Epstein–Barr virus (EBV), a gamma-1 herpesvirus, has tropism for B lymphocytes and epithelial cells of the upper aerodigestive tract. Despite most adults being asymptomatic carriers of an EBV infection obtained during adolescence, in some individuals EBV is oncogenic: it drives several types of lymphoma and some epithelial malignancies, principally nasopharyngeal carcinoma (NPC) [1]. EBV latent membrane protein 1 (LMP1), an active transmembrane receptor, appears to mediate malignant transformation by activating the nuclear-factor-kappa B (NF-ᴋB), c-Jun N-terminal kinase (JNK) and phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathways [2].
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