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Paternally Derived H19 Is Differentially Expressed in Malignant and Nonmalignant Trophoblast

Department of Animal Development and Genetics, University of Uppsala, Norbyvägen 18A, S-752 36 Uppsala, Sweden [C. W., S. J. M., R. O.]; Cancer Research Campaign Laboratories, Department of Medical Oncology and Biochemistry, Charing Cross and Westminister Medical School, St. Dunstan's Road, London W6 8RP, United Kingdom [R. A. F.]; and Department of Obstetrics and Gynecology, Karolinska Hospital, Post Box 140, S-171 76, Stockholm, Sweden [F. F.]

The paternal allele of the H19 gene has been shown to be transcriptionally inactive in the developing human embryo. Using reverse transcription PCR and RNase protection assays, we demonstrate that expression of H19 is predominantly, but not exclusively, from the maternal allele in the human placenta. In situ hybridization analysis shows strong expression of the H19 gene in eight complete hydatidiform moles, hyperplastic tissues consisting of trophoblasts which contain only paternally derived genetic material, indicating that H19 is not functionally imprinted in this tissue. H19, a putative growth suppressor, is oppositely imprinted to the neighboring insulin-like growth factor II (IGF2) gene and an up-regulation of IGF2 expression has been linked previously to a down-regulation of H19 expression in the progression to Wilms' tumor. Two cases of complete hydatidiform mole which progressed to choriocarcinoma show high levels of expression of both H19 and IGF2. The choriocarcinomas which developed from these complete hydatidiform moles showed similar expression of IGF2 but a decreased number of H19-positive cells, which may reflect selection for cells expressing IGF2 and against those expressing H19 in this tissue.

¹ To whom requests for reprints should be addressed.

Received 9/ 9/94. Accepted 12/30/94.

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