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The adjacent insulin-like growth factor 2 ( IGF2 ) and  H19  genes are imprinted in most normal human tissues, but imprinting is often lost in tumors. The mechanisms involved in maintenance of imprinting (MOI) and loss of imprinting (LOI) are unresolved. We show here that osteosarcoma (OS) tumors with  IGF2/H19  MOI exhibit allele-specific differential methylation of a CTCF-binding site upstream of  H19 . LOI of  IGF2  or  H19  in OS occurs in a mutually exclusive manner, and occurs with monoallelic expression of the other gene. Bisulfite sequencing reveals  IGF2  LOI occurs with biallelic CpG methylation of the CTCF-binding site, while  H19  LOI occurs with biallelic hypomethylation of this site. Our data demonstrate that  IGF2  LOI and  H19  LOI are accompanied by reciprocal methylation changes at a critical CTCF-binding site. We propose a model in which incomplete gain or loss of methylation at this CTCF-binding site during tumorigenesis explains the complex and often conflicting expression patterns of  IGF2  and  H19  in tumors.

Loss of imprinting of IGF2 and H19 in osteosarcoma is accompanied by reciprocal methylation changes of a CTCF-binding site