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dc.contributor.authorSouza, Bárbara Kunzlerpt_BR
dc.contributor.authorFreire, Natália Hogetoppt_BR
dc.contributor.authorJaeger, Mariane da Cunhapt_BR
dc.contributor.authorFarias, Caroline Brunetto dept_BR
dc.contributor.authorBrunetto, Algemir Lunardipt_BR
dc.contributor.authorBrunetto, Andre Tessainerpt_BR
dc.contributor.authorRoesler, Rafaelpt_BR
dc.date.accessioned2022-04-07T04:47:52Zpt_BR
dc.date.issued2021pt_BR
dc.identifier.issn1422-0067pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/236683pt_BR
dc.description.abstractEpigenetic mechanisms, including post-translational modifications of DNA and histones that influence chromatin structure, regulate gene expression during normal development and are also involved in carcinogenesis and cancer progression. The histone methyltransferase G9a (euchromatic histone lysine methyltransferase 2, EHMT2), which mostly mediates mono- and dimethylation by histone H3 lysine 9 (H3K9), influences gene expression involved in embryonic development and tissue differentiation. Overexpression of G9a has been observed in several cancer types, and different classes of G9a inhibitors have been developed as potential anticancer agents. Here, we review the emerging evidence suggesting the involvement of changes in G9a activity in brain tumors, namely glioblastoma (GBM), the main type of primary malignant brain cancer in adults, and medulloblastoma (MB), the most common type of malignant brain cancer in children. We also discuss the role of G9a in neuroblastoma (NB) and the drug development of G9a inhibitors.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofInternational journal of molecular sciences. Basel. Vol. 22, no. 20 (Oct. 2021), 11292, 11 p.pt_BR
dc.rightsOpen Accessen
dc.subjectHistona-lisina N-metiltransferasept_BR
dc.subjectG9aen
dc.subjectMetilação de DNApt_BR
dc.subjectEHMT2en
dc.subjectGlioblastomaen
dc.subjectEpigênese genéticapt_BR
dc.subjectMedulloblastomaen
dc.subjectNeoplasias encefálicaspt_BR
dc.subjectEpigeneticsen
dc.subjectBrain tumoren
dc.titleEHMT2/G9a as an epigenetic target in pediatric and adult brain tumorspt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001137381pt_BR
dc.type.originEstrangeiropt_BR


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