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dc.contributor.authorMemari, F
dc.contributor.authorJoneidi, Z
dc.contributor.authorTaheri, B
dc.contributor.authorAval, SF
dc.contributor.authorRoointan, A
dc.contributor.authorZarghami, N
dc.date.accessioned2018-08-26T08:53:55Z
dc.date.available2018-08-26T08:53:55Z
dc.date.issued2018
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/54045
dc.description.abstractEpigenetic variations can play remarkable roles in different normal and abnormal situations. Such variations have been shown to have a direct role in the pathogenesis of various diseases either through inhibition of tumor suppressor genes or increasing the expression of oncogenes. Enzymes involving in epigenetic machinery are the main actors in tuning the epigenetic-based controls on gene expressions. Aberrant expression of these enzymes can trigger a big chaos in the cellular gene expression networks and finally lead to cancer progression. This situation has been shown in different types of leukemia, where high or low levels of an epigenetic enzyme are partly or highly responsible for involvement or progression of a disease. DNA hypermethylation, different histone modifications, and aberrant miRNA expressions are three main epigenetic variations, which have been shown to play a role in leukemia progression. Epigenetic based treatments now are considered as novel and effective therapies in order to decrease the abnormal epigenetic modifications in patient cells. Different epigenetic-based approaches have been developed and tested to inhibit or reverse the unusual expression of epigenetic agents in leukemia. The reciprocal behavior of miRNAs in the regulation of epigenetic modifiers, while being regulated by them, unlocks a new opportunity in order to design some epigenetic-based miRNAs able to silence or sensitize these effectors in leukemia. é 2018 Elsevier Masson SAS
dc.language.isoEnglish
dc.relation.ispartofBiomedicine and Pharmacotherapy
dc.titleEpigenetics and Epi-miRNAs: Potential markers/therapeutics in leukemia
dc.typeLetter
dc.citation.volume106
dc.citation.spage1668
dc.citation.epage1677
dc.citation.indexScopus
dc.identifier.DOIhttps://doi.org/10.1016/j.biopha.2018.07.133


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