Ontology highlight
ABSTRACT: Background
Imprinted domains have been identified as targets for aberrant DNA methylation during carcinogenesis, but it remains unclear when these epigenetic alterations occur and how they contribute to tumor progression. Epigenetic instability at key cis-regulatory elements within imprinted domains can concomitantly activate proto-oncogenes and turn off tumor suppressor genes. Thus, to further characterize the epigenetic response of imprinted domains during carcinogenesis, we compared the stability of DNA methylation at a variety of cis-regulatory elements within imprinted domains in two fundamentally different mouse tumors, benign and malignant, induced by the KrasG12D mutation.Results
We report that imprinted domains remain stable in benign processes
SUBMITTER: Bretz CL
PROVIDER: S-EPMC5572065 | biostudies-literature | 2017
REPOSITORIES: biostudies-literature