Unknown

Dataset Information

0

Myeloid cell differentiation arrest by miR-125b-1 in myelodysplastic syndrome and acute myeloid leukemia with the t(2;11)(p21;q23) translocation.


ABSTRACT: 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.

SUBMITTER: Bousquet M 

PROVIDER: S-EPMC2571925 | biostudies-literature |

REPOSITORIES: biostudies-literature

Similar Datasets

| S-EPMC3003065 | biostudies-literature
| S-EPMC7366384 | biostudies-literature
| S-EPMC3533560 | biostudies-literature
| S-EPMC3060294 | biostudies-literature
2014-05-22 | E-GEOD-46745 | biostudies-arrayexpress
2014-05-22 | GSE46745 | GEO
| S-EPMC5346668 | biostudies-literature
| S-EPMC3972113 | biostudies-literature
| S-EPMC5520910 | biostudies-literature
| S-EPMC8489933 | biostudies-literature