OncoTargets and therapy最新文献

{"title":"Recent Advances in Understanding the Clinical Responses of Brentuximab Vedotin in Lymphoma and the Correlation with CD30 Expression.","authors":"Wen Chen, Zhihong Zhang","doi":"10.2147/OTT.S487088","DOIUrl":"10.2147/OTT.S487088","url":null,"abstract":"<p><p>Brentuximab vedotin (BV) is an antibody-drug conjugate that combines the CD30 monoclonal antibody with the microtubule-disrupting agent, monomethyl auristatin E, which induces apoptosis in the tumor cell upon its release from the conjugate. The safety and efficacy of BV have been assessed in several studies in patients with T- and B-cell lymphomas. This article reviews the currently available data on the distribution of CD30 expression in T- and B-cell lymphomas, as well as the various levels of CD30 positivity cutoff used in the literature. It also analyzes the relationship between CD30 expression levels and the clinical response to BV in clinical trials for both T- and B-cell lymphomas and investigates BV efficacy in patients with low or undetectable levels of CD30 and examines potential mechanisms by which BV exerts its effect on these patients. This review contributes to the growing evidence suggesting that CD30 expression levels do not predict the clinical benefit of BV as the drug demonstrated substantial efficacy in patients across a wide range of CD30 expression levels while suggesting that the antitumor activity was not associated with CD30 expression levels. Furthermore, the potential of BV as a targeted approach along with its mechanism of action is also summarized to explain its key role in the future treatments of lymphomas, especially for CD30-expressing lymphomas.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"18 ","pages":"1-14"},"PeriodicalIF":2.7,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11720807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971748","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":"Progress of Immune Checkpoint Inhibitors Therapy for pMMR/MSS Metastatic Colorectal Cancer.","authors":"Fanjie Qu, Shuang Wu, WeiWei Yu","doi":"10.2147/OTT.S500281","DOIUrl":"10.2147/OTT.S500281","url":null,"abstract":"<p><p>Immunotherapy is one of the research hotspots in colorectal cancer field in recent years. The colorectal cancer patients with mismatch repair-deficient (dMMR) or high microsatellite instability (MSI-H) are the primary beneficiaries of immunotherapy. However, the vast majority of colorectal cancers are mismatch repair proficient (pMMR) or microsatellite stability (MSS), and their immune microenvironment is characterized by \"cold tumors\" that are generally insensitive to single immunotherapy based on immune checkpoint inhibitors (ICIs). Studies have shown that some pMMR/MSS colorectal cancer patients regulate the immune microenvironment by combining other treatments, such as multi-target tyrosine kinase inhibitors, anti-vascular endothelial growth factor (VEGF) monoclonal antibodies, chemotherapy, radiotherapy, anti-epithelial growth factor receptor (EGFR) monoclonal antibodies, and mitogen-activated protein kinase (MAPK) signaling pathway inhibitors and oncolytic viruses, etc. to transform \"cold tumor\" into \"hot tumor\", thereby improving the response to immunotherapy. In addition, screening for potential prognostic biomarkers can also enrich the population benefiting from immunotherapy for microsatellite stable colorectal cancer. Therefore, in pMMR or MSS metastatic colorectal cancer (mCRC), the optimization of immunotherapy regimens and the search for effective efficacy prediction biomarkers are currently important research directions. In this paper, we review the progress of efficacy of immunotherapy (mainly ICIs) in pMMR /MSS mCRC, challenges and potential markers, in order to provide research ideas for the development of immunotherapy for mCRC.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1223-1253"},"PeriodicalIF":2.7,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903347","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":"Development of a Prognostic Risk Model for Esophageal Cancer Based on M0 Macrophage-Related Genes.","authors":"Xiaoping Zuo, Fuqiang Wang, Guofeng Liu, Shenglong Xie, Senyi Deng, Yun Wang","doi":"10.2147/OTT.S483536","DOIUrl":"10.2147/OTT.S483536","url":null,"abstract":"<p><strong>Background: </strong>This study investigates the prognostic value of M0 macrophage-related genes (M0MRGs) in esophageal cancer (ESCA) and identifies novel targets for immunotherapy.</p><p><strong>Methods: </strong>Differentially expressed genes (DEGs) were screened with ESCA-related expression profile data (GSE5364 and GSE17351) from the GEO database, followed by GO and KEGG pathway enrichment analyses. Then, immune cell infiltration was examined with the CIBERSORT algorithm and multiplex fluorescence-based immunohistochemistry (MP-IHC). ESCA-related gene expression data and relevant clinical information were retrieved from TCGA. M0MRGs were identified with TCGA-ESCA based on Spearman's correlation coefficient. Additionally, LASSO and Cox regression analyses were conducted to further construct an M0MRG-related prognostic model. ATP6V0D2 and MMP12 expression in ESCA was analyzed with tissue microarray. Finally, the half maximal inhibitory concentrations (IC50) of commonly used chemotherapeutics in TCGA-ESCA were calculated with the \"oncoPredict\" R package.</p><p><strong>Conclusion: </strong>In summary, ATP6V0D2 and MMP12 were crucial components in a prognostic risk model for ESCA and were associated with poor prognoses, implicating the involvement of elevated M0 macrophages in disease progression and providing potential therapeutic targets and strategies for ESCA.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1209-1222"},"PeriodicalIF":2.7,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903345","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":"CRISPR-Cas13a Targeting the FGFR3-TACC3 Fusion Gene Inhibits Proliferation of Bladder Cancer Cells in vitro and in vivo.","authors":"Yadong Wang, Jinjin Zhu, Shangwen Liu, Zhengbo Sun, Guibiao Wen, Dakun Huang, Mianxiong Chen, Yuchen Liu, Feng Lin","doi":"10.2147/OTT.S492659","DOIUrl":"10.2147/OTT.S492659","url":null,"abstract":"<p><strong>Introduction: </strong>The FGFR3-TACC3 fusion gene exists in a variety of malignant tumors, including bladder cancer. In our ongoing research on the CRISPR-Cas13a gene-editing system, we reported the use of CRISPR-Cas13a gene-editing system to knockout FGFR3-TACC3 and inhibit the proliferation of bladder tumor cells.</p><p><strong>Purpose: </strong> This study aimed to use the CRISPR-Cas13a gene-editing system to target the FGFR3-TACC3 fusion gene in bladder cancer cells, which has the potential to be a new and effective treatment for bladder cancer.</p><p><strong>Materials and methods: </strong>The efficacy of the CRISPR-Cas13a gene-editing system was analysed by qRT-PCR. The inhibitory effects of Cas13a-mediated knockdown of the FGFR3-TACC3 fusion gene on the proliferation of RT4 and RT112 cell lines were assessed utilizing CCK-8, EdU, and organoid formation assays. Subsequently, the comparative tumorigenic capability of RT4 cells with FGFR3-TACC3 knockdown achieved by Cas13a was examined in a nude mouse model.</p><p><strong>Results: </strong>At the cellular level, the comparative analysis of FGFR3-TACC3 knockdown efficacy between CRISPR-Cas13a and shRNA revealed a more pronounced reduction with the former. This knockdown effectively curtailed cellular proliferation, with CRISPR-Cas13a-mediated knockdown exhibiting a superior inhibitory effect over shRNA-mediated knockdown. In organoid cultures derived from RT4 cells, a similar trend was observed, with Cas13a-mediated knockdown of FGFR3-TACC3 leading to a more substantial suppression of proliferation compared to shRNA-mediated knockdown. In vivo tumor models corroborated these findings, demonstrating a significantly diminished tumor volume in the Cas13a-treated cohort relative to both the control and shRNA-treated groups.</p><p><strong>Conclusion: </strong>The CRISPR-Cas13a gene-editing system has been demonstrated to significantly suppress tumor proliferation both in vitro and in vivo, thereby presenting itself as a promising candidate for a novel and efficacious therapeutic intervention in bladder cancer treatment.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1197-1207"},"PeriodicalIF":2.7,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882324","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":"Erratum: Long Non-Coding RNA TRG-AS1 Promoted Proliferation and Invasion of Lung Cancer Cells Through the miR-224-5p/SMAD4 Axis [Retraction] [Corrigendum].","authors":"","doi":"10.2147/OTT.S511815","DOIUrl":"10.2147/OTT.S511815","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.2147/OTT.S474055.].</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1195-1196"},"PeriodicalIF":2.7,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876899","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":"Silencing of Long Noncoding RNA LINC00346 Inhibits the Tumorigenesis of Colorectal Cancer Through Targeting MicroRNA-148b [Retraction].","authors":"","doi":"10.2147/OTT.S511336","DOIUrl":"https://doi.org/10.2147/OTT.S511336","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.2147/OTT.S242715.].</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1187-1188"},"PeriodicalIF":2.7,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11648281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838737","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":"Hyperbilirubinemia in a Patient Receiving Alectinib for Anaplastic Lymphoma Kinase Positive Non-Small-Cell Lung Cancer: A Histological Features.","authors":"Qian Zhang, Lei Yan, Yujie Bao, Xiaoling Yuan, Donglin Yin, Jie Xu","doi":"10.2147/OTT.S486860","DOIUrl":"10.2147/OTT.S486860","url":null,"abstract":"<p><strong>Background: </strong>Alectinib is a second generation of anaplastic lymphoma kinase (ALK) inhibitor that has been approved for the treatment of advanced non-small-cell lung cancer (NSCLC) with ALK rearrangements. Hepatotoxicity is the most common adverse drug reaction. However, there is currently no published report on the pathologic findings of alectinib-induced hyperbilirubinemia.</p><p><strong>Case presentation: </strong>Here, we report a case of a patient with NSCLC and chronic hepatitis B (CHB) who was treated with alectinib and developed grade 4 hyperbilirubinemia after 3 years on therapy. Alectinib was discontinued, and an artificial liver support system (ALSS) was used to decline blood bilirubin levels. The pathological manifestations from a liver biopsy showed the hepatocytes with scattered focal necrosis, bile stasis, and vesicular steatosis, bile emboli in capillaries, and star-shaped fibers proliferation in the portal area.</p><p><strong>Conclusion: </strong>This is the first report of alectinib-induced hyperbilirubinemia which was confirmed by liver histopathology and successfully relieved by ALSS treatment and drug discontinuation.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1189-1193"},"PeriodicalIF":2.7,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11646391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829484","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":"Screening and Studying of Blood miRNAs as Potential Diagnostic Markers for Papillary Thyroid Carcinoma.","authors":"Xize Li, Wen Qin, Wenting Wang, Weilin Liu, Tianyi Dong, Aixiang Liu, Haojie Cai, Zhouhan Xu, Jiping Zeng","doi":"10.2147/OTT.S489559","DOIUrl":"10.2147/OTT.S489559","url":null,"abstract":"<p><strong>Objective: </strong>MiRNAs play a pivotal role in tumorigenesis and development by exerting negative regulation on the expression of target genes. In this study, bioinformatics techniques and online database were employed to investigate the specific miRNA-target gene regulatory network in PTC, which was subsequently validated using human blood samples and compared to existing tumor markers.</p><p><strong>Methods: </strong>The miRNA (GSE50901) and Gene Expression (GSE113629) chip screening data of human PTC tissues were retrieved from GEO database. A comparative analysis was conducted using the GEO2R to identify differentially expressed miRNAs and target genes of the patients with PTC. Prediction of the miRNA-target gene regulatory network, related signal transduction pathways, biological effects and their relationship to prognosis was performed based on GO, KEGG, qRT-PCR detection of human blood samples, analysis of correlation on the existing pathological tumor markers, and ROC.</p><p><strong>Results: </strong>Compared to the corresponding normal thyroid tissues, a total of 2116 miRNAs were found to be differentially expressed in PTC patients, including 1968 up-regulated and 148 down-regulated genes. The abnormally expressed genes primarily participated in signal pathways associated with tumorigenesis and abnormal gene transcription. By utilizing data from the GEO database, five miRNAs closely linked to PTC prognosis were identified, which were miR-221-3p, miR-222-3p, miR-182-5p, miR-135a-5p, and miR-34a-5p, with elucidating the target genes. Experimental validation, correlation analysis with tumor markers along with bioinformatics analysis revealed a significant increase in expression levels of miR-182-5p in PTC patients which positively correlated with poor prognosis. These molecules could play crucial roles in both initiation and progression of PTC.</p><p><strong>Conclusion: </strong>This study identified potential novel blood-based miRNA biomarkers for PTC through bioinformatics analysis combined with the detection of human blood samples, thereby offering new possibilities for significant biomarkers associated with diagnosis and prognosis of PTC.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1173-1185"},"PeriodicalIF":2.7,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11645959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829485","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":"Ubiquitination-Binding Enzyme 2C is Associated with Cancer Development and Prognosis and is a Potential Therapeutic Target.","authors":"Mengjie Zhao, Jielong Li, Rui Wang, Lida Mi, Yan Gu, Rongjin Chen, Yangyang Li, Woda Shi, Yajun Zhang","doi":"10.2147/OTT.S485053","DOIUrl":"10.2147/OTT.S485053","url":null,"abstract":"<p><p>UBE2C (Ubiquitination-binding enzyme 2C), one of the E2 enzymes encoded in the human genome, is a component of the ubiquitin proteasome system and plays a pivotal role in regulating cell cycle progression. Moreover, UBE2C is highly expressed and may play a pivotal role in both high-incidence and high-mortality malignancies, including lung cancers, breast cancers, and esophageal cancers. UBE2C influences a number of key processes, including cell cycle progression, tumor invasion and metastasis, proliferation, and drug resistance. However, few articles have systematically summarized the role of UBE2C in cancer. The aim of this review is to describe the structure and function of UBE2C, focusing on the current status of UBE2C research in malignant tumors. Furthermore, this review presents the potential of UBE2C as a new therapeutic target and a diagnostic and prognostic biomarker. Finally, future research directions for UBE2C are proposed. It is of great value to explore the mechanism of action of UBE2C in the tumor microenvironment (TME). A comprehensive and coherent comprehension of UBE2C will undoubtedly facilitate its transition from fundamental research to clinical applications.</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1159-1171"},"PeriodicalIF":2.7,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829486","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":"Long Non Coding RNA SNHG16 Facilitates Proliferation, Migration, Invasion and Autophagy of Neuroblastoma Cells via Sponging miR-542-3p and Upregulating ATG5 Expression [Retraction].","authors":"","doi":"10.2147/OTT.S509994","DOIUrl":"https://doi.org/10.2147/OTT.S509994","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.2147/OTT.S226915.].</p>","PeriodicalId":19534,"journal":{"name":"OncoTargets and therapy","volume":"17 ","pages":"1157-1158"},"PeriodicalIF":2.7,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11634940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818808","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}