Most chromosomal translocations in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) involve oncogenes which 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 responsible for a strong up-regulation of miR-125b (6 to 90 fold). In vitro experiments revealed that miR-125b was able to block monocytic and granulocytic differentiation of leukemic cells and primary CD34+ human blasts. 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 clinico-pathological entity.

Topics:
leukemia, myelocytic, acute, myeloid cells, translocation (genetics), leukemic cells, myelodysplastic syndrome, neoplasms, blast cells, chimera organism, granulocytes, monocytes

Disclosures: No relevant conflicts of interest to declare.

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2008, The American Society of Hematology
2008
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