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Articles Published Processes
9/15/2014 8:39:00 AM | Browse: 1252 | Download: 1175
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Received |
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2012-12-05 09:46 |
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Peer-Review Started |
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2012-12-05 18:17 |
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To Make the First Decision |
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2013-01-17 11:00 |
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Return for Revision |
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2013-01-17 19:38 |
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Revised |
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2013-04-04 02:28 |
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Second Decision |
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2013-04-10 17:03 |
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Accepted by Journal Editor-in-Chief |
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Accepted by Executive Editor-in-Chief |
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2013-04-11 05:43 |
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Articles in Press |
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Publication Fee Transferred |
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Edit the Manuscript by Language Editor |
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Typeset the Manuscript |
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2013-04-16 14:26 |
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Publish the Manuscript Online |
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2013-05-09 13:09 |
Category |
Virology |
Manuscript Type |
Topic Highlights |
Article Title |
How virus persistence can initiate the tumorigenesis process
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Manuscript Source |
Invited Manuscript |
All Author List |
Simone Avanzi, Gualtiero Alvisi and Alessandro Ripalti |
Funding Agency and Grant Number |
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Corresponding Author |
Dr. Alessandro Ripalti, Department of Oncology, Hematology and Laboratory Medicine, Operative Unit of Microbiology, A.O-U. di Bologna Policlinico S. Orsola-Malpighi, via Massarenti 9, 40138 Bologna, Italy. alessandro.ripalti@unibo.it
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Key Words |
Virus; Carcinogenesis; Tumor; Oncogene; Latency; Viral persistence |
Core Tip |
Current models for viral driven oncogenesis cannot explain why tumor development in carriers of tumorigenic viruses is a very rare event, occurring decades after virus infection. Considering that viruses are mutagenic agents per se and human oncogenic viruses additionally establish latent and persistent infections, we attempt here to provide a general mechanism of tumor initiation both for RNA and DNA viruses, suggesting viruses could be both necessary and sufficient in triggering human tumorigenesis initiation.
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Publish Date |
2013-05-09 13:09 |
Citation |
Avanzi S, Alvisi G, Ripalti A. How virus persistence can initiate the tumorigenesis process. World J Virol 2013; 2(2): 102-109 |
URL |
http://www.wjgnet.com/2220-3249/full/v2/i2/102.htm |
DOI |
http://dx.doi.org/10.5501/wjv.v2.i2.102 |
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