Genome-wide methylation sequencing identifies progression-related epigenetic drivers in myelodysplastic syndromes.

Cell Death & Disease
Jing-dong ZhouJun Qian

Abstract

The potential mechanism of myelodysplastic syndromes (MDS) progressing to acute myeloid leukemia (AML) remains poorly elucidated. It has been proved that epigenetic alterations play crucial roles in the pathogenesis of cancer progression including MDS. However, fewer studies explored the whole-genome methylation alterations during MDS progression. Reduced representation bisulfite sequencing was conducted in four paired MDS/secondary AML (MDS/sAML) patients and intended to explore the underlying methylation-associated epigenetic drivers in MDS progression. In four paired MDS/sAML patients, cases at sAML stage exhibited significantly increased methylation level as compared with the matched MDS stage. A total of 1090 differentially methylated fragments (DMFs) (441 hypermethylated and 649 hypomethylated) were identified involving in MDS pathogenesis, whereas 103 DMFs (96 hypermethylated and 7 hypomethylated) were involved in MDS progression. Targeted bisulfite sequencing further identified that aberrant GFRA1, IRX1, NPY, and ZNF300 methylation were frequent events in an additional group of de novo MDS and AML patients, of which only ZNF300 methylation was associated with ZNF300 expression. Subsequently, ZNF300 hypermethylation in l...Continue Reading

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Citations

Jul 11, 2021·Molecular Oncology·Carlo GaniniGerry Melino

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Datasets Mentioned

BETA
PRJNA670308

Methods Mentioned

BETA
MDS
PCR
RRBS
flow cytometry
methylation profiling
transfection

Software Mentioned

GraphPad Prism
CpGplot
Bismark
SPSS
MethylTarget
Methyl Primer Express
Coremine

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