MicroRNA expression in tumor cells from Waldenstrom's macroglobulinemia reflects both their normal and malignant cell counterparts

• Published in: Blood cancer journal (New York) Vol. 1; no. 6; p. e24
• Main Authors: Hodge, L S, Elsawa, S F, Grote, D M, Price-Troska, T L, Asmann, Y W, Fonseca, R, Gertz, M A, Witzig, T E, Novak, A J, Ansell, S M
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.06.2011; Springer Nature B.V; Nature Publishing Group
• Subjects: 631/250/2502/2055; 692/699/67/1990; Biomedical and Life Sciences; Biomedicine; Cancer Research; Hematology; Oncology; Original; original-article; B lymphocyte; microRNA; Waldenstrom's macroglobulinemia; plasma cell
• ISSN: 2044-5385; 2044-5385
• DOI: 10.1038/bcj.2011.25

MicroRNAs (miRNAs) are involved in the regulation of many cellular processes including hematopoiesis, with the aberrant expression of differentiation-stage specific miRNA associated with lymphomagenesis. miRNA profiling has been essential for understanding the underlying biology of many hematological malignancies; however the miRNA signature of the diverse tumor clone associated with Waldenstrom's macroglobulinemia (WM), consisting of B lymphocytes, plasmacytes and lymphoplasmacytic cells, has not been characterized. We have investigated the expression of over 13 000 known and candidate miRNAs in both CD19 + and CD138 + WM tumor cells, as well as in their malignant and non-malignant counterparts. Although neither CD19 + nor CD138 + WM cells were defined by a distinct miRNA profile, the combination of all WM cells revealed a unique miRNA transcriptome characterized by the dysregulation of many miRNAs previously identified as crucial for normal B-cell lineage differentiation. Specifically, miRNA-9 * /152/182 were underexpressed in WM, whereas the expression of miRNA-21/125b/181a/193b/223/363 were notably increased (analysis of variance; P <0.0001). Future studies focusing on the effects of these dysregulated miRNAs will provide further insight into the mechanisms responsible for the pathogenesis of WM.