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(American Journal of Pathology. 2000;157:1393-1403.)
© 2000 American Society for Investigative Pathology

Regular Articles

p57KIP2 Is Not Mutated in Hepatoblastoma but Shows Increased Transcriptional Activity in a Comparative Analysis of the Three Imprinted Genes p57KIP2, IGF2, and H19

Wolfgang Hartmann*, Andreas Waha*, Arend Koch*, Cynthia G. Goodyer{dagger}, Steffen Albrecht{ddagger}, Dietrich von Schweinitz§ and Torsten Pietsch*

From the Department of Neuropathology,*
University of Bonn Medical Center, Bonn, Germany; the Department of Endocrinology,{dagger}
Montreal Children’s Hospital, McGill University, Montreal, Canada; the Department of Pathology,{ddagger}
Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Canada; and the Department of Pediatric Surgery,§
University of Basel Medical Center, Basel, Switzerland

Hepatoblastomas (HBs), representing malignant liver tumors of childhood, show frequent loss of heterozygosity (LOH) in the chromosomal region 11p15.5. This loss is of maternal origin suggesting the presence of a monoallelically expressed tumor suppressor gene in this region. p57KIP2 (KIP2) located at 11p15.5 is predominantly expressed from the maternal allele and encodes a cyclin-dependent kinase inhibitor. We screened a series of 56 HB tumors and five HB cell lines for allelic loss (LOH) of the KIP2 locus by microsatellite analysis and KIP2 coding sequence mutations by single-strand conformation polymorphism analysis. Although LOH at the KIP2 locus occurred in 25% of the cases, no mutations were found. Analysis of KIP2 mRNA expression by competitive reverse transcriptase-polymerase chain reaction revealed up-regulation in nine of 12 HBs compared to matching liver samples. In contrast, mRNA levels of the putative suppressor gene H19 on 11p15.5 were decreased in 10 of 12 tumors, indicating that KIP2 and H19 are not co-regulated in HBs. IGF2 mRNA expression was increased in 11 of 12 HB samples. All HBs showed monoallelic KIP2 expression. However, the overexpression of KIP2 in HBs with maternal loss of 11p15.5 suggests a reactivation of the paternal allele in these cases. Overexpression of KIP2 in HBs argues against a role as a HB suppressor gene.




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