Role of epigenetics in chronic myeloid leukemia
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
23296408
PubMed Central
PMC3578734
DOI
10.1007/s11899-012-0152-z
Knihovny.cz E-zdroje
- MeSH
- bcr-abl fúzní proteiny antagonisté a inhibitory genetika terapeutické užití MeSH
- chemorezistence MeSH
- chronická myeloidní leukemie farmakoterapie genetika patologie MeSH
- epigenomika * MeSH
- inhibitory proteinkinas farmakologie terapeutické užití MeSH
- lidé MeSH
- metylace DNA MeSH
- mikro RNA fyziologie MeSH
- protinádorové látky farmakologie terapeutické užití MeSH
- regulace genové exprese u leukemie účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- bcr-abl fúzní proteiny MeSH
- inhibitory proteinkinas MeSH
- mikro RNA MeSH
- protinádorové látky MeSH
The efficacy of therapeutic modalities in chronic myeloid leukemia (CML) depends on both genetic and epigenetic mechanisms. This review focuses on epigenetic mechanisms involved in the pathogenesis of CML and in resistance of tumor cells to tyrosine kinase inhibitors leading to the leukemic clone escape and propagation. Regulatory events at the levels of gene regulation by transcription factors and microRNAs are discussed in the context of CML pathogenesis and therapeutic modalities.
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