Current cancer drug targets最新文献

{"title":"Exosome-mediated Induction of Apoptosis in Cisplatin-treated Gastric Cancer Cells as a Strategy to Mitigate Side Effects.","authors":"Jiaqi Zhu, Hui Wang, Yijie Liu, Wen Li, Li Cao, Wenjing Wang, Suoni Li, Jin Shang, Yannan Qin, Chen Huang, Bo Guo","doi":"10.2174/0115680096369817250407164352","DOIUrl":"https://doi.org/10.2174/0115680096369817250407164352","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer is the third most lethal malignancy worldwide. While cisplatin has shown remarkable efficacy at a low cost, it is also associated with severe side effects. Exosomes play a key role in mediating the bystander effect of radiation and have the capacity to deliver apoptosis signals for targeted destruction of tumor cell. However, there remains a paucity of research on exosome-mediated bystander effects in the context of chemotherapeutic drugs.</p><p><strong>Objective: </strong>This study aims to investigate the ability of cisplatin-induced exosomes to deliver apoptosis signals to gastric cancer cells, with the aim of mitigating the adverse effects associated with chemotherapy.</p><p><strong>Methods: </strong>Differential ultracentrifugation was used to isolate apoptotic exosomes secreted by cisplatin-induced gastric cancer MKN-28 cells. Characterization and identification of these exosomes were performed by transmission electron microscopy, particle size analyzer, flow cytometry, and Western blotting. The transduction efficiency of the exosomes was confirmed through immunefluorescence. The effects of apoptotic exosomes on the proliferation, apoptosis, migration, cycle, senescence, and tumor formation of MKN-28 cells in vitro and in vivo were investigated by live cell workstation, flow cytometry, HE staining, and tumor-igenicity assays.</p><p><strong>Results: </strong>Cisplatin-induced apoptotic exosomes, termed DDP-EXO, exhibited a significantly enhanced inhibitory effect on the proliferation of MKN-28 cells compared to gastric epithelial GES-1 cells. Moreover, DDP-EXO was able to deliver apoptotic signals to MKN-28 cells, leading to an increase in the apoptotic population in recipient cells, possibly through the involvement of Caspase-9. Furthermore, DDP-EXO showed limited impacts on cell migration, cell cycle, or cell senescence. In vivo, DDP-EXO effectively suppressed tumorigenesis in a subcutaneous tumor model without causing detectable pathological changes in main organs and blood samples, suggesting a favorable safety profile.</p><p><strong>Conclusion: </strong>In summary, this study provides new perspectives on the potential application of exosomes as an innovative therapeutic approach for gastric cancer.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992997","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":"MND1 Promotes the Proliferation of Prostate Cancer Cell via the CCNB1/p53 Signaling Pathway.","authors":"Zhongxiang Zhao, Yesong Zou, Qian Lv, Chenxiao Wu, Ke Tang, Fazhong Dai, Jiayao Feng, Hongshen Lai, Wenjie Lai, Xiaofu Qiu","doi":"10.2174/0115680096391591250506064859","DOIUrl":"https://doi.org/10.2174/0115680096391591250506064859","url":null,"abstract":"<p><strong>Introduction: </strong>Prostate cancer (PCa) is one of the most commonly diagnosed can-cers in men, with a high global incidence. The Meiotic Nuclear Division 1 (MND1) protein is essential for the repair of DNA double-strand breaks during meiosis, but its role in PCa re-mains poorly understood. This study aims to explore the function of MND1 in PCa progression and the mechanism involved.</p><p><strong>Methods: </strong>RNA-Seq data from the TCGA and GEO databases were analyzed. Kaplan-Meier (KM) method and χ2 test examined the association between MND1 expression, prognosis, and clinical parameters. PCa cell lines (22RV1 and C4-2) were used for functional assays. CCK-8, EdU, colony formation assay, flow cytometry analysis and xenograft model were used to evaluate the effects of MND1 on PCa cell proliferation in vitro and in vivo.</p><p><strong>Results: </strong>MND1 expression was significantly upregulated in PCa tissues, particularly in cases with Gleason scores ≥8, and correlated with poorer disease-free survival (DFS) and adverse clinical features. Functionally, elevated MND1 expression promoted PCa cell proliferation both in vitro and in vivo. Mechanistically, MND1 facilitated cell cycle progression from G0/G1 to S phase via activation of the CCNB1/p53 signaling pathway.</p><p><strong>Conclusion: </strong>MND1 promotes prostate cancer progression by facilitating the G0/G1 to S phase transition via the CCNB1/p53 pathway, making it a promising prognostic marker and potential therapeutic target.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966924","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":"CREC Family Genes as Biomarkers and Therapeutic Targets in Lung Adenocarcinoma: In vitro and In silico Insights.","authors":"Yimin Jiang, Guangfu Zhu, Xueqin Cheng, Xinyue Mo, Yi Chen, Fengqi Xu, MeiFang Wang, Yijun Tang","doi":"10.2174/0115680096363759250401045735","DOIUrl":"https://doi.org/10.2174/0115680096363759250401045735","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer (NSCLC), characterized by poor prognosis and limited treatment options.</p><p><strong>Material and methods: </strong>This study investigated the expression patterns and functional roles of the CREC family genes (RCN1, RCN2, RCN3, SDF2, and CALU) in LUAD using vari-ous detailed molecular and in silico experiments.</p><p><strong>Results: </strong>RT-qPCR analysis revealed significant upregulation of all five genes in LUAD cell lines compared to normal controls, with ROC curve analysis suggesting their potential as di-agnostic biomarkers. Validation using independent datasets (Oncomine, UALCAN, and HPA) confirmed these findings at both the transcript and protein levels. Stage-specific ex-pression and promoter methylation analyses demonstrated that RCN1 and CALU exhibit higher expression in advanced stages, while promoter hypomethylation correlated with gene overexpression in LUAD. Mutation and copy number variation (CNV) analyses indicated that CREC gene alterations are common in LUAD, with CALU and RCN3 frequently mu-tated. Functional assays revealed that knockdown of SDF2 and CALU significantly reduced cell proliferation, colony formation, and wound healing abilities in A549 cells, suggesting their roles in promoting LUAD progression. Gene enrichment and miRNA interaction anal-yses highlighted the involvement of CREC genes in processes like calcium binding, oxida-tive stress response, and immune regulation. CALU emerged as a potential prognostic mark-er, showing a significant association with poorer survival outcomes.</p><p><strong>Conclusion: </strong>Together, the findings of this study suggested that CREC family genes may serve as promising diagnostic and therapeutic targets in LUAD.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981690","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":"Ergodic Manipulation of Genome Chaos: Innovative Strategies against Malignant Progression.","authors":"Sergey Shityakov, Viacheslav Kravtsov","doi":"10.2174/0115680096379988250415094558","DOIUrl":"https://doi.org/10.2174/0115680096379988250415094558","url":null,"abstract":"<p><p>Genome instability is a key driver of malignant progression in cancer and is char-acterized by chromoanagenesis, including spontaneous events, such as chromothripsis, chromoanasynthesis, and chromoplexy. These genome catastrophes create the heterogeneity necessary for tumor cells to adapt, evolve, and resist therapy. Ergodic anticancer therapy rep-resents a novel strategy for targeting cancer stem cells by manipulating their genome chaos. Two approaches have been proposed: ergodynamic anticancer therapy (EDAT), which en-hances genome chaos beyond a critical threshold and leads to self-destruction, and ergostatic anticancer therapy (ESAT), which suppresses chaos and limits malignant progression. This brief review explores the conceptual foundations, molecular mechanisms, and therapeutic potential of ergostatic and ergodynamic therapies in treating cancer, highlighting their role in personalized medicine.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970278","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":"Arctigenin Suppresses Melanoma via Mitophagy Activation In vitro and Enhances Dacarbazine Sensitivity In vivo.","authors":"Ling Jiang, Yang Lu, Hongyan Zhao, Weiyang He","doi":"10.2174/0115680096373796250414062644","DOIUrl":"https://doi.org/10.2174/0115680096373796250414062644","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the effect and mechanism of arctigenin (ARG) on the sensitization of dacarbazine (DTIC) via the regulation of mitophagy.</p><p><strong>Methods: </strong>In vitro experiments were conducted to explore the effects of ARG on the biologi-cal behavior of melanoma cells, mitochondrial autophagy mediated by PINK1/Parkin, and the role of reactive oxygen species (ROS)-mitochondrial autophagy in the regulation of the biological behavior of melanoma cells by an ROS quenching agent, a mitochondrial autoph-agy inhibitor, and an activator. The effects of ARG and dacarbazine in nude mice were as-sessed.</p><p><strong>Results: </strong>CCK8 assays revealed that ARG inhibited the proliferation of the human melanoma cell lines A375 and SK-MEL-2. The observation of submicroscopic structures demonstrated mitochondrial damage. Flow cytometry further verified that ARG induced apoptosis. West-ern blot analysis revealed that the protein expression levels of cleaved caspase 3 and Bax in-creased, whereas that of Bcl-2 decreased. In addition, ARG increased ROS levels. LC3II/I, PINK1, and Parkin were increased. ARG-induced apoptosis was related to increased mito-chondrial oxidative stress and promoted the occurrence of mitochondrial autophagy. After the addition of the autophagy inhibitor Mdivi-1 or the ROS quencher N-acetylcysteine (NAC), the antiproliferative effect of ARG was markedly attenuated. The expression levels of PINK1, Parkin, LC3II/I, cleaved caspase 3, and Bax were increased, whereas that of Bcl-2 was decreased. The formation of mitochondrial autophagosomes was observed by transmis-sion electron microscopy. ARG inhibited the proliferation and induced the apoptosis of mel-anoma cells in vivo.</p><p><strong>Conclusion: </strong>Autophagy-mediated cell apoptosis was activated through the PINK1/Parkin pathway by ARG, effectively inhibiting the proliferation of human melanoma cells.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978486","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":"Synergistic Targeting of EGFR, ESR1, BCL2, and TP53 Pathways: A Multi-Pronged Approach for Advanced Breast Cancer Therapy.","authors":"Harneet Marwah, Hitesh Kumar Dewangan","doi":"10.2174/0115680096366956250314043513","DOIUrl":"https://doi.org/10.2174/0115680096366956250314043513","url":null,"abstract":"<p><p>Breast cancer is a heterogeneous disease driven by complex molecular signaling pathways that influence tumor progression, metastasis, and treatment resistance. This review provides a comprehensive analysis of the molecular mechanisms underlying breast cancer, with a focus on key pathways such as EGFR, ESR1, BCL2, and TP53. We examine the roles of these pathways in regulating critical cellular processes, including proliferation, survival, apoptosis, and migration. EGFR's involvement in cell proliferation and migration, as well as its overexpression and mutations in breast cancer, are discussed, alongside the impact of ESR1 signaling in hormone-receptor-positive breast cancer and resistance to endocrine ther-apies. Additionally, the review highlights the function of BCL2 in apoptosis regulation and its overexpression in conferring resistance while also exploring the role of TP53 in cell cycle control and apoptosis, particularly its mutations that contribute to poor prognosis. Further-more, the interplay between these molecular pathways-such as the crosstalk between EGFR and ESR1, BCL2-TP53 interactions, and the EGFR-TP53 mutational relationships-illustrates the complexity of resistance mechanisms and the need for multi-targeted thera-peutic strategies. The concept of synergistic targeting, including the integration of the PI3K/AKT/mTOR pathway, is explored, with evidence supporting the potential for over-coming resistance and improving therapeutic outcomes. We also discuss the emerging role of personalized medicine, emphasizing biomarker-driven approaches for patient selection and tailored treatments. Finally, advancements in nanoparticle-based drug delivery systems are reviewed, addressing their potential to enhance therapeutic efficacy and address current challenges in cancer therapy. This review highlights the critical importance of understanding the molecular underpinnings of breast cancer and the need for integrated, multi-targeted ap-proaches to overcome therapeutic resistance, offering insights into future directions for im-proving clinical outcomes in breast cancer treatment.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968790","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 Comprehensive Evaluation of the Effectiveness and Safety of Pembrolizumab for the Treatment of Metastatic Colorectal Cancer: A Systematic Review and Meta-Analysis.","authors":"Chao Huang, Yue He, Yidian Yang, Weizeng Shen","doi":"10.2174/0115680096357426250310070752","DOIUrl":"https://doi.org/10.2174/0115680096357426250310070752","url":null,"abstract":"<p><strong>Aim: </strong>This comprehensive assessment and quantitative synthesis aimed to assess the effectiveness and safety profile of pembrolizumab, an antagonist of the programmed cell death protein 1 [PD-1] pathway, for individuals with metastatic colorectal carcinoma [mCRC].</p><p><strong>Methods: </strong>A comprehensive search of scholarly articles was performed using the PubMed and Web of Science [WOS] databases from January 2015 to August 2024. The scope of the search was limited to randomized controlled trials and clinical studies that reported the effectiveness of pembrolizumab in patients with metastatic colorectal cancer [mCRC], which emphasized critical indicators, such as overall survival, progression-free survival, objective response rate, and disease control rate. The research also considered secondary outcomes, including the incidence of severe adverse events and mortality rates. Data ex-traction was performed by two independent reviewers, who employed a standardized data collection form. The subsequent meta-analysis was performed using RevMan 5.0, a soft-ware tool for statistical analysis.</p><p><strong>Results: </strong>Six studies with 1,634 patients were included, and of these patients, 812 were in the pembrolizumab group, and 822 were in the control group. The results of the meta-analysis indicated via the standard mean difference [SMD] that the overall survival [OS] of patients in the pembrolizumab group was significantly different from that of patients in the control group [SMD = 0.21, 95% CI [0.09, 0.32], P = 0.0005]. The progression-free survival [PFS] of patients in the pembrolizumab group was slightly longer than that of pa-tients in the control group according to the SMD, and this difference was statistically sig-nificant [SMD = 0.11, 95% CI [0.01, 0.22], P = 0.03]. Compared with the objective re-sponse rate [ORR] of patients in the control group, that of patients in the pembrolizumab group was significantly higher [OR = 1.71, 95% CI [1.34, 2.17], P < 0.0001]. The mortali-ty rate in the pembrolizumab group was also significantly different from that in the control group [OR = 0.67, 95% CI [0.52, 0.87], P = 0.002].</p><p><strong>Conclusion: </strong>Pembrolizumab may help improve overall survival [OS] and progression-free survival [PFS] in patients with metastatic colorectal cancer, which can potentially reduce the mortality rate. More research using larger, well-designed studies is needed to further confirm these findings.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996133","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":"MED10 Increases Cisplatin Resistance by Promoting PTEN Ubiquitination of Hepatocellular Carcinoma","authors":"Qiucheng Cai, Jianyong Liu, Junyang Xiao, Jianwei Chen, Lizhi Lv, Fang Yang","doi":"10.2174/0115680096330893241221141235","DOIUrl":"10.2174/0115680096330893241221141235","url":null,"abstract":"<p><strong>Objective: </strong>Hepatocellular carcinoma (HCC) is a highly prevalent malignant tumor, ranking as the third leading cause of cancer-related deaths worldwide. Despite advances in chemotherapy, many patients exhibit limited therapeutic efficacy, ultimately leading to cisplatin resistance. Thus, an in-depth investigation into the molecular mechanisms underlying cisplatin resistance is critically needed.</p><p><strong>Materials and methods: </strong>This study utilized the GEPIA dataset to analyze MED10 expression and its association with HCC. MED10 expression levels in normal and HCC tissues were quantified via PCR and immunohistochemistry. HCC cell proliferation was assessed through cell viability and colony formation assays, while apoptosis rates were measured using flow cytometry. To examine PTEN ubiquitination, Western blot analysis was conducted in vitro. Additionally, xenograft tumor models were employed using BALB/c nude mice (male/female, 6 weeks old, 18-22 g) to evaluate cellular proliferation in vivo.</p><p><strong>Results: </strong>The findings reveal a pivotal role for MED10 in driving cisplatin resistance in HCC by promoting PTEN ubiquitination. MED10 expression correlated with HCC malignancy, and MED10 knockdown significantly reduced the IC50 of cisplatin in SMMC-7721, HepG2, and MHCC97-H cell lines. MED10 overexpression significantly decreased PTEN protein levels, which was reversed by the ubiquitination inhibitor TAK-243, while PTEN mRNA levels remained unaffected by MED10 overexpression or TAK-243. Both in vitro and in vivo, MED10 enhanced cisplatin resistance by promoting PTEN ubiquitination in HCC cells. These results offer valuable insights into the molecular mechanisms underlying MED10 expression and its role in cisplatin resistance in HCC.</p><p><strong>Conclusions: </strong>MED10 enhances cisplatin resistance by promoting PTEN ubiquitination in HCC cells.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779367","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":"HDL Cholesterol Levels and Pancreatic Cancer Risk: Protective Effects Revealed.","authors":"Yiming Shao, Rui Hao, Si Si Lin, Ba-Fang Ma, Jun-Nan Ye, Mayila Maimaiti, Yasen Maimaitiyiming","doi":"10.2174/0115680096334509241218141459","DOIUrl":"https://doi.org/10.2174/0115680096334509241218141459","url":null,"abstract":"<p><strong>Background: </strong>The causal relationship between lipoprotein traits and the risk of pancre-atic cancer (PC) remains unclear. In this study, we employed a two-sample Mendelian randomiza-tion (MR) approach to explore the untangled relationship between lipoprotein traits and PC.</p><p><strong>Methods: </strong>Univariable MR analyses were used to determine the causal connection between lipo-protein traits and PC. Instrumental variables corresponding to lipoprotein traits were taken from the Global Lipids Genetics Consortium (GLGC) (n = 188,578). The outcome dataset was created from PC summary-level data (n case = 1896, n control = 1939) from a genome-wide association study of European ancestry. Causal effects were evaluated using the inverse variance weighted (IVW) method. For sensitivity analysis, both the weighted median (WM) and MR-Egger methods, among others, were utilized. We also conducted multivariable MR analyses to examine potential confounders.</p><p><strong>Results: </strong>In univariable MR, IVW methods supported evidence that HDL cholesterol (OR = 0.463, 95% CI: 0.313-0.685; P = 1.10×10-4) was linked with a decreased risk of PC. These findings were consistent across other MR methods, including MR-Egger (OR = 0.340, 95% CI: 0.182-0.638; P = 1.30×10-3) and WM (OR = 0.367, 95% CI: 0.195-0.692; P = 1.90×10-3). Our results displayed no significant heterogeneity or horizontal pleiotropy. Furthermore, these associations persisted in the multivariable MR analysis after adjusting for confounding factors such as smok-ing, alcohol consumption, and body mass index (BMI).</p><p><strong>Conclusions: </strong>Our comprehensive MR analyses consistently demonstrate a protective association between higher HDL cholesterol levels and decreased PC risk, even after adjustments for key life-style factors and BMI.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718217","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":"Is the Use of SGLT-2 Associated with an Increased Risk of Cancer?","authors":"Sadique Hussain, Gyas Khan, Gaurav Gupta","doi":"10.2174/0115680096383119250307083130","DOIUrl":"https://doi.org/10.2174/0115680096383119250307083130","url":null,"abstract":"","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656384","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}