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Downregulation but lack of promoter hypermethylation or somatic mutations of the potential tumor suppressor CXXC5 in MDS and AML with deletion 5q

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During recent years mutations in epigenetic modulators have been identified in several human cancers, including acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS)[1]. CXXC5 has been found to be necessary for retinoic acid induced differentiation of myelocytic leukemia cells, identifying CXXC5 as a candidate tumor suppressor for myeloid transformation[2]. CXXC5 belongs to the CXXC-zinc finger domain family comprising 13 proteins. © 2012 John Wiley & Sons A/S.
OriginalsprogEngelsk
TidsskriftEuropean Journal of Haematology
Vol/bind90
Udgave nummer3
Sider (fra-til)259-60
ISSN0902-4441
DOI
StatusUdgivet - 2013

ID: 36545526