechanisms hastening bile duct cancer malignancy. Our findings advance the understanding of regulating CCA malignancy and may offer a novel target for its treatment.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"711-722"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12424537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315773","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}

引用次数: 0

Overcoming refractory leptomeningeal metastasis in nonsmall cell lung cancer with intrathecal pemetrexed and osimertinib: a case report. 包膜内培美曲塞和奥西替尼治疗难治性非小细胞肺癌轻脑膜转移1例。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-07-15 DOI: 10.1097/CAD.0000000000001748

Li Xue, Xuhui Zhao, Xiaohui Tai, XuXia Zhang, Lingfang Zhang, Hongling Li

{"title":"Overcoming refractory leptomeningeal metastasis in nonsmall cell lung cancer with intrathecal pemetrexed and osimertinib: a case report.","authors":"Li Xue, Xuhui Zhao, Xiaohui Tai, XuXia Zhang, Lingfang Zhang, Hongling Li","doi":"10.1097/CAD.0000000000001748","DOIUrl":"10.1097/CAD.0000000000001748","url":null,"abstract":"Leptomeningeal metastasis (LM), a devastating complication of advanced nonsmall cell lung cancer (NSCLC), severely compromises patient survival and quality of life. Currently, standardized diagnostic criteria and treatment protocols for NSCLC-associated LM remain undefined, posing significant clinical challenges. Here, we present a case of a 58-year-old female with advanced epidermal growth factor receptor (EGFR)-mutated (exon 19 deletion) lung adenocarcinoma who developed LM after failing first-line gefitinib therapy. Initial treatment with osimertinib (80 mg/day), a third-generation EGFR-tyrosine kinase inhibitor (TKI), achieved 8 months of disease control before LM progression. Cerebrospinal fluid genomic analysis revealed acquired EGFR mutations (exon19 L747-A750delins and exon18 L718Q). Combination therapy with intrathecal pemetrexed and standard-dose osimertinib temporarily alleviated neurological symptoms. Upon disease recurrence after 6 months, therapeutic intensification through increased intrathecal pemetrexed frequency and high-dose osimertinib (160 mg/day) resulted in sustained neurological improvement and prolonged survival with manageable toxicity. This case demonstrates the potential of optimized intrathecal/systemic TKI combination strategies for EGFR-mutant NSCLC with LM, providing clinical insights for this therapeutic dilemma.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"764-769"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636000","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}

引用次数: 0

LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial-mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1: Erratum. LncRNA FOXP4-AS1沉默通过miR-136-5p/MAPK1抑制鼻咽癌转移和上皮-间质转化：更正。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-09-10 DOI: 10.1097/CAD.0000000000001726

Jin Yan, Qi Zhou

引用次数: 0

Progression of drug resistance or multiple primary lung cancer: a case report and literature review of a patient with mesenchymal-epithelial transition factor exon 14 skipping alterations lung adenocarcinoma. 耐药或多发性原发性肺癌的进展：一例间充质上皮转移因子外显子14跳变肺腺癌的病例报告和文献综述。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-06-12 DOI: 10.1097/CAD.0000000000001747

Liang Gong, Lihang Zhou, Pan Yang, Fu Xiong, Xin Li, Chunlan Tang

{"title":"Progression of drug resistance or multiple primary lung cancer: a case report and literature review of a patient with mesenchymal-epithelial transition factor exon 14 skipping alterations lung adenocarcinoma.","authors":"Liang Gong, Lihang Zhou, Pan Yang, Fu Xiong, Xin Li, Chunlan Tang","doi":"10.1097/CAD.0000000000001747","DOIUrl":"10.1097/CAD.0000000000001747","url":null,"abstract":"Mesenchymal-epithelial transition factor (MET) exon 14 skipping alterations are rare mutations in non-small-cell lung cancer, associated with high malignancy and poor prognosis. This article presents a case of a patient diagnosed with advanced left upper lung adenocarcinoma characterized by a MET14 skipping mutation. Following first-line treatment with crizotinib, there was a significant reduction in the size of the primary lesion; however, during the course of treatment, an increase in size and prominence of solid components were observed in the right upper lung lesion. A biopsy and subsequent genetic testing revealed an epidermal growth factor receptor L858R mutation in the right upper lung adenocarcinoma, indicating the presence of multiple primary lung cancers. The patient opted against surgical intervention and local treatments, choosing instead a combination therapy regimen that included almonertinib and crizotinib. This treatment approach led to a significant reduction in the size of the right upper lung lesion. The patient's condition has remained stable without any signs of progression, resulting in an overall survival duration exceeding 53 months.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"759-763"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12424535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282230","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}

引用次数: 0

FH-2001 is a novel FGFR/VEGFR dual inhibitor with immune-modulating activity. FH-2001是一种具有免疫调节活性的新型FGFR/VEGFR双抑制剂。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-06-24 DOI: 10.1097/CAD.0000000000001743

Aiguo Liu, Longfei Huang, Xin Gao, Lei Liu, Xiang Li, Xiaohong Yu, Chunyan Zhao

{"title":"FH-2001 is a novel FGFR/VEGFR dual inhibitor with immune-modulating activity.","authors":"Aiguo Liu, Longfei Huang, Xin Gao, Lei Liu, Xiang Li, Xiaohong Yu, Chunyan Zhao","doi":"10.1097/CAD.0000000000001743","DOIUrl":"10.1097/CAD.0000000000001743","url":null,"abstract":"Multiple cancers are driven by aberrant fibroblast growth factor receptor (FGFR) signaling and vascular endothelial growth factor receptor (VEGFR)-linked angiogenesis. Several therapeutic agents targeting FGFR and VEGFR have been developed and approved for use in solid cancers; however, there is still a high unmet medical need for new agents that have a more powerful antitumor activity and a broader antitumor spectrum. Here, we report the discovery of FH-2001, a novel and potent FGFR/VEGFR dual inhibitor, with additional activity of modulating programmed cell death ligand 1 (PD-L1) gene expression. In biochemical assays, FH-2001 showed potent inhibition of FGFR1, 2, 3, and 4, with half-maximal inhibitory concentration (IC 50 ) of 0.2, 0.2, 0.4, and 2.0 nM, respectively, and VEGFR1, 2, and 3, with IC 50 values of 2.0, 0.3, and 0.5 nM, respectively. FH-2001 significantly suppressed the cell growth of FGFR- or VEGFR-driven cancer cell lines. In representative cell line- and patient-derived tumor xenografts with aberrant FGFR or VEGFR signaling, FH-2001 substantially inhibited tumor growth. Furthermore, FH-2001 demonstrated marked antitumor activities when treated alone or combined with PD-L1 or PD-1 antibody in syngeneic mouse models. Flow cytometric analysis revealed that FH-2001 alone or in combination with anti-PD-L1 increased T and natural killer cells and decreased myeloid cells in the tumor microenvironment. Mechanistically, FH-2001 treatment dramatically reduced c-Myc and PD-L1 mRNA and protein levels in a dose-dependent manner in vitro . Taken together, FH-2001 is a promising dual-target inhibitor of FGFR and VEGFR and also modulates cancer immunity, while its robust antitumor activity positions it as a potentially class-leading anticancer agent.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"703-710"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473842","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}

引用次数: 0

The mTOR pathway inhibition with everolimus in pseudomyogenic hemangioendothelioma harboring SERPINE1-FOSB gene fusion: a case report and review of the literature. 依维莫司抑制含有SERPINE1-FOSB基因融合的假肌源性血管内皮瘤的mTOR通路：一例报告和文献综述。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-07-03 DOI: 10.1097/CAD.0000000000001752

Cevat İlteriş Kikili, Bahadir Köylü, Fatih Kemik, Nazan Demir, Mehmet Ali Deveci, Fatih Selçukbiricik

引用次数: 0

Discovery and optimization of oxidative phosphorylation inhibitors from a phenotypic screen. 从表型筛选中发现并优化氧化磷酸化抑制剂。

IF 2.2 4区医学

Anti-Cancer Drugs Pub Date : 2025-10-01 Epub Date: 2025-06-20 DOI: 10.1097/CAD.0000000000001750

Mahmoud El Shemerly, Florian Richalet, Dimitri Robay, Claude Nuoffer, Alexandra Kunz, Luc Bury, Claire Hisler, Norbert Hermann, Jochen Spickermann, Sven Weiler, Paul M J McSheehy, Laurenz Kellenberger, Heidi A Lane

{"title":"Discovery and optimization of oxidative phosphorylation inhibitors from a phenotypic screen.","authors":"Mahmoud El Shemerly, Florian Richalet, Dimitri Robay, Claude Nuoffer, Alexandra Kunz, Luc Bury, Claire Hisler, Norbert Hermann, Jochen Spickermann, Sven Weiler, Paul M J McSheehy, Laurenz Kellenberger, Heidi A Lane","doi":"10.1097/CAD.0000000000001750","DOIUrl":"10.1097/CAD.0000000000001750","url":null,"abstract":"Tumor metabolism and metabolic reprogramming in cancer cells represent a promising area in oncology research, offering new avenues for therapeutic intervention. While the 'Warburg effect' highlights the reliance of many tumors on aerobic glycolysis, emerging evidence indicates that some cancers also depend on mitochondrial oxidative phosphorylation (OXPHOS) for energy production, cancer cell survival, tumor progression, metastasis, and drug resistance. We conducted a high-throughput, differential, phenotypic screening followed by a focused medicinal chemistry campaign, leading to the identification of novel, potent OXPHOS inhibitors. These lead compounds selectively target complex I of the mitochondrial electron transport chain, thereby disrupting ATP production and oxygen consumption in cancer cells. In-vitro studies in breast cancer cell lines, along with published data, suggest that MCT4 expression may serve as a biomarker for drug sensitivity. Notably, low MCT4 expression correlated with higher potency in cell growth assays. The identified compounds exhibited favorable drug-like properties, including good pharmacokinetics and oral bioavailability in mice. Daily oral dosing significantly inhibited tumor growth in two in-vivo breast cancer models with low MCT4 expression levels. This efficacy, however, was accompanied by body weight loss, indicating the need to enhance the therapeutic index through optimization or rational combination therapy strategies. These findings highlight the therapeutic potential of targeting mitochondrial OXPHOS in cancers with defined metabolic dependencies, offering a novel approach for exploiting tumor-specific metabolic vulnerabilities for improved cancer treatment.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"731-741"},"PeriodicalIF":2.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332342","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}

引用次数: 0