File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Aberrant DNA Methylation in Acute Myeloid Leukemia and Its Clinical Implications

TitleAberrant DNA Methylation in Acute Myeloid Leukemia and Its Clinical Implications
Authors
KeywordsAcute myeloid leukemia
DNA methylation
epigenetic biomarker
therapeutics
Issue Date2019
PublisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms
Citation
International Journal of Molecular Sciences, 2019, v. 20, p. article no. 4576 How to Cite?
AbstractAcute myeloid leukemia (AML) is a heterogeneous disease that is characterized by distinct cytogenetic or genetic abnormalities. Recent discoveries in cancer epigenetics demonstrated a critical role of epigenetic dysregulation in AML pathogenesis. Unlike genetic alterations, the reversible nature of epigenetic modifications is therapeutically attractive in cancer therapy. DNA methylation is an epigenetic modification that regulates gene expression and plays a pivotal role in mammalian development including hematopoiesis. DNA methyltransferases (DNMTs) and Ten-eleven-translocation (TET) dioxygenases are responsible for the dynamics of DNA methylation. Genetic alterations of DNMTs or TETs disrupt normal hematopoiesis and subsequently result in hematological malignancies. Emerging evidence reveals that the dysregulation of DNA methylation is a key event for AML initiation and progression. Importantly, aberrant DNA methylation is regarded as a hallmark of AML, which is heralded as a powerful epigenetic marker in early diagnosis, prognostic prediction, and therapeutic decision-making. In this review, we summarize the current knowledge of DNA methylation in normal hematopoiesis and AML pathogenesis. We also discuss the clinical implications of DNA methylation and the current therapeutic strategies of targeting DNA methylation in AML therapy.
Persistent Identifierhttp://hdl.handle.net/10722/287956
ISSN
2023 Impact Factor: 4.9
2023 SCImago Journal Rankings: 1.179
PubMed Central ID
ISI Accession Number ID
Grants

 

DC FieldValueLanguage
dc.contributor.authorYANG, X-
dc.contributor.authorWong, MPM-
dc.contributor.authorNg, RK-
dc.date.accessioned2020-10-05T12:05:43Z-
dc.date.available2020-10-05T12:05:43Z-
dc.date.issued2019-
dc.identifier.citationInternational Journal of Molecular Sciences, 2019, v. 20, p. article no. 4576-
dc.identifier.issn1661-6596-
dc.identifier.urihttp://hdl.handle.net/10722/287956-
dc.description.abstractAcute myeloid leukemia (AML) is a heterogeneous disease that is characterized by distinct cytogenetic or genetic abnormalities. Recent discoveries in cancer epigenetics demonstrated a critical role of epigenetic dysregulation in AML pathogenesis. Unlike genetic alterations, the reversible nature of epigenetic modifications is therapeutically attractive in cancer therapy. DNA methylation is an epigenetic modification that regulates gene expression and plays a pivotal role in mammalian development including hematopoiesis. DNA methyltransferases (DNMTs) and Ten-eleven-translocation (TET) dioxygenases are responsible for the dynamics of DNA methylation. Genetic alterations of DNMTs or TETs disrupt normal hematopoiesis and subsequently result in hematological malignancies. Emerging evidence reveals that the dysregulation of DNA methylation is a key event for AML initiation and progression. Importantly, aberrant DNA methylation is regarded as a hallmark of AML, which is heralded as a powerful epigenetic marker in early diagnosis, prognostic prediction, and therapeutic decision-making. In this review, we summarize the current knowledge of DNA methylation in normal hematopoiesis and AML pathogenesis. We also discuss the clinical implications of DNA methylation and the current therapeutic strategies of targeting DNA methylation in AML therapy.-
dc.languageeng-
dc.publisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms-
dc.relation.ispartofInternational Journal of Molecular Sciences-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAcute myeloid leukemia-
dc.subjectDNA methylation-
dc.subjectepigenetic biomarker-
dc.subjecttherapeutics-
dc.titleAberrant DNA Methylation in Acute Myeloid Leukemia and Its Clinical Implications-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/ijms20184576-
dc.identifier.pmid31527484-
dc.identifier.pmcidPMC6770227-
dc.identifier.scopuseid_2-s2.0-85072270257-
dc.identifier.hkuros315766-
dc.identifier.volume20-
dc.identifier.spagearticle no. 4576-
dc.identifier.epagearticle no. 4576-
dc.identifier.isiWOS:000489100500255-
dc.publisher.placeSwitzerland-
dc.relation.projectEpigenetic regulation of C/EBP-epsilon enhancer activity in MLL-rearranged leukemia-
dc.identifier.issnl1422-0067-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats