scholarly journals Presence of Human Papillomavirus and Epstein–Barr Virus, but Absence of Merkel Cell Polyomavirus, in Head and Neck Cancer of Non-Smokers and Non-Drinkers

2021 ◽  
Vol 10 ◽  
Author(s):  
Frans J. Mulder ◽  
Faisal Klufah ◽  
Famke M. E. Janssen ◽  
Farzaneh Farshadpour ◽  
Stefan M. Willems ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Human Papillomavirus ◽  
Head And Neck ◽  
Epstein Barr Virus ◽  
Merkel Cell Polyomavirus ◽  
Merkel Cell ◽  
Cell Cycle Proteins ◽  
P53 Expression ◽  
Barr Virus ◽  
Epstein Barr

ObjectiveDetermine the presence and prognostic value of human papillomavirus (HPV), Epstein-Barr virus (EBV), Merkel cell polyomavirus (MCPyV), and cell cycle proteins in head and neck squamous cell carcinoma (HNSCC) of non-smokers and non-drinkers (NSND).MethodsClinical characteristics and tumors of 119 NSND with HNSCC were retrospectively collected and analyzed on tissue microarrays. RNAscope in situ hybridization (ISH) was used to screen for the presence of HPV and MCPyV mRNA. Immunohistochemistry was performed for expression of p16 as surrogate marker for HPV, Large T-antigen for MCPyV, and cell cycle proteins p53 and pRb. Positive virus results were confirmed with polymerase chain reaction. For EBV, EBV encoded RNA ISH was performed. Differences in 5-year survival between virus positive and negative tumors were determined by log rank analysis.ResultsAll oropharyngeal tumors (OPSCC) (n = 10) were HPV-positive, in addition to one oral (OSCC) and one nasopharyngeal tumor (NPSCC). The other three NPSCC were EBV-positive. MCPyV was not detected. Patients with HPV or EBV positive tumors did not have a significantly better 5-year disease free or overall survival. Over 70% of virus negative OSCC showed mutant-type p53 expression.ConclusionIn this cohort, all OPSCC and NPSCC showed HPV or EBV presence. Besides one OSCC, all other oral (n = 94), hypopharyngeal (n = 1), and laryngeal (n = 9) tumors were HPV, EBV, and MCPyV negative. This argues against a central role of these viruses in the ethiopathogenesis of tumors outside the oro- and nasopharynx in NSND. So, for the majority of NSND with virus negative OSCC, more research is needed to understand the carcinogenic mechanisms in order to consider targeted therapeutic options.

scholarly journals Infection and coinfection by human papillomavirus, Epstein–Barr virus and Merkel cell polyomavirus in patients with squamous cell carcinoma of the larynx: a retrospective study

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5834 ◽  
Author(s):  
Jose Manuel Vazquez-Guillen ◽  
Gerardo C. Palacios-Saucedo ◽  
Lydia Guadalupe Rivera-Morales ◽  
Monica Valeria Alonzo-Morado ◽  
Saira Berenice Burciaga-Bernal ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Human Papillomavirus ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epstein Barr Virus ◽  
Merkel Cell Polyomavirus ◽  
Merkel Cell ◽  
Barr Virus ◽  
Hpv Genotypes ◽  
Epstein Barr

Background Human papillomavirus (HPV) is recognized as an important risk factor for laryngeal carcinogenesis. Although HPV-16 and 18 have been strongly implicated, the presence of other high-risk HPV (HR-HPV) genotypes or the coinfection with Epstein-Barr virus (EBV) or Merkel cell polyomavirus (MCPV) may increase the risk, but their etiological association has not been definitively established. Methods We characterized the genotype-specific HPV and the frequency of EBV and MCPV infections through the detection of their DNA in 195 laryngeal specimens of squamous cell carcinoma (SCC) histologically confirmed. Results HPV DNA was detected in 93 (47.7%) specimens. HPV-11 was the most frequent with 68 cases (73.1%), and HPV-52 was the most frequently HR-HPV found with 51 cases, which corresponds to 54.8% of all HPV-positive specimens. EBV DNA was detected in 54 (27.7%) tumor tissue specimens of which 25 (46.3%) were in coinfection with HPV. MCPV DNA was detected only in 11 (5.6%) cases of which 5 (45.4%) were in coinfection with an HR-HPV. No association between the presence of DNA of the three examined viruses and the patient smoking habits, alcohol consumption, age, the keratinization status, differentiation grade, or localization of the tumor in the larynx were found. Discussion HPV-52 was the most prevalent HR-HPV, which may suggest that this and other genotypes in addition to HPV-16 and 18 could be considered for prophylaxis. However, further studies including non-cancer larynx cases and the evaluation of other molecular markers and viral co-infection mechanisms are needed to determine the role of the different HR-HPV genotypes, EBV, and MCPV in the etiology of SCC of the larynx.

scholarly journals Human Papillomavirus and Epstein-Barr Virus Infection, p53 Expression, and Cellular Proliferation in Laryngeal Carcinoma

2006 ◽  
Vol 126 (2) ◽  
pp. 284-293 ◽  
Author(s):  
Deilson Elgui de Oliveira ◽  
Maura M. Bacchi ◽  
Ricardo S.S. Macarenco ◽  
José Vicente Tagliarini ◽  
Ricardo C. Cordeiro ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Virus Infection ◽  
Laryngeal Carcinoma ◽  
Epstein Barr Virus ◽  
Cellular Proliferation ◽  
Epstein Barr Virus Infection ◽  
P53 Expression ◽  
Barr Virus ◽  
Epstein Barr ◽  
Barr Virus Infection

scholarly journals Detection of Epstein-Barr virus and human papillomavirus in head and neck tumors.

1993 ◽  
Vol 31 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Y S Tyan ◽  
S T Liu ◽  
W R Ong ◽  
M L Chen ◽  
C H Shu ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Head And Neck ◽  
Epstein Barr Virus ◽  
Head And Neck Tumors ◽  
Barr Virus ◽  
Neck Tumors ◽  
Epstein Barr

scholarly journals Genetic Dissection of Cell Growth Arrest Functions Mediated by the Epstein-Barr Virus Lytic Gene Product, Zta

1999 ◽  
Vol 73 (11) ◽  
pp. 9029-9038 ◽  
Author(s):  
Antonio Rodriguez ◽  
Monica Armstrong ◽  
Daniel Dwyer ◽  
Erik Flemington
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Epstein Barr Virus ◽  
Kinase Inhibitors ◽  
Growth Arrest ◽  
Lytic Replication ◽  
P53 Expression ◽  
Cell Growth Arrest ◽  
Barr Virus ◽  
Epstein Barr

ABSTRACT Expression of the Epstein-Barr virus (EBV) latency-associated genes activates cell cycle progression and drives immortalization of the infected cell. In contrast, progression of the EBV replication program occurs most efficiently in growth-arrested cells. Previous studies showed that the EBV-encoded immediate-early transcription factor, Zta, can induce expression of the cyclin-dependent kinase inhibitors, p21 and p27, the tumor suppressor, p53, and cell growth arrest. Moreover, Zta-mediated induction of growth arrest occurs independently of its transcriptional transactivation function. Here we show that substitution of Zta’s basic DNA binding domain with the analogous region of the Zta homologue, c-Fos, abrogates Zta’s ability to induce growth arrest and to induce p21, p27, or p53 expression, suggesting that protein-protein interactions between this region of Zta and key cell cycle control proteins are involved in signaling cell cycle arrest. We also show that despite the crucial role for Zta’s basic domain in eliciting cell growth arrest, its amino terminus is required for efficient induction of p27 and it modulates the level of p53 induction. Last, we provide evidence that Zta-mediated inductions of p21, p27, and p53 occur, at least in part, through distinct pathways. Therefore, Zta interacts with multiple growth arrest pathways, a property which may have evolved partly as a means to ensure that lytic replication occurs in a growth-arrested setting in multiple different tissues in various states of differentiation.

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