Document Detail


Molecular piracy: the viral link to carcinogenesis.
MedLine Citation:
PMID:  9930354     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The vast majority of the human experience with viral infections is associated with acute symptoms, such as malaise, fever, chills, rhinitis and diarrhea. With this acute or lytic phase, the immune system mounts a response and eliminates the viral agent while acquiring antibodies to that specific viral subtype. With latent or chronic infections, the viral agent becomes incorporated into the human genome. Viral agents capable of integration into the host's genetic material are particularly dangerous and may commandeer the host's ability to regulate normal cell growth and proliferation. The oncogenic viruses may immortalize the host cell, and facilitate malignant transformation. Cell growth and proliferation may be enhanced by viral interference with tumor suppressor gene function (p53 and pRb). Viruses may act as vectors for mutated proto-oncogenes (oncogenes). Overexpression of these oncogenes in viral-infected cells interferes with normal cell function and allows unregulated cell growth and proliferation, which may lead to malignant transformation and tumour formation. Development of oral neoplasms, both benign and malignant, has been linked to several viruses. Epstein-Barr virus is associated with oral hairy leukoplakia, lymphoproliferative disease, lymphoepithelial carcinoma, B-cell lymphomas, and nasopharyngeal carcinoma. Human herpesvirus-8 has been implicated in all forms of Kaposi's sarcoma, primary effusion lymphomas, multiple myeloma, angioimmunoblastic lymphadenopathy, and Castleman's disease. Human herpesvirus-6 has been detected in lymphoproliferative disease, lymphomas, Hodgkin's disease, and oral squamous cell carcinoma. The role of human papillomavirus in benign (squamous papilloma, focal epithelial hyperplasia, condyloma acuminatum, verruca vulgaris), premalignant (oral epithelial dysplasia), and malignant (squamous cell carcinoma) neoplasms within the oral cavity is well recognized. Herpes simplex virus may participate as a cofactor in oral squamous cell carcinoma development by enhancing activation, amplification, and overexpression of pre-existing oncogenes within neoplastic tissues. Because of the integral role of viruses in malignant transformation of host cells, innovative antiviral therapy may prevent tumour development, involute neoplastic proliferations, or arrest malignant progression.
Authors:
C M Flaitz; M J Hicks
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Oral oncology     Volume:  34     ISSN:  1368-8375     ISO Abbreviation:  Oral Oncol.     Publication Date:  1998 Nov 
Date Detail:
Created Date:  1999-02-17     Completed Date:  1999-02-17     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9709118     Medline TA:  Oral Oncol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  448-53     Citation Subset:  IM; X    
Affiliation:
Department of Stomatology, University of Texas, Houston Health Science Center 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
Cell Division
Cell Transformation, Neoplastic
HIV / pathogenicity
Herpesviridae / pathogenicity
Humans
Mouth Neoplasms / virology*
Oncogenic Viruses / pathogenicity*
Papillomaviridae / pathogenicity

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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