International Journal of Hematology

, 77:37

Hodgkin’s Lymphoma and CD30 Signal Transduction

Authors

    • Fourth Department of Internal MedicineKitasato University, School of Medicine
    • Division of Pathology, Department of Cancer Research, The Institute of Medical ScienceThe University of Tokyo
  • Masaaki Higashihara
    • Fourth Department of Internal MedicineKitasato University, School of Medicine
  • Toshiki Watanabe
    • Division of Pathology, Department of Cancer Research, The Institute of Medical ScienceThe University of Tokyo
Review Article

DOI: 10.1007/BF02982601

Cite this article as:
Horie, R., Higashihara, M. & Watanabe, T. Int J Hematol (2003) 77: 37. doi:10.1007/BF02982601

Abstract

Advances in molecular biology have shed light on the biological basis of Hodgkin’s lymphoma (HL). Knowledge of the biological basis has enabled us to understand that most Hodgkin and Reed-Sternberg (H-RS) cells are derived from germinal center B-cells and constitutive nuclear factor κB (NF-κ) activation is a common molecular feature. Molecular mechanisms responsible for constitutive NF-κB activation, Epstein Barr virus latent membrane protein 1, and defective IκBα and IκB kinase activation have been clarified in the past several years. A recent study revealed the biological link between 2 characteristic features of H-RS cells: CD30 overexpression and constitutive NF-κB activation. Ligand-independent signaling by over-expressed CD30 was shown to be a common mechanism that induced constitutive NF-κB activation in these cells. These results suggest the self-growth—promoting potential of H-RS cells and redefine the biology of HL composed of H-RS cells and lymphocytes.

Key words:

Hodgkin’s lymphomaHodgkin and Reed-Sternberg cellCD30NF-κ BIκBα
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Copyright information

© The Japanese Society of Hematology 2003