Copy number rather than epigenetic alterations are the major dictator of imprinted methylation in tumors.

ABSTRACT: It has been postulated that imprinting aberrations are common in tumors. To understand the role of imprinting in cancer, we have characterized copy-number and methylation in over 280 cancer cell lines and confirm our observations in primary tumors. Imprinted differentially methylated regions (DMRs) regulate parent-of-origin monoallelic expression of neighboring transcripts in cis. Unlike single-copy CpG islands that may be prone to hypermethylation, imprinted DMRs can either loose or gain methylation during tumorigenesis. Here, we show that methylation profiles at imprinted DMRs often not represent genuine epigenetic changes but simply the accumulation of underlying copy-number aberrations (CNAs), which is independent of the genome methylation state inferred from cancer susceptible loci. O

SUBMITTER: Martin-Trujillo A 

PROVIDER: S-EPMC5589900 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature