柯萨奇病毒A21对耐药肿瘤B细胞的疗效。

IF 5.3 2区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
Matthew Holmes, Gina B Scott, Samuel Heaton, Tyler Barr, Basem Askar, Louise M E Müller, Victoria A Jennings, Christy Ralph, Cathy Burton, Alan Melcher, Peter Hillmen, Christopher Parrish, Fiona Errington-Mais
{"title":"柯萨奇病毒A21对耐药肿瘤B细胞的疗效。","authors":"Matthew Holmes,&nbsp;Gina B Scott,&nbsp;Samuel Heaton,&nbsp;Tyler Barr,&nbsp;Basem Askar,&nbsp;Louise M E Müller,&nbsp;Victoria A Jennings,&nbsp;Christy Ralph,&nbsp;Cathy Burton,&nbsp;Alan Melcher,&nbsp;Peter Hillmen,&nbsp;Christopher Parrish,&nbsp;Fiona Errington-Mais","doi":"10.1016/j.omto.2023.03.002","DOIUrl":null,"url":null,"abstract":"<p><p>Primary drug resistance and minimal residual disease are major challenges in the treatment of B cell neoplasms. Therefore, this study aimed to identify a novel treatment capable of eradicating malignant B cells and drug-resistant disease. Oncolytic viruses eradicate malignant cells by direct oncolysis and activation of anti-tumor immunity, have proven anti-cancer efficacy, and are safe and well tolerated in clinical use. Here, we demonstrate that the oncolytic virus coxsackievirus A21 can kill a range of B cell neoplasms, irrespective of an anti-viral interferon response. Moreover, CVA21 retained its capacity to kill drug-resistant B cell neoplasms, where drug resistance was induced by co-culture with tumor microenvironment support. In some cases, CVA21 efficacy was actually enhanced, in accordance with increased expression of the viral entry receptor ICAM-1. Importantly, the data confirmed preferential killing of malignant B cells and CVA21 dependence on oncogenic B cell signaling pathways. Significantly, CVA21 also activated natural killer (NK) cells to kill neoplastic B cells and drug-resistant B cells remained susceptible to NK cell-mediated lysis. Overall, these data reveal a dual mode of action of CVA21 against drug-resistant B cells and support the development of CVA21 for the treatment of B cell neoplasms.</p>","PeriodicalId":18869,"journal":{"name":"Molecular Therapy Oncolytics","volume":"29 ","pages":"17-29"},"PeriodicalIF":5.3000,"publicationDate":"2023-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106520/pdf/main.pdf","citationCount":"1","resultStr":"{\"title\":\"Efficacy of coxsackievirus A21 against drug-resistant neoplastic B cells.\",\"authors\":\"Matthew Holmes,&nbsp;Gina B Scott,&nbsp;Samuel Heaton,&nbsp;Tyler Barr,&nbsp;Basem Askar,&nbsp;Louise M E Müller,&nbsp;Victoria A Jennings,&nbsp;Christy Ralph,&nbsp;Cathy Burton,&nbsp;Alan Melcher,&nbsp;Peter Hillmen,&nbsp;Christopher Parrish,&nbsp;Fiona Errington-Mais\",\"doi\":\"10.1016/j.omto.2023.03.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Primary drug resistance and minimal residual disease are major challenges in the treatment of B cell neoplasms. Therefore, this study aimed to identify a novel treatment capable of eradicating malignant B cells and drug-resistant disease. Oncolytic viruses eradicate malignant cells by direct oncolysis and activation of anti-tumor immunity, have proven anti-cancer efficacy, and are safe and well tolerated in clinical use. Here, we demonstrate that the oncolytic virus coxsackievirus A21 can kill a range of B cell neoplasms, irrespective of an anti-viral interferon response. Moreover, CVA21 retained its capacity to kill drug-resistant B cell neoplasms, where drug resistance was induced by co-culture with tumor microenvironment support. In some cases, CVA21 efficacy was actually enhanced, in accordance with increased expression of the viral entry receptor ICAM-1. Importantly, the data confirmed preferential killing of malignant B cells and CVA21 dependence on oncogenic B cell signaling pathways. Significantly, CVA21 also activated natural killer (NK) cells to kill neoplastic B cells and drug-resistant B cells remained susceptible to NK cell-mediated lysis. Overall, these data reveal a dual mode of action of CVA21 against drug-resistant B cells and support the development of CVA21 for the treatment of B cell neoplasms.</p>\",\"PeriodicalId\":18869,\"journal\":{\"name\":\"Molecular Therapy Oncolytics\",\"volume\":\"29 \",\"pages\":\"17-29\"},\"PeriodicalIF\":5.3000,\"publicationDate\":\"2023-06-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106520/pdf/main.pdf\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular Therapy Oncolytics\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.omto.2023.03.002\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Therapy Oncolytics","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.omto.2023.03.002","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 1

摘要

原发性耐药和微小残留病是B细胞肿瘤治疗的主要挑战。因此,本研究旨在确定一种能够根除恶性B细胞和耐药疾病的新治疗方法。溶瘤病毒通过直接溶瘤和激活抗肿瘤免疫来消灭恶性细胞,已被证明具有抗癌功效,临床应用安全且耐受性良好。在这里,我们证明了溶瘤病毒柯萨奇病毒A21可以杀死一系列B细胞肿瘤,而不考虑抗病毒干扰素反应。此外,CVA21保留了其杀死耐药B细胞肿瘤的能力,其中通过与肿瘤微环境支持共培养诱导耐药。在某些情况下,CVA21的功效实际上是增强的,这与病毒进入受体ICAM-1表达的增加是一致的。重要的是,这些数据证实了恶性B细胞的优先杀伤和CVA21对致癌B细胞信号通路的依赖。值得注意的是,CVA21还激活自然杀伤(NK)细胞杀死肿瘤B细胞,耐药B细胞仍然对NK细胞介导的裂解敏感。总的来说,这些数据揭示了CVA21对耐药B细胞的双重作用模式,并支持CVA21治疗B细胞肿瘤的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Efficacy of coxsackievirus A21 against drug-resistant neoplastic B cells.

Primary drug resistance and minimal residual disease are major challenges in the treatment of B cell neoplasms. Therefore, this study aimed to identify a novel treatment capable of eradicating malignant B cells and drug-resistant disease. Oncolytic viruses eradicate malignant cells by direct oncolysis and activation of anti-tumor immunity, have proven anti-cancer efficacy, and are safe and well tolerated in clinical use. Here, we demonstrate that the oncolytic virus coxsackievirus A21 can kill a range of B cell neoplasms, irrespective of an anti-viral interferon response. Moreover, CVA21 retained its capacity to kill drug-resistant B cell neoplasms, where drug resistance was induced by co-culture with tumor microenvironment support. In some cases, CVA21 efficacy was actually enhanced, in accordance with increased expression of the viral entry receptor ICAM-1. Importantly, the data confirmed preferential killing of malignant B cells and CVA21 dependence on oncogenic B cell signaling pathways. Significantly, CVA21 also activated natural killer (NK) cells to kill neoplastic B cells and drug-resistant B cells remained susceptible to NK cell-mediated lysis. Overall, these data reveal a dual mode of action of CVA21 against drug-resistant B cells and support the development of CVA21 for the treatment of B cell neoplasms.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Molecular Therapy Oncolytics
Molecular Therapy Oncolytics Medicine-Oncology
CiteScore
10.90
自引率
3.50%
发文量
152
审稿时长
6 weeks
期刊介绍: Molecular Therapy — Oncolytics is an international, online-only, open access journal focusing on the development and clinical testing of viral, cellular, and other biological therapies targeting cancer.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信