MicroRNA-451 in chronic myeloid leukemia: miR-451-BCR-ABL regulatory loop?
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
21511335
DOI
10.1016/j.leukres.2011.03.029
PII: S0145-2126(11)00165-2
Knihovny.cz E-resources
- MeSH
- Fusion Proteins, bcr-abl antagonists & inhibitors MeSH
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics MeSH
- Genes, abl physiology MeSH
- Humans MeSH
- MicroRNAs genetics MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Fusion Proteins, bcr-abl MeSH
- MicroRNAs MeSH
- MIRN451 microRNA, human MeSH Browser
Chronic myeloid leukemia (CML) is caused by constituve activity of BCR-ABL tyrosine kinase. Despite of high efficiency of imatinib, selective BCR-ABL inhibitor, about 30% of patients develop resistance. Novel markers and targets for therapy are thus necessary. MicroRNAs are small intereference RNAs whose role in physiological and malignant hematopoiesis has been shown. This study is focused on miR-451 in CML. Following our observation of miR-451 downregulation in CML, we further show its relation to BCR-ABL activity. Our data together with current literature indicate a more complex relationship of miR-451 and BCR-ABL in CML.
Department of Molecular Genetics Institute of Hematology and Blood Transfusion Prague Czech Republic
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