PMC:2065877 / 1024-1735 JSONTXT

{"project":"sentences","denotations":[{"id":"T10","span":{"begin":0,"end":14},"obj":"Sentence"},{"id":"T11","span":{"begin":16,"end":173},"obj":"Sentence"},{"id":"T12","span":{"begin":174,"end":355},"obj":"Sentence"},{"id":"T13","span":{"begin":356,"end":487},"obj":"Sentence"},{"id":"T14","span":{"begin":488,"end":574},"obj":"Sentence"},{"id":"T15","span":{"begin":575,"end":710},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Author Summary\n\nEpstein-Barr virus (EBV) is linked to the development of multiple cancers, including post-transplant lymphoma, Hodgkin disease, and nasopharyngeal carcinoma. Latent membrane protein 1 (LMP1) is expressed in many EBV-associated cancers and is responsible for most of the altered cellular growth properties that are induced by EBV infection. This study reveals that LMP1 induces lymphomas in B-1a lymphocytes, a cell type that is susceptible to transformation in aged mice. The lymphomas require Akt, NFκB, and Stat3 signaling for enhanced growth and survival. The activation of the Stat3, Akt, and NFκB signaling pathways likely underlies the ability of LMP1 to promote malignant transformation. "}