EXPRESSION OF CD44 VARIANT ISOFORMS IN PERIPHERAL-BLOOD LEUKOCYTES INMALIGNANT-LYMPHOMA AND LEUKEMIA - INVERSE CORRELATION BETWEEN EXPRESSION AND TUMOR PROGRESSION

In a variety of human tumors, including high grade Non-Hodgkin's lymph oma (hgNHL), a linkage between expression of CD44 variant isoforms (CD 44v) and tumor progression has been described. In search of an easily accessible diagnostic parameter, expression of CD44 standard (CD44s) a nd CD44 variant isoforms (exons v5, v6, v7 and v10) in peripheral bloo d lymphocytes (PBLs) of patients with hematological malignancies was e valuated by fluorescence activated cell scanning. The analysis of 30 b lood samples of healthy donors and patients with non-malignant disease s and of 183 blood samples of patients with malignant hematological di sorders revealed that only in patients with malignant disorders did a measurable proportion of PBLs express CD44 variant isoforms, mostly ex ons v5, v6, v7 and, less frequently, exon v10. Elevated levels of CD44 v expression were noted in PBLs of patients with acute and chronic mye loid leukemia (AML: 16%, CML: 25%), Hodgkin's disease (HD: 17%), multi ple myeloma (MM: 22%), polycythemia vera (PV: 33%), acute lymphoid leu kemia (ALL: 23%) and, most frequently, in PBLs of patients with non-Ho dgkin's lymphoma (NHL: 54%). CD44v expression was not restricted to th e malignant phenotype, but instead was also noted in T cells, B cells and monocytes, preferentially in a subpopulation of large cells. Furth ermore, expression of CD44v in PBLs was not linked to the histological grading or clinical staging. There was, however, an inverse correlati on with tumor progression, whereas response to therapy was frequently accompanied by upregulation of CD44v. Thus, expression of CD44v in the PBLs of patients with NHL mainly reflected immune responsiveness. Sin ce NHL manifests itself primarily in lymphoid organs, its progression is difficult to follow. Monitoring of CD44v in PBLs could be used as a n additional and convenient parameter for surveying the course of dise ase. Copyright (C) 1996 Elsevier Science Ltd