Tumour Virus Research最新文献_第7页

Detection of high-risk HPV in FFPE specimens of various tumours using the BD Onclarity™ HPV Assay 使用BD Onclarity™HPV Assay检测各种肿瘤FFPE标本中的高危HPV

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200243

Robert van der Geize , Natalie Methorst , Maarten Niemantsverdriet

引用次数: 0

HPV and head and neck cancers: Towards early diagnosis and prevention HPV和头颈癌:早期诊断和预防

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200245

Luisa Galati , Susanna Chiocca , Daria Duca , Marta Tagliabue , Cindy Simoens , Tarik Gheit , Marc Arbyn , Massimo Tommasino

{"title":"HPV and head and neck cancers: Towards early diagnosis and prevention","authors":"Luisa Galati , Susanna Chiocca , Daria Duca , Marta Tagliabue , Cindy Simoens , Tarik Gheit , Marc Arbyn , Massimo Tommasino","doi":"10.1016/j.tvr.2022.200245","DOIUrl":"10.1016/j.tvr.2022.200245","url":null,"abstract":"<div><p>Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide with an increasing trend of its incidence. Alcohol consumption, smoking, and viral infections, such as the mucosal high-risk (HR) human papillomaviruses (HPVs) are major risk factors for HNSCC development. In particular, HR HPVs are mainly associated with a subset of oropharyngeal squamous cell carcinoma (OPSCC), while other head and neck sites are marginally affected by HPV infection. HPV16 is the most frequently HR HPV type associated with HNSCC. In contrast to the cervix, no screening programs or identifiable pre-malignant lesions have been characterized for HPV-related HNSCC. Therefore, identification of general diagnostic algorithms and HPV biomarkers that could facilitate the early diagnosis, disease evolution and recurrence for HPV-driven HNSCCs are urgently needed. We herein review the role of HPV in HNSCC with a focus on epidemiology, biology, applied diagnostic algorithms and available biomarkers in body fluids as early diagnostic tools in HPV-driven HNSCCs.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"14 ","pages":"Article 200245"},"PeriodicalIF":4.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4a/e5/main.PMC9420391.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10514877","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: 8

Synergistic targeting of the PI3K/mTOR and MAPK/ERK pathways in Merkel cell carcinoma 默克尔细胞癌中PI3K/mTOR和MAPK/ERK通路的协同靶向

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200244

Arturo Temblador , Dimitrios Topalis , Graciela Andrei , Robert Snoeck

{"title":"Synergistic targeting of the PI3K/mTOR and MAPK/ERK pathways in Merkel cell carcinoma","authors":"Arturo Temblador , Dimitrios Topalis , Graciela Andrei , Robert Snoeck","doi":"10.1016/j.tvr.2022.200244","DOIUrl":"10.1016/j.tvr.2022.200244","url":null,"abstract":"<div><p>Merkel cell carcinoma (MCC) is an aggressive type of skin cancer, which is caused either by integration of the oncogenic Merkel cell polyomavirus (MCPyV) or by accumulation of UV-light induced mutations. Since the response to immune-checkpoint inhibitors is limited, new therapeutic agents need to be explored. Previous studies have shown that MCC cell lines and xenografts are sensitive to MLN0128, a dual mTOR1/2 inhibitor. Prompted by these results and considering that the PI3K/mTOR and MAPK/ERK pathways are the most commonly deregulated pathways in cancer, the combination of MLN0128 with the MEK1/2 inhibitor trametinib was investigated. Importantly, the combined targeting showed to be synergistic in MCC cell lines and induced alterations in the protein levels of downstream elements of the targeted pathways. This synergistic activity implies a reduction in the dose of each inhibitor necessary to reach the same effect that when used as single agents. Therefore, this is a promising approach to improve the clinical management of MCC and to overcome the limited efficacy of single drug regimens owed to the appearance of toxicity or drug resistance.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"14 ","pages":"Article 200244"},"PeriodicalIF":4.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/de/a9/main.PMC9449649.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10517406","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: 1

Synonymous nucleotide changes drive papillomavirus evolution 同义核苷酸变化驱动乳头瘤病毒进化

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200248

Kelly M. King , Esha Vikram Rajadhyaksha , Isabelle G. Tobey , Koenraad Van Doorslaer

引用次数: 2

Programmed death-ligand 1 (PD-L1) polymorphisms as predictive biomarkers for the development of liver cirrhosis and hepatocellular carcinoma in HCV Egyptian patients 程序性死亡配体1 (PD-L1)多态性作为HCV埃及患者肝硬化和肝细胞癌发展的预测性生物标志物

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200249

Marwa Hassan , Mohammed Saad Attia , Zainab Ali-Eldin , Gamal El Attar , Mohamed Elzallat , Hany Haroun Kaisar Saad , Amira Isaac

{"title":"Programmed death-ligand 1 (PD-L1) polymorphisms as predictive biomarkers for the development of liver cirrhosis and hepatocellular carcinoma in HCV Egyptian patients","authors":"Marwa Hassan , Mohammed Saad Attia , Zainab Ali-Eldin , Gamal El Attar , Mohamed Elzallat , Hany Haroun Kaisar Saad , Amira Isaac","doi":"10.1016/j.tvr.2022.200249","DOIUrl":"10.1016/j.tvr.2022.200249","url":null,"abstract":"<div><h3>Background</h3><p>Considering the immune evasion role of programmed death-ligand 1 (PD-L1) in cancer development, its genomic variations might be closely associated with disease development and cancer risks. Accordingly, this study was performed to investigate how the PD-L1 gene polymorphisms affect the susceptibility to hepatitis C virus (HCV)-induced liver cirrhosis and cancer development in the Egyptian population.</p></div><div><h3>Methodology</h3><p>Two single nucleotide polymorphisms of the PD-L1 gene; rs2297136 (A > G) and rs4143815 (C > G), were studied in 50 HCV, 51 liver cirrhosis, and 52 hepatocellular carcinoma (HCC) patients as well as 50 healthy subjects using real-time PCR.</p></div><div><h3>Results</h3><p>The frequencies of PD-L1 rs2297136 AA and rs4143815 GG genotypes were significantly higher in the liver cirrhosis than the control and HCV groups. The rs4143815 CG and GG genotypes were linked to a higher risk of developing HCC and were positively associated with the clinicopathological features of HCC.</p></div><div><h3>Conclusions</h3><p>The PD-L1 rs2297136 AA and rs4143815 GG genotypes increase the susceptibility to liver cirrhosis. The rs4143815 CG and GG genotypes are positively associated with HCC risk and its clinicopathological characteristics. Therefore, HCV patients carrying the PD-L1 rs4143815 G-allele should be followed up on a regular basis to allow for early HCC management.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"14 ","pages":"Article 200249"},"PeriodicalIF":4.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9594630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9081249","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: 1

Small DNA tumor viruses and human cancer: Preclinical models of virus infection and disease 小DNA肿瘤病毒和人类癌症:病毒感染和疾病的临床前模型

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200239

Megan E. Spurgeon

{"title":"Small DNA tumor viruses and human cancer: Preclinical models of virus infection and disease","authors":"Megan E. Spurgeon","doi":"10.1016/j.tvr.2022.200239","DOIUrl":"10.1016/j.tvr.2022.200239","url":null,"abstract":"<div><p>Human tumor viruses cause various human cancers that account for at least 15% of the global cancer burden. Among the currently identified human tumor viruses, two are small DNA tumor viruses: human papillomaviruses (HPVs) and Merkel cell polyomavirus (MCPyV). The study of small DNA tumor viruses (adenoviruses, polyomaviruses, and papillomaviruses) has facilitated several significant biological discoveries and established some of the first animal models of virus-associated cancers. The development and use of preclinical <em>in vivo</em> models to study HPVs and MCPyV and their role in human cancer is the focus of this review. Important considerations in the design of animal models of small DNA tumor virus infection and disease, including host range, cell tropism, choice of virus isolates, and the ability to recapitulate human disease, are presented. The types of infection-based and transgenic model strategies that are used to study HPVs and MCPyV, including their strengths and limitations, are also discussed. An overview of the current models that exist to study HPV and MCPyV infection and neoplastic disease are highlighted. These comparative models provide valuable platforms to study various aspects of virus-associated human disease and will continue to expand knowledge of human tumor viruses and their relationship with their hosts.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"14 ","pages":"Article 200239"},"PeriodicalIF":4.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/24/a8/main.PMC9194455.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10507337","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: 3

Differences in integration frequencies and APOBEC3 profiles of five high-risk HPV types adheres to phylogeny 五种高危型HPV的整合频率和APOBEC3谱的差异与系统发育有关

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200247

Alexander Hesselberg Løvestad , Adina Repesa , Jean-Marc Costanzi , Sonja Lagström , Irene Kraus Christiansen , Trine B. Rounge , Ole Herman Ambur

{"title":"Differences in integration frequencies and APOBEC3 profiles of five high-risk HPV types adheres to phylogeny","authors":"Alexander Hesselberg Løvestad , Adina Repesa , Jean-Marc Costanzi , Sonja Lagström , Irene Kraus Christiansen , Trine B. Rounge , Ole Herman Ambur","doi":"10.1016/j.tvr.2022.200247","DOIUrl":"10.1016/j.tvr.2022.200247","url":null,"abstract":"<div><p>Persistent infection with Human Papillomavirus (HPV) is responsible for almost all cases of cervical cancers, and HPV16 and HPV18 associated with the majority of these. These types differ in the proportion of viral minor nucleotide variants (MNVs) caused by APOBEC3 mutagenesis as well as integration frequencies. Whether these traits extend to other types remains uncertain. This study aimed to investigate and compare genomic variability and chromosomal integration in the two phylogenetically distinct Alpha-7 and Alpha-9 clades of carcinogenic HPV types. The TaME-seq protocol was employed to sequence cervical cell samples positive for HPV31, HPV33 or HPV45 and combine these with data from a previous study on HPV16 and HPV18. APOBEC3 mutation signatures were found in Alpha-9 (HPV16/31/33) but not in Alpha-7 (HPV18/45). HPV45 had significantly more MNVs compared to the other types. Alpha-7 had higher integration frequency compared to Alpha-9. An increase in integration frequency with increased diagnostic severity was found for Alpha-7. The results highlight important differences and broaden our understanding of the molecular mechanisms behind cervical cancer induced by high-risk HPV types from the Alpha-7 and Alpha-9 clades.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"14 ","pages":"Article 200247"},"PeriodicalIF":4.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/47/fb/main.PMC9485212.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10517127","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: 4

Editorial board member 编委会成员

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/S2666-6790(22)00017-9

引用次数: 0

The oncogenic gamma herpesviruses Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) hijack retinoic acid-inducible gene I (RIG-I) facilitating both viral and tumour immune evasion 致癌性γ疱疹病毒eb病毒(EBV)和卡波西肉瘤相关疱疹病毒(KSHV)劫持维甲酸诱导基因I (RIG-I)，促进病毒和肿瘤的免疫逃避

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200246

Alana Nash , Elizabeth J. Ryan

{"title":"The oncogenic gamma herpesviruses Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) hijack retinoic acid-inducible gene I (RIG-I) facilitating both viral and tumour immune evasion","authors":"Alana Nash , Elizabeth J. Ryan","doi":"10.1016/j.tvr.2022.200246","DOIUrl":"10.1016/j.tvr.2022.200246","url":null,"abstract":"<div><p>Herpesviruses evade host immunity to establish persistent lifelong infection with dormant latent and replicative lytic phases. Epstein-Barr virus (EBV) and Kaposi's Sarcoma-associated virus (KSHV) are double-stranded DNA herpesviruses that encode components to activate RNA sensors, (Retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA5). Yet both viruses can effectively evade the antiviral immune response. The ability of these viruses to disarm RIG-I to evade immunity allowing viral persistency can contribute to the creation of a protected niche that facilitates tumour growth and immune evasion. Alternatively, viral nucleic acids present in the cytosol during the replicative phase of the viral lifecycle can activate pro-inflammatory signaling downstream of RIG-I augmenting tumour promoting inflammation.</p><p>Understanding how these viral proteins disrupt innate immune pathways could help identify mechanisms to boost immunity, clearing viral infection and enhancing the efficacy of immunotherapy for virally induced cancers. Here we review literature on the strategies EBV and KSHV use to either enhance or inhibit RLR signaling.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"14 ","pages":"Article 200246"},"PeriodicalIF":4.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9424536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10507953","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: 4

Women with a positive high-risk human papillomavirus (HPV) test remain at increased risk of HPV infection and cervical precancer ≥15 years later 高危人乳头瘤病毒(HPV)检测阳性的妇女在HPV感染和宫颈癌前病变≥15年后仍有增加的风险

IF 4.3

Tumour Virus Research Pub Date : 2022-12-01 DOI: 10.1016/j.tvr.2022.200240

Federica Inturrisi , Johannes A. Bogaards , Albert G. Siebers , Chris J.L.M. Meijer , Daniëlle A.M. Heideman , Johannes Berkhof

{"title":"Women with a positive high-risk human papillomavirus (HPV) test remain at increased risk of HPV infection and cervical precancer ≥15 years later","authors":"Federica Inturrisi , Johannes A. Bogaards , Albert G. Siebers , Chris J.L.M. Meijer , Daniëlle A.M. Heideman , Johannes Berkhof","doi":"10.1016/j.tvr.2022.200240","DOIUrl":"10.1016/j.tvr.2022.200240","url":null,"abstract":"<div><p>Little is known about the long-term association between high-risk human papillomavirus (hrHPV) test results in women participating in a hrHPV-based cervical cancer screening program. To address this question, we collected data of 2217 women who participated in the POBASCAM hrHPV-based screening trial (enrolment 1999/2002) and also attended the Dutch hrHPV-based screening program between January 2017 and March 2018. Among 143 women who tested hrHPV-positive in 1999/2002, 45 (31.5%) had ≥ CIN2 or hysterectomy before 2017 and 17 (11.9%) tested hrHPV-positive at the 2017/2018 screen. In comparison, among 2074 women who tested hrHPV-negative in 1999/2002, 10 (0.5%) had ≥ CIN2 or hysterectomy before 2017 and 119 (5.7%) tested hrHPV-positive at the 2017/2018 screen. It follows that in the group of women who were not treated for ≥ CIN2 or had a hysterectomy in between the two screens 15 years apart (N = 2162), women who were hrHPV-positive in 1999/2002 had a higher risk of being hrHPV-positive in 2017/2018 than those who were hrHPV-negative in 1999/2002 (OR 3.4, 95% CI 1.8–6.1). A similar association was found at the genotype level for genotype-concordant results (5.1, 1.0–11.3) and for genotype non-concordant results (3.7, 1.6–6.7). Women who were hrHPV-positive in 2017/2018 had a higher risk of CIN3 after a hrHPV-positive result in 1999/2002 than after a hrHPV-negative result (5.8, 1.0–27.8). In conclusion, a positive hrHPV result in screening gives a long-term increased risk of a hrHPV-positive result, also for different genotypes, and a long-term increased risk of CIN3. This supports the concept of risk-stratification in hrHPV-based cervical cancer screening where previous hrHPV results are included in screening recommendations.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"14 ","pages":"Article 200240"},"PeriodicalIF":4.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9190048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10507341","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: 1