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

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.