Journal Article

Viral carcinogenesis: revelation of molecular mechanisms and etiology of human disease

Janet S. Butel

in Carcinogenesis

Volume 21, issue 3, pages 405-426
Published in print March 2000 | ISSN: 0143-3334
Published online March 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.3.405
Viral carcinogenesis: revelation of molecular mechanisms and etiology of human disease

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The RNA and DNA tumor viruses have made fundamental contributions to two major areas of cancer research. Viruses were vital, first, to the discovery and analysis of cellular growth control pathways and the synthesis of current concepts of cancer biology and, second, to the recognition of the etiology of some human cancers. Transforming retroviruses carry oncogenes derived from cellular genes that are involved in mitogenic signalling and growth control. DNA tumor viruses encode oncogenes of viral origin that are essential for viral replication and cell transformation; viral oncoproteins complex with cellular proteins to stimulate cell cycle progression and led to the discovery of tumor suppressors. Viral systems support the concept that cancer development occurs by the accumulation of multiple cooperating events. Viruses are now accepted as bona fide etiologic factors of human cancer; these include hepatitis B virus, Epstein–Barr virus, human papillomaviruses, human T-cell leukemia virus type I and hepatitis C virus, plus several candidate human cancer viruses. It is estimated that 15% of all human tumors worldwide are caused by viruses. The infectious nature of viruses distinguishes them from all other cancer-causing factors; tumor viruses establish long-term persistent infections in humans, with cancer an accidental side effect of viral replication strategies. Viruses are usually not complete carcinogens, and the known human cancer viruses display different roles in transformation. Many years may pass between initial infection and tumor appearance and most infected individuals do not develop cancer, although immunocompromised individuals are at elevated risk of viral-associated cancers. Variable factors that influence viral carcinogenesis are reviewed, including possible synergy between viruses and environmental cofactors. The difficulties in establishing an etiologic role for a virus in human cancer are discussed, as well as the different approaches that proved viral links to cancer. Future directions for tumor virus studies are considered.

Keywords: AIDS, acquired immunodeficiency syndrome; ATL, adult T-cell leukemia; BKV, BK virus; BL, Burkitt's lymphoma; EBNA, Epstein–Barr virus-encoded nuclear antigen; EBV, Epstein–Barr virus; EV, epidermodysplasia verruciformis; HAM/TSP, HTLV-I-associated myelopathy/tropical spastic paraparesis; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HHV-8(KSHV), human herpesvirus type 8 (Kaposi's sarcoma-associated herpesvirus); HIV, human immunodeficiency virus; HPV, human papillomavirus; HTLV-I, human T-cell leukemia virus type I; JCV, JC virus; KS, Kaposi's sarcoma; MCV, molluscum contagiosum virus; MHC, major histocompatibility complex; MMTV, mouse mammary tumor virus; NPC, nasopharyngeal carcinoma; PCR, polymerase chain reaction; RDA, representational difference analysis; RSV, Rous sarcoma virus; SV40, simian virus 40; T-ag, large T-antigen; TRAF, tumor necrosis factor receptor-associated factors; VLP, virus-like particle.

Journal Article.  19666 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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