Pathogenesis of Burkitt lymphoma: expression of an activated c-myc oncogene causes the tumorigenic conversion of EBV-infected human B lymphoblasts.
To study the pathogenesis of Burkitt lymphoma, we introduced activated c-myc genes into human EBV-infected lymphoblastoid cells derived from in vitro infection of normal cord blood or directly from infected peripheral blood from AIDS patients. In both cell types the constitutive expression of exogenous c-myc caused negative regulation of endogenous c-myc expression, changes in growth properties typical of transformed cells, and acquisition of tumorigenicity in immunodeficient mice. In all myc-transfected populations the degree of malignancy directly correlated with the level of c-myc mRNA. EBV infection and c-myc activation are thus sufficient for the tumorigenic conversion of human B cells in vitro, strongly supporting the hypothesis that these same two pathogenetic steps may be involved in the in vivo development of Burkitt lymphoma.
D001402:B-Lymphocytes / Q000382:microbiology / Q000502:physiology*; D002051:Burkitt Lymphoma / Q000235:genetics*; D002453:Cell Cycle; D002472:Cell Transformation, Viral; D005786:Gene Expression Regulation; D004854:Herpesvirus 4, Human / Q000235:genetics; D006801:Humans; D066298:In Vitro Techniques; D009857:Oncogenes; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D014162:Transfection
D011518:Proto-Oncogene Proteins