Terrence Hensle

TL;DR: In most WTs (18/25), H19 RNA was reduced at least 20–fold from fetal kidney levels and expression patterns were consistent with IGF2/H19 enhancer competition without obligate inverse coupling, implicate genetic and epigenetic inactivation of H19 in Wilms' tumorigenesis.

TL;DR: Highlights two molecular classes of Wilms' tumor, and indicate strong selection for stabilization of beta-catenin in the WT1-mutant class, likely critical in tumor formation after loss of WT1.

TL;DR: Data indicate coordinately reduced expression of two linked paternally imprinted genes in most WTs and also suggest mechanistic differences in the maintenance of imprinting at these two loci.

TL;DR: LOH mapping showed that the entire domain, including IGF2/H19, is within the minimal WT2 region, and pre-existing massive allelic asymmetry for DNA methylation and hyper-dependence of transcription on methylation status may underlie the mechanism of gene-specific silencing of H19 in Wilms' tumorigenesis.

TL;DR: Data is reviewed and extended to indicate that a majority of WTs show a bipaternal epigenotype at these loci, with H19 inactive and IGF2 biallelically active.