Tumour Virus Research最新文献_第2页

De-regulation of aurora kinases by oncogenic HPV; implications in cancer development and treatment 致瘤性HPV对极光激酶的去调控作用对癌症发展和治疗的影响。

IF 4.7

Tumour Virus Research Pub Date : 2025-02-07 DOI: 10.1016/j.tvr.2025.200314

Kemi Hannah Oladipo , Joanna L. Parish

{"title":"De-regulation of aurora kinases by oncogenic HPV; implications in cancer development and treatment","authors":"Kemi Hannah Oladipo , Joanna L. Parish","doi":"10.1016/j.tvr.2025.200314","DOIUrl":"10.1016/j.tvr.2025.200314","url":null,"abstract":"<div><div>Human papillomaviruses (HPVs) cause diseases ranging from benign warts to invasive cancers. HPVs are the cause of almost all cervical cancers and a sub-set of other epithelial malignancies including head and neck cancers, specifically within the oropharynx. The oncogenic properties of HPV are largely mediated through the viral oncoproteins E6 and E7, which disrupt many cellular pathways to drive uncontrolled cell proliferation. One family of proteins targeted by HPV is the Aurora kinase family. Aurora kinases are serine/threonine kinases including Aurora kinase A (AURKA), B (AURKB), and C (AURKC) which are often dysregulated in many cancer types, including HPV driven cancers. All three family members play essential roles in mitotic regulation and accurate cell division.</div><div>The deregulation of Aurora kinases by HPV infection highlights their potential as therapeutic targets in HPV-associated malignancies. Targeting Aurora kinase activity, in combination with current HPV therapies, may provide new avenues for treating HPV-induced cancers and reducing the burden of HPV-related diseases. Combinatorial inhibition targets distinct but overlapping functions of these kinases, thereby reducing the potential for cancer cells to develop resistance. This broad impact emphasizes the capability for Aurora kinase inhibitors not only as anti-mitotic agents but also as modulators of multiple oncogenic pathways. This review explores the combinatorial effects of Aurora kinase inhibition, offering insights into novel therapeutic strategies for the treatment of HPV-driven cancers.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200314"},"PeriodicalIF":4.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

How can HPV E6 manipulate host cell differentiation process to maintain the reservoir of infection HPV E6如何操纵宿主细胞分化过程以维持感染库。

IF 4.7

Tumour Virus Research Pub Date : 2025-01-19 DOI: 10.1016/j.tvr.2025.200313

Yuwen Chen , Nagayasu Egawa , Ke Zheng , John Doorbar

引用次数: 0

Rapid-onset cancer 迅速发生癌症。

IF 4.7

Tumour Virus Research Pub Date : 2025-01-02 DOI: 10.1016/j.tvr.2024.200312

Andrea Bilger, Paul F. Lambert

引用次数: 0

Too many cooks in the kitchen: HPV driven carcinogenesis – The result of collaboration or competition? 厨房里的厨师太多：HPV驱动的致癌作用——是合作还是竞争的结果？

IF 4.7

Tumour Virus Research Pub Date : 2024-12-27 DOI: 10.1016/j.tvr.2024.200311

Weimer Kathleen

引用次数: 0

Editorial: Tumour Virus Research on Virus Host Interactions and Cell Transformation 社论：肿瘤病毒在病毒宿主相互作用和细胞转化方面的研究。

IF 4.7

Tumour Virus Research Pub Date : 2024-12-20 DOI: 10.1016/j.tvr.2024.200310

Lawrence Banks, Peter Stern

引用次数: 0

Drugs and drug targets for the treatment of HPV-positive cervical cancer 治疗hpv阳性子宫颈癌的药物和药物靶点。

IF 4.7

Tumour Virus Research Pub Date : 2024-12-19 DOI: 10.1016/j.tvr.2024.200309

Carly A. Burmeister, Saif F. Khan, Sharon Prince

{"title":"Drugs and drug targets for the treatment of HPV-positive cervical cancer","authors":"Carly A. Burmeister, Saif F. Khan, Sharon Prince","doi":"10.1016/j.tvr.2024.200309","DOIUrl":"10.1016/j.tvr.2024.200309","url":null,"abstract":"<div><div>Cervical cancer is primarily driven by persistent infection with high-risk human papillomavirus (HPV) strains and remains a significant global health challenge, particularly in low- and middle-income countries where late-stage diagnoses is common. While vaccination and screening programs have reduced incidence rates, the need for novel and more effacacious and cost-effective therapeutic options is therefore critical especially for advanced cervical cancer. This review highlights several key advances in the understanding of HPV-induced carcinogenesis and the development of therapeutic strategies over the past five years. Important areas of focus include the role of HPV oncoproteins E5, E6 and E7 in modulating signalling pathways, treatment strategies for precancerous lesions, the potential of natural compounds to target cervical cancer cells, and the emergence of immunotherapies, checkpoint inhibitors, antibody-drug conjugates, and novel drug combinations to treat cervical cancer. Additionally, lifestyle recommendations and the integration of natural supplements are discussed for their potential to enhance treatment efficacy and improve patient outcomes. The developments reported in this review underscore the evolving landscape of cervical cancer treatment and the need for continued research to validate and integrate these emerging therapies into clinical practice.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200309"},"PeriodicalIF":4.7,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Intraperitoneal delivery of cannabidiol (CBD) and Δ9-tetrahydocannabinol (THC) promotes papillomavirus infections in athymic nude mice 腹腔注射大麻二酚（CBD）和Δ9-tetrahydocannabinol （THC）促进乳突裸鼠乳头瘤病毒感染。

IF 4.7

Tumour Virus Research Pub Date : 2024-12-16 DOI: 10.1016/j.tvr.2024.200307

Sarah A. Brendle , Jingwei Li , Dongxiao Sun , Junjia Zhu , Angela N. Henderson-Redmond , Daniel J. Morgan , Karla K. Balogh , Danielle Covington , Debra A. Shearer , Jiafen Hu

{"title":"Intraperitoneal delivery of cannabidiol (CBD) and Δ9-tetrahydocannabinol (THC) promotes papillomavirus infections in athymic nude mice","authors":"Sarah A. Brendle , Jingwei Li , Dongxiao Sun , Junjia Zhu , Angela N. Henderson-Redmond , Daniel J. Morgan , Karla K. Balogh , Danielle Covington , Debra A. Shearer , Jiafen Hu","doi":"10.1016/j.tvr.2024.200307","DOIUrl":"10.1016/j.tvr.2024.200307","url":null,"abstract":"<div><div>We used our mouse papillomavirus (MmuPV1) model to test the hypothesis that two primary psychoactive ingredients of marijuana, Δ<sup>9</sup>-tetrahydrocannabinol (THC) and cannabidiol (CBD), promote papillomavirus persistence in the oral mucosa of infected mice. We conducted intraperitoneal (ip) injections of a moderate dose (3 mg/kg) of either CBD and/or THC in both male and female athymic nude mice and followed the mice up to 20 weeks post-infection. These doses are comparable to what is estimated for human conventional cannabis consumption. All mice were infected with MmuPV1 in the oral cavity at week 4 post-ip delivery of CBD, THC, or a combination of THC and CBD (T + C). THC and CBD were detected in the blood of treated mice for up to 72 h after ip injection. Significantly higher levels of viral DNA were detected in males from both CBD and T + C-treated groups compared to those in the control group at 9- 10-and 12-weeks post infection. A marginally increased viral RNA was also detected in the infected tongues of males in all tested groups compared to that in males in the vehicle control group; the opposite was observed in females. We detected significantly higher levels of dermal dendritic cells (CD205<sup>+</sup>CD11c<sup>+</sup>), granulocytes (Ly6G<sup>+</sup>), but macrophages (F4-80+) recruited to the infected tongues of CBD-treated females. Our findings suggest that CBD may play a role in promoting MmuPV1 persistence in the oral cavity.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200307"},"PeriodicalIF":4.7,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical indications for host-cell DNA methylation markers in cervical screening and management of cervical intraepithelial neoplasia: A review 宫颈上皮内瘤变筛查和治疗中宿主细胞DNA甲基化标志物的临床适应症综述

IF 4.7

Tumour Virus Research Pub Date : 2024-12-16 DOI: 10.1016/j.tvr.2024.200308

S. Dick , D.A.M. Heideman , J. Berkhof , R.D.M. Steenbergen , M.C.G. Bleeker

引用次数: 0

The adenoviral E4orf4 protein: A multifunctional protein serving as a guide for treating cancer, a multifactorial disease 腺病毒E4orf4蛋白：一种多功能蛋白，作为治疗癌症（一种多因素疾病）的指南。

IF 4.7

Tumour Virus Research Pub Date : 2024-12-15 DOI: 10.1016/j.tvr.2024.200303

Amir Basis, Rakefet Sharf, Tamar Kleinberger

{"title":"The adenoviral E4orf4 protein: A multifunctional protein serving as a guide for treating cancer, a multifactorial disease","authors":"Amir Basis, Rakefet Sharf, Tamar Kleinberger","doi":"10.1016/j.tvr.2024.200303","DOIUrl":"10.1016/j.tvr.2024.200303","url":null,"abstract":"<div><div>Viruses exploit several cellular pathways to support their replication, and many of these virus-targeted pathways are also important for cancer growth. Consequently, studying virus-host interactions offers valuable insights into tumorigenesis and can suggest the development of novel anti-cancer therapies, with oncolytic viruses being one well-known example. The adenovirus E4orf4 protein, which disrupts several host regulatory pathways to facilitate viral infection, also functions as a potent anti-cancer agent when expressed independently. E4orf4 can selectively kill a wide range of cancer cell lines while sparing non-cancerous cells. Moreover, it effectively eliminated cancer in an <em>in vivo Drosophila</em> model without causing significant harm to normal tissues.</div><div>In this study we provide evidence that an E4orf4-mimicking drug cocktail, comprising sublethal doses of four FDA-approved drugs targeting the pathways disrupted by E4orf4, significantly enhanced cancer cell death in many cancer cell types compared with individual drugs or less inclusive drug combinations. The quadruple drug cocktail was not toxic in non-cancerous cells. These findings provide a proof-of-principle for the potential application of virus-host interaction studies to design an effective E4orf4-based cancer therapy. Further investigation of E4orf4 interactions with the host cell will likely improve this E4orf4-based therapy by adding drugs that disrupt additional pathways.</div><div>Crucially, the E4orf4-based approach offers a strategic advantage by avoiding the time-consuming development of novel drugs. Instead, it leverages existing drugs, including those that might be too toxic for use as monotherapies, by employing them at sublethal concentrations in combination. Thus, it provides a feasible and efficient method for advancing cancer therapy.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200303"},"PeriodicalIF":4.7,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142840250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Polyomavirus large T antigens: Unraveling a complex interactome 多瘤病毒大T抗原：揭示一个复杂的相互作用组。

IF 4.7

Tumour Virus Research Pub Date : 2024-12-13 DOI: 10.1016/j.tvr.2024.200306

Matthew R. Googins, Ping An, Christian H. Gauthier, James M. Pipas

{"title":"Polyomavirus large T antigens: Unraveling a complex interactome","authors":"Matthew R. Googins, Ping An, Christian H. Gauthier, James M. Pipas","doi":"10.1016/j.tvr.2024.200306","DOIUrl":"10.1016/j.tvr.2024.200306","url":null,"abstract":"<div><div>All members of the polyomavirus family encode a large T antigen (LT) protein that plays essential roles in viral DNA replication, regulation of viral gene expression, and the manipulation of numerous cellular pathways. Over 100 polyomaviruses have been discovered in hosts ranging from arthropods and fish to mammals, including fourteen that infect humans. LT is among the most studied viral proteins with thousands of articles describing its functions in viral productive infection and tumorigenesis. However, nearly all knowledge of LT activities is based on the studies of simian virus 40 (SV40) and a few other viruses. Comparative studies of LT proteins of different polyomaviruses have revealed a remarkable diversity in the mechanisms by which LT proteins function across different polyomavirus species. This review focuses on human polyomaviruses highlights the similarities and differences between polyomavirus LTs and highlights gaps in our understanding of this protein family. The concentration of knowledge around SV40 LT and the corresponding lack of mechanistic studies on LT proteins encoded by other human and animal polyomaviruses severely constrains our understanding of the biology of this important virus family.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200306"},"PeriodicalIF":4.7,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11720896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0