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

Cell. 1987 Apr 24;49(2):161-70. doi: 10.1016/0092-8674(87)90556-3.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • B-Lymphocytes / microbiology
  • B-Lymphocytes / physiology*
  • Burkitt Lymphoma / genetics*
  • Cell Cycle
  • Cell Transformation, Viral
  • Gene Expression Regulation
  • Herpesvirus 4, Human / genetics
  • Humans
  • In Vitro Techniques
  • Oncogenes*
  • Proto-Oncogene Proteins / genetics*
  • Transfection

Substances

  • Proto-Oncogene Proteins