alexa Pathogenesis of Burkitt lymphoma: expression of an activated c-myc oncogene causes the tumorigenic conversion of EBV-infected human B lymphoblasts.
Oncology

Oncology

Chemotherapy: Open Access

Author(s): Lombardi L, Newcomb EW, DallaFavera R

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Abstract 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.
This article was published in Cell and referenced in Chemotherapy: Open Access

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