Most chromosomal translocations in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) involve oncogenes that are either up-regulated or form part of new chimeric genes. The t(2;11)(p21;q23) translocation has been cloned in 19 cases of MDS and AML. In addition to this, we have shown that this translocation is associated with a strong up-regulation of miR-125b (from 6- to 90-fold). In vitro experiments revealed that miR-125b was able to interfere with primary human CD34+cell differentiation, and also inhibited terminal (monocytic and granulocytic) differentiation in HL60 and NB4 leukemic cell lines. Therefore, miR-125b up-regulation may represent a new mechanism of myeloid cell transformation, and myeloid neoplasms carrying the t(2;11) translocation define a new clinicopathological entity.

dx.doi.org/10.1084/jem.20080285, hdl.handle.net/1765/29228
The Journal of Experimental Medicine
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Erasmus MC: University Medical Center Rotterdam

Bousquet, M, Quelen, C, Rosati, R, Mas, V.M.D, Starza, R.L, Bastard, C, … Brousset, P. (2008). Myeloid cell differentiation arrest by miR-125b-1 in myelodysplasic syndrome and acute myeloid leukemia with the t(2;11)(p21;q23) translocation. The Journal of Experimental Medicine, 205(11), 2499–2506. doi:10.1084/jem.20080285