PubMed · 14372998
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J SPRINDRICH, V KOLAR. 1954. Lymphogranulom.. https://pubmed.ncbi.nlm.nih.gov/14372998/
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The WHO classification of malignant lymphoma presents a list of disease entities well defined by clinical, immunologic and genetic features. The disease entities are primarily exemplified by mantle cell lymphoma (the relative incidence, 3%, related with an aberrant expression of cyclin D1 activated by t(11;14) chromosomal translocation), follicular lymphoma (7%, with BCL2 by t(14;18) translocation), marginal zone B-cell lymphoma of MALT type (8%, with MALT1 by t(11;18) or t(14;18) translocation), adult T-cell leukemia/lymphoma (7%, but 20% in Kyushu, with human T-cell leukemia virus type 1 [HTLV1]), extranodal NK/T-cell lymphoma of nasal type (2%, with Epstein-Barr virus [EBV]), and anaplastic large cell lymphoma (2%, with ALK by t(2;5) translocation). The genetic alterations or agents related with their pathogenesis are of great relevance to the diagnoses of these entities. Conversely, the category of diffuse large B-cell lymphoma occupies the largest percentage (33%), and is heterogeneous, including several subtypes. The diagnoses of lymphoma subtypes, except for the main entities described above, largely depends on the phenotypic analysis, in addition to their clinical manifestations and histologic evaluations. Therefore, much attention should be paid to the diagnostic pitfalls in the phenotypic analysis of T-cell lymphomas in regard to incorrect classification of lymphoma, due to lack of awareness or incomplete immunophenotypic evaluation; incorrect interpretation of immunophenotypic data, due to failure to correlate them with the other laboratory data; and suboptimal quality of immunohistochemical stains, leading to a wrong conclusion.
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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.