Hodgkin’s Lymphoma and CD30 Signal Transduction
- Cite this article as:
- Horie, R., Higashihara, M. & Watanabe, T. Int J Hematol (2003) 77: 37. doi:10.1007/BF02982601
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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.