scholarly journals HPV AND HEAD NECK MALIGNANCIES – ROLE OF VACCINATION

2018 ◽  
Vol VOLUME 6 (VOLUME 6 NUMBER 2 DECEMBER 2018) ◽  
pp. 22-26
Author(s):  
Sumit Sharma

Human papillomavirus is a DNA virus from the papillomavirus family and it not only causes genital and anal cancers, but also causes a subset of head and neck squamous cell carcinoma. It has both sexual and non sexual modes of transmission, former being predominant. Other factors associates with higher risk of HPV induced carcinogenesis are -- Smoking and HIV-infection, male sex and older age. Vaccines are available to prevent HPV infection and are to be given to boys and girls between 14-26 years of age preferably before first sexual contact, and if you already have an HPV infection, getting the HPV vaccine can’t treat it, but it can protect you from getting other types of HPV infections.

Sexual Health ◽  
2010 ◽  
Vol 7 (3) ◽  
pp. 394 ◽  
Author(s):  
Carol Chelimo ◽  
Trecia A. Wouldes ◽  
Linda D. Cameron

Two-hundred undergraduate students completed an anonymous questionnaire after viewing a human papillomavirus (HPV) vaccine television commercial. Eight-four percent of participants would accept a free HPV vaccine, whereas 47% were unconcerned about future personal HPV infection risk. Males were less likely to accept a free HPV vaccine and to be concerned about future personal HPV infection risk. Perceived HPV vaccine effectiveness was significantly greater among participants who had previously heard of the vaccine and who knew that HPV is sexually transmitted. More education on the role of sexual behavioural characteristics of both males and females in HPV transmission is necessary to promote awareness and concern of personal HPV infection risk and acceptance of HPV vaccination.


2020 ◽  
Vol 68 (9) ◽  
pp. 595-606
Author(s):  
Hesham Mohamed ◽  
Caj Haglund ◽  
Lauri Jouhi ◽  
Timo Atula ◽  
Jaana Hagström ◽  
...  

Oropharyngeal squamous cell carcinoma (OPSCC) is subclassified by the World Health Organization into two different entities: human papillomavirus (HPV)-positive and HPV-negative tumors. HPV infection promotes the epithelial-to-mesenchymal transition (EMT) and transformation of keratinocyte stem cells into cancer stem cells. EMT is a crucial process in the carcinogenesis of epithelial-derived malignancies, and we aimed to study the role of its markers in OPSCC. This study consists of 202 consecutive OPSCC patients diagnosed and treated with curative intent. We examined E-cadherin, β-catenin, and vimentin expression using immunohistochemistry and compared these with tumor and patient characteristics and treatment outcome. We found that the cell-membranous expression of β-catenin was stronger in HPV-positive than in HPV-negative tumors, and it was stronger in the presence of regional metastasis. The stromal vimentin expression was stronger among HPV-positive tumors. A high E-cadherin expression was associated with tumor grade. No relationship between these markers and survival emerged. In conclusion, β-catenin and vimentin seem to play different roles in OPSCC: the former in the tumor tissue itself, and the latter in the tumor stroma. HPV infection may exploit the β-catenin and vimentin pathways in carcinogenic process. More, β-catenin may serve as a marker for the occurrence of regional metastasis:


2011 ◽  
Vol 6 (1) ◽  
pp. 4 ◽  
Author(s):  
Giuseppe Pannone ◽  
Angela Santoro ◽  
Silvana Papagerakis ◽  
Lorenzo Lo Muzio ◽  
Gaetano De Rosa ◽  
...  

2004 ◽  
Vol 15 (4) ◽  
pp. 188-196 ◽  
Author(s):  
Patrick K. Ha ◽  
Joseph A. Califano

Human papillomavirus (HPV) infection with high-risk types 16 and 18 has widely been reported as one of the prominent mechanisms behind the development of cervical squamous cell carcinoma. Links between HPV and oral cavity cancer have been suggested as well, based on epidemiologic and molecular means, though the association is less well-established. It is likely that HPV plays a role in oral cavity carcinogenesis, though only in a small subset of cases. The difficulty in providing true causal evidence of HPV’s role in oral cancer lies in our lack of understanding of the significance of mechanisms by which HPV leads to oral carcinogenesis, as well as limitations in the molecular analysis of HPV. Further studies are necessary for the contribution of HPV in oral cavity malignancy to be better demonstrated.


2019 ◽  
Vol 45 (2) ◽  
pp. e85
Author(s):  
L. Bognar ◽  
S. Bellyei ◽  
I. Hegedus ◽  
K. Gombos ◽  
O.P. Horvath ◽  
...  

2018 ◽  
Vol 13 (1) ◽  
Author(s):  
Laura Bognár ◽  
Ivett Hegedűs ◽  
Szabolcs Bellyei ◽  
Éva Pozsgai ◽  
László Zoltán ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Maria Pujantell ◽  
Roger Badia ◽  
Iván Galván-Femenía ◽  
Edurne Garcia-Vidal ◽  
Rafael de Cid ◽  
...  

AbstractInfection by human papillomavirus (HPV) alters the microenvironment of keratinocytes as a mechanism to evade the immune system. A-to-I editing by ADAR1 has been reported to regulate innate immunity in response to viral infections. Here, we evaluated the role of ADAR1 in HPV infection in vitro and in vivo. Innate immune activation was characterized in human keratinocyte cell lines constitutively infected or not with HPV. ADAR1 knockdown induced an innate immune response through enhanced expression of RIG-I-like receptors (RLR) signaling cascade, over-production of type-I IFNs and pro-inflammatory cytokines. ADAR1 knockdown enhanced expression of HPV proteins, a process dependent on innate immune function as no A-to-I editing could be identified in HPV transcripts. A genetic association study was performed in a cohort of HPV/HIV infected individuals followed for a median of 6 years (range 0.1–24). We identified the low frequency haplotype AACCAT significantly associated with recurrent HPV dysplasia, suggesting a role of ADAR1 in the outcome of HPV infection in HIV+ individuals. In summary, our results suggest that ADAR1-mediated innate immune activation may influence HPV disease outcome, therefore indicating that modification of innate immune effectors regulated by ADAR1 could be a therapeutic strategy against HPV infection.


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