The Role of EBV-Induced Hypermethylation in Gastric Cancer Tumorigenesis.
Viruses
; 12(11)2020 10 28.
Article
de En
| MEDLINE
| ID: mdl-33126718
ABSTRACT
Epstein-Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the host and viral genome following initial infection of gastric epithelial cells. Many studies have been completed in an attempt to identify genes that frequently become hypermethylated and therefore significant pathways that become silenced to promote tumorigenesis. It is clear that EBV-induced hypermethylation silences key tumor suppressor genes, cell cycle genes and cellular differentiation factors to promote a highly proliferative and poorly differentiated cell population. EBV infection has been shown to induce methylation in additional malignancies including Nasopharyngeal Carcinoma and Burkitt's Lymphoma though not to the same level as in EBVaGC. Lastly, some genes silenced in EBVaGC are common to other heavily methylated tumors such as colorectal and breast tumors; however, some genes are unique to EBVaGC and can provide insights into the major pathways involved in tumorigenesis.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Tumeurs de l'estomac
/
Herpèsvirus humain de type 4
/
Méthylation de l'ADN
/
Carcinogenèse
Type d'étude:
Prognostic_studies
Limites:
Humans
Langue:
En
Journal:
Viruses
Année:
2020
Type de document:
Article
Pays d'affiliation:
États-Unis d'Amérique