Human Papillomavirus 16 E6/E7 Transcript and E2 Gene Status in Patients with Cervical Neoplasia

2004 ◽  
Vol 8 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Narayanan Sathish ◽  
Priya Abraham ◽  
Abraham Peedicayil ◽  
Gopalan Sridharan ◽  
Subhashini John ◽  
...  
2006 ◽  
Vol 65 (3) ◽  
pp. 760-765 ◽  
Author(s):  
Katja Lindel ◽  
Ethel-Michele de Villiers ◽  
Philipp Burri ◽  
Ueli Studer ◽  
Hans J. Altermatt ◽  
...  

2013 ◽  
Vol 121 (2, PART 1) ◽  
pp. 321-329 ◽  
Author(s):  
Doo Byung Chay ◽  
Hanbyoul Cho ◽  
Bo Wook Kim ◽  
Eun Suk Kang ◽  
Eunseop Song ◽  
...  

2008 ◽  
Vol 131 (1) ◽  
pp. 106-110 ◽  
Author(s):  
K. Lee ◽  
I. Magalhaes ◽  
C. Clavel ◽  
J. Briolat ◽  
P. Birembaut ◽  
...  

2004 ◽  
Vol 94 (2) ◽  
pp. 509-514 ◽  
Author(s):  
Nobuo Masumoto ◽  
Takuma Fujii ◽  
Mitsuya Ishikawa ◽  
Makio Mukai ◽  
Akiko Ono ◽  
...  

2004 ◽  
Vol 85 (6) ◽  
pp. 1433-1444 ◽  
Author(s):  
Rosa M. Ordóñez ◽  
Ana María Espinosa ◽  
Dolores Javier Sánchez-González ◽  
Juan Armendáriz-Borunda ◽  
Jaime Berumen

Asian-American (AA) variants of human papillomavirus 16 (HPV-16) are linked to a high incidence of cervical cancer in Mexico, with some evidence strongly suggesting that they are more oncogenic than European (E) variants, including their association with younger women and their higher associated risk of cervical cancer. Differences in the regulation of viral E6/E7 oncogene transcription by the E2 protein may be involved in the higher oncogenicity of AA variants. In E variants, E6/E7 oncogene transcription is repressed by the E2 protein and is frequently up-regulated by the destruction of the E2 gene during viral integration. In contrast, the E2 gene is retained in full in most AA-positive carcinomas, raising the possibility of alternative mechanisms for increasing viral oncogene transcription. The authors investigated whether the higher oncogenicity of AA variants is linked to differences in E6/E7 oncogene transcription and the mechanism of E2 deactivation. E6/E7 and E1/E2 transcripts were explored by RT-PCR in 53 HPV-16-positive cervical carcinomas, 39 retaining (20 European and 19 AA) and 14 having lost (12 European and 2 AA) the E1/E2 genes, and transcription repression activity of the AA E2 genes was tested in four cell lines that constitutively express the β-galactosidase reporter or E6/E7 genes driven by the viral long control region. E6/E7 oncogene transcripts were found in all carcinomas, but only those positive for AA variants with E1/E2 genes had complete E2 transcripts. E2 transcripts were down-regulated by splicing in E-positive carcinomas retaining E1/E2. AA E2 genes were impaired for repression of E6/E7 oncogene transcription in vivo. These results suggest that E6/E7 oncogene expression starts earlier in AA than E variant infections, since E variants need E2 to be destroyed or down-regulated.


Virology ◽  
2014 ◽  
Vol 448 ◽  
pp. 314-321 ◽  
Author(s):  
Mina Kalantari ◽  
Kathryn Osann ◽  
Itzel E. Calleja-Macias ◽  
Seong Kim ◽  
Bing Yan ◽  
...  

2010 ◽  
Vol 70 (10) ◽  
pp. 4081-4091 ◽  
Author(s):  
Elizabeth Gray ◽  
Mark R. Pett ◽  
Dawn Ward ◽  
David M. Winder ◽  
Margaret A. Stanley ◽  
...  

2006 ◽  
Vol 194 (12) ◽  
pp. 1706-1712 ◽  
Author(s):  
Jo L. K. Cheung ◽  
Keith W. K. Lo ◽  
Tak‐Hong Cheung ◽  
Julian W. Tang ◽  
Paul K. S. Chan

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