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Epstein-Barr virus and gastric carcinoma: virus-host interactions leading to carcinoma.
Cancer Sci. 2008 Sep; 99(9):1726-33.CS

Abstract

Epstein-Barr virus (EBV)-associated gastric carcinoma (GC) is a distinct subgroup of GC, comprising 10% of all cases of GC. EBV-associated carcinoma is the monoclonal growth of EBV-infected epithelial cells, and it represents a model of virus-host interactions leading to carcinoma. EBV-infected cells express several latent proteins (latency I program of viral latent gene expression) in EBV-associated GC. However, latent membrane protein 2A (LMP2A) up-regulates the cellular survivin gene through the NFkB pathway, conferring resistance to apoptotic stimuli on the neoplastic cells. EBV-associated GC also shows characteristic abnormality, that is, global and non-random CpG island methylation of the promoter region of many cancer-related genes. Since the viral genes are also regulated by promoter methylation in the infected cells, the DNA methylation mechanism specific to EBV-associated GC may be an exaggeration of the cellular mechanism, which is primarily for defense against foreign DNA. Production of several immunomodulator molecules, inducing tumor-infiltrating lymphocyte and macrophages, serves to form the characteristic histologic pattern in EBV-associated GC. The proposed sequence of events within the mucosa is as follows: EBV infection of certain gastric stem cells; expression of viral latent genes; abnormality of signal pathways caused by viral gene products; DNA methylation-mediated repression of tumor suppressor genes; and monoclonal growth of EBV-infected cells through interaction with other etiologic factors. Potentially useful therapeutic approaches to EBV-associated GC are those that utilize the virus-host interactions, such as bortezomib-induced and viral enzyme-targeted radiotherapy.

Authors+Show Affiliations

Department of Pathology and Diagnostic Pathology, Graduate School of Medicine, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan. mfukayama-tky@umin.ac.jpNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

18616681

Citation

Fukayama, Masashi, et al. "Epstein-Barr Virus and Gastric Carcinoma: Virus-host Interactions Leading to Carcinoma." Cancer Science, vol. 99, no. 9, 2008, pp. 1726-33.
Fukayama M, Hino R, Uozaki H. Epstein-Barr virus and gastric carcinoma: virus-host interactions leading to carcinoma. Cancer Sci. 2008;99(9):1726-33.
Fukayama, M., Hino, R., & Uozaki, H. (2008). Epstein-Barr virus and gastric carcinoma: virus-host interactions leading to carcinoma. Cancer Science, 99(9), 1726-33. https://doi.org/10.1111/j.1349-7006.2008.00888.x
Fukayama M, Hino R, Uozaki H. Epstein-Barr Virus and Gastric Carcinoma: Virus-host Interactions Leading to Carcinoma. Cancer Sci. 2008;99(9):1726-33. PubMed PMID: 18616681.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epstein-Barr virus and gastric carcinoma: virus-host interactions leading to carcinoma. AU - Fukayama,Masashi, AU - Hino,Rumi, AU - Uozaki,Hiroshi, Y1 - 2008/07/04/ PY - 2008/7/12/pubmed PY - 2008/12/17/medline PY - 2008/7/12/entrez SP - 1726 EP - 33 JF - Cancer science JO - Cancer Sci. VL - 99 IS - 9 N2 - Epstein-Barr virus (EBV)-associated gastric carcinoma (GC) is a distinct subgroup of GC, comprising 10% of all cases of GC. EBV-associated carcinoma is the monoclonal growth of EBV-infected epithelial cells, and it represents a model of virus-host interactions leading to carcinoma. EBV-infected cells express several latent proteins (latency I program of viral latent gene expression) in EBV-associated GC. However, latent membrane protein 2A (LMP2A) up-regulates the cellular survivin gene through the NFkB pathway, conferring resistance to apoptotic stimuli on the neoplastic cells. EBV-associated GC also shows characteristic abnormality, that is, global and non-random CpG island methylation of the promoter region of many cancer-related genes. Since the viral genes are also regulated by promoter methylation in the infected cells, the DNA methylation mechanism specific to EBV-associated GC may be an exaggeration of the cellular mechanism, which is primarily for defense against foreign DNA. Production of several immunomodulator molecules, inducing tumor-infiltrating lymphocyte and macrophages, serves to form the characteristic histologic pattern in EBV-associated GC. The proposed sequence of events within the mucosa is as follows: EBV infection of certain gastric stem cells; expression of viral latent genes; abnormality of signal pathways caused by viral gene products; DNA methylation-mediated repression of tumor suppressor genes; and monoclonal growth of EBV-infected cells through interaction with other etiologic factors. Potentially useful therapeutic approaches to EBV-associated GC are those that utilize the virus-host interactions, such as bortezomib-induced and viral enzyme-targeted radiotherapy. SN - 1349-7006 UR - https://www.unboundmedicine.com/medline/citation/18616681/Epstein_Barr_virus_and_gastric_carcinoma:_virus_host_interactions_leading_to_carcinoma_ L2 - https://doi.org/10.1111/j.1349-7006.2008.00888.x DB - PRIME DP - Unbound Medicine ER -