The role of human papillomavirus in carcinoma

1991 ◽  
Vol 25 (4) ◽  
pp. 698-705 ◽  
Author(s):  
Matthew Brett Quan ◽  
Ronald Leonard Moy
Keyword(s):  
2021 ◽  
Vol 9 (5) ◽  
pp. 891
Author(s):  
Takashi Hatano ◽  
Daisuke Sano ◽  
Hideaki Takahashi ◽  
Nobuhiko Oridate

The incidence of oropharyngeal cancer (OPC) is increasing remarkably among all head and neck cancers, mainly due to its association with the human papillomavirus (HPV). Most HPVs are eliminated by the host’s immune system; however, because HPV has developed an effective immune evasion mechanism to complete its replication cycle, a small number of HPVs are not eliminated, leading to persistent infection. Moreover, during the oncogenic process, the extrachromosomal HPV genome often becomes integrated into the host genome. Integration involves the induction and high expression of E6 and E7, leading to cell cycle activation and increased genomic instability in the host. Therefore, integration is an important event in oncogenesis, although the associated mechanism remains unclear, especially in HPV-OPC. In this review, we summarize the current knowledge on HPV-mediated carcinogenesis, with special emphasis on immune evasion and integration mechanisms, which are crucial for oncogenesis.


2015 ◽  
Vol 10 (1) ◽  
Author(s):  
Yi Zhou ◽  
Jinyuan Li ◽  
Yuting Ji ◽  
Ming Ren ◽  
Bo Pang ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (2) ◽  
pp. e0116618 ◽  
Author(s):  
Suzette M. Matthijsse ◽  
Joost van Rosmalen ◽  
Jan A. C. Hontelez ◽  
Roel Bakker ◽  
Inge M. C. M. de Kok ◽  
...  

2007 ◽  
Vol 86 (1) ◽  
pp. 94-98 ◽  
Author(s):  
José Eleutério Jr ◽  
Paulo César Giraldo ◽  
Ana Katherine Gonçalves ◽  
Diane Isabelle Magno Cavalcante ◽  
Francisco Valdeci de Almeida Ferreira ◽  
...  

2018 ◽  
Vol 122 ◽  
pp. 92-97 ◽  
Author(s):  
Giorgio Bogani ◽  
Umberto Leone Roberti Maggiore ◽  
Mauro Signorelli ◽  
Fabio Martinelli ◽  
Antonino Ditto ◽  
...  

2010 ◽  
Vol 43 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Arezoo Aghakhani ◽  
Rasool Hamkar ◽  
Mahmoud Parvin ◽  
Nastaran Ghavami ◽  
Mahsa Nadri ◽  
...  

2004 ◽  
Vol 78 (13) ◽  
pp. 7199-7207 ◽  
Author(s):  
Kenneth Raj ◽  
Samuel Berguerand ◽  
Shirley Southern ◽  
John Doorbar ◽  
Peter Beard

ABSTRACT The human papillomavirus (HPV) E1∧E4 protein is the most abundantly expressed viral protein in HPV-infected epithelia. It possesses diverse activities, including the ability to bind to the cytokeratin network and to DEAD-box proteins, and in some cases induces the collapse of the former. E1∧E4 is also able to prevent the progression of cells into mitosis by arresting them in the G2 phase of the cell cycle. In spite of these intriguing properties, the role of this protein in the life cycle of the virus is not clear. Here we report that after binding to and collapsing the cytokeratin network, the HPV type 16 E1∧E4 protein binds to mitochondria. When cytokeratin is not present in the cell, E1∧E4 appears associated with mitochondria soon after its synthesis. The leucine cluster within the N-terminal portion of the E1∧E4 protein is pivotal in mediating this association. After the initial binding to mitochondria, the E1∧E4 protein induces the detachment of mitochondria from microtubules, causing the organelles to form a single large cluster adjacent to the nucleus. This is followed by a severe reduction in the mitochondrial membrane potential and an induction of apoptosis. HPV DNA replication and virion production occur in terminally differentiating cells which are keratin-rich, rigid squamae that exfoliate after completion of the differentiation process. Perturbation of the cytokeratin network and the eventual induction of apoptotic properties are processes that could render these unyielding cells more fragile and ease the exit of newly synthesized HPVs for subsequent rounds of infection.


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