The molecular basis for the generation of Hodgkin and Reed-Sternberg cells in Hodgkin's lymphoma

Int J Hematol. 2003 May;77(4):330-5. doi: 10.1007/BF02982639.

Abstract

Hodgkin's lymphoma (HL) is a lymphoid neoplasm with a low frequency of malignant tumor cells, known as Hodgkin and Reed-Sternberg (H-RS) cells, in a background of mixed cellular infiltrates. Despite extensive studies on H-RS cells, the molecular mechanisms of their growth and regulation have remained uncertain for a long period. Recently, constitutively activated nuclear factor-kappaB (NF-kappaB) was reported to be a unique and common characteristic of H-RS cells that prevents the cells from undergoing apoptosis. NF-kappaB triggers proliferation and provides a molecular basis for these cells' aberrant growth and cytokine gene expression. In HL pathogenesis associated with Epstein-Barr virus infection, the activation of NF-kappaB is induced by viral latent membrane protein 1 (LMP1). Coupled with recent insights into the molecular mechanisms of activation of NF-kappaB signaling in H-RS cells, this review discusses a linkage between LMP1 and HL via CD99, which has recently been reported to be down-regulated by LMP1 through the NF-kappaB signaling pathway. This down-regulation leads to the generation of cells with H-RS phenotypes related to the clinical and histologic characteristics of HL.

Publication types

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

MeSH terms

  • 12E7 Antigen
  • Antigens, CD / metabolism
  • Cell Adhesion Molecules / metabolism
  • Hodgkin Disease / etiology
  • Hodgkin Disease / pathology*
  • Humans
  • NF-kappa B / metabolism
  • Reed-Sternberg Cells / pathology*
  • Viral Matrix Proteins / physiology

Substances

  • 12E7 Antigen
  • Antigens, CD
  • CD99 protein, human
  • Cell Adhesion Molecules
  • EBV-associated membrane antigen, Epstein-Barr virus
  • NF-kappa B
  • Viral Matrix Proteins