Aberrant silencing of cancer-related genes by CpG hypermethylation occurs independently of their spatial organization in the nucleus.

ABSTRACT: Aberrant promoter DNA-hypermethylation and repressive chromatin constitutes a frequent mechanism of gene inactivation in cancer. There is great interest in dissecting the mechanisms underlying this abnormal silencing. Studies have shown changes in the nuclear organization of chromatin in tumor cells as well as the association of aberrant methylation with long-range silencing of neighboring genes. Furthermore, certain tumors show a high incidence of promoter methylation termed as the CpG island methylator phenotype. Here, we have analyzed the role of nuclear chromatin architecture for genes in hypermethylated inactive versus nonmethylated active states and its relation with long-range silencing and CpG island methylator phenotype. Using combined immunostaining for active/repressive chromati

SUBMITTER: Easwaran HP 

PROVIDER: S-EPMC3031132 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature