The origin and clonal proliferation of malignant altered cells in Hodgkin's disease
Krizanac-Bengez, L.; Boranic, M.
Lijecnicki Vjesnik 112(1-2): 50-52
1990
ISSN/ISBN: 0024-3477 PMID: 2366621 Document Number: 365183
Monoclonal antibodies and techniques of molecular genetics have shown Hodgkin's disease to be a clonal neoplasm, and that Hodgkin's and Reed-Sternberg cells--malignant cells in this lymphoma--are either of B-lymphoid, T-lymphoid, or myelo-monocytic cell origin. Hodgkin and Reed-Sternberg cells have high multiplicative potential. Their scarcity in lymphoma tissue in relation to nonneoplastic cells has been attributed a) to prolonged cell-cycle, or b) to secretion of lymphokines by which malignant cells attract reactive cells and become "diluted" in formed lymphogranuloma. Different histological subtypes of Hodgkin's disease seem to be correlated with different origin of malignant cell clones. In lymphocytic depletion, malignant cells are usually of B-lymphoid origin; in mixed cellularity and nodular sclerosis they are usually of T-lymphoid origin. In some cases, malignant cell clone is neither of B-lymphoid, neither of T-lymphoid origin; these cells might be "frozen" at a very low differentiation stage.