PubMed · 14026445
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R DEGOS, E LORTAT-JACOB, J F TINTHOIN. [Late diffuse ichthyosis with lymph node reticulosarcoma].. https://pubmed.ncbi.nlm.nih.gov/14026445/
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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 kappaB (NF-kappaB) activation is a common molecular feature. Molecular mechanisms responsible for constitutive NF-kappaB activation, Epstein Barr virus latent membrane protein 1, and defective IkappaBalpha and IkappaB 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-kappaB activation. Ligand-independent signaling by overexpressed CD3O was shown to be a common mechanism that induced constitutive NF-kappaB 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.
The sensitivity of pediatric Hodgkin disease to radiation and chemotherapy has resulted in cure for most children and adolescents who have been diagnosed in the past three decades. Identification of prognostic factors in clinical trials has allowed for tailoring of therapeutic approaches to improve outcome in sequential trials. Tumor burden, symptoms, clinical features, pathology, response to therapy, biology, and host factors are reviewed in this context. New developments should be directed toward identification of factors associated with biologic mechanisms of disease to facilitate the development of biologically targeted therapies that will be more efficacious and less toxic.