Genomics

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Recruitment of MYC to target genes in ramos and mutu3 cells


ABSTRACT: Follicular lymphomas and diffuse large B-cell lymphomas have markedly different biological phenotypes and yet all originate from mature, germinal center B-cells. We hypothesized that alterations in DNA methylation patterning might help explain the clinical heterogeneity of these diseases. We report that intra- and inter-individual patient heterogeneity in cytosine methylation is associated with disease severity, and that methylation heterogeneity originates in germinal centers and is amplified during disease progression. Abnormal methylation patterns differ between chromosomal regions and depend on local gene density and the methylation status of neighboring genes. Lymphomagenic transcriptional regulators, such as BCL6, MYC and EZH2, perturb DNA methylation in a target gene-specific manner. Furthermore, aberrant epigenetic states – especially hypomethylation – tend to spread along DNA in a non-specific manner while insulator elements like CTCF inhibit such spreading. Our findings suggest mechanisms through which altered cytosine methylation contributes to the distinct phenotypes of tumors derived from mature B-cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31110 | GEO | 2012/11/27

SECONDARY ACCESSION(S): PRJNA144677

REPOSITORIES: GEO

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