MicroRNA-451 in chronic myeloid leukemia: miR-451-BCR-ABL regulatory loop?
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
21511335
DOI
10.1016/j.leukres.2011.03.029
PII: S0145-2126(11)00165-2
Knihovny.cz E-zdroje
- MeSH
- bcr-abl fúzové proteiny antagonisté a inhibitory MeSH
- chronická myeloidní leukemie genetika MeSH
- geny abl fyziologie MeSH
- lidé MeSH
- mikro RNA genetika MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- bcr-abl fúzové proteiny MeSH
- mikro RNA MeSH
- MIRN451 microRNA, human MeSH Prohlížeč
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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