Epigenetic lesions at the H19 locus in Wilms' tumour patients View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1994-07

AUTHORS

Thomas Moulton, Taria Crenshaw, Yue Hao, Josh Moosikasuwan, Na Lin, Francine Dembitzer, Terrence Hensle, Lawrence Weiss, Lydia McMorrow, Thomas Loew, Wilma Kraus, William Gerald, Benjamin Tycko

ABSTRACT

To test the potential role of H19 as a tumour suppressor gene we have examined its expression and DNA methylation in Wilms' tumours (WTs). In most WTs (18/25), H19 RNA was reduced at least 20–fold from fetal kidney levels. Of the expression–negative tumours ten retained 11p15.5 heterozygosity: in nine of these, H19 DNA was biallelically hypermethylated and in two cases hypermethylation locally restricted to H19 sequences was also present in the non–neoplastic kidney parenchyma. IGF2 mRNA was expressed in most but not all WTs and expression patterns were consistent with IGF2/H19 enhancer competition without obligate inverse coupling. These observations implicate genetic and epigenetic inactivation of H19 in Wilms' tumorigenesis. More... »

PAGES

440-447

Journal

TITLE

Nature Genetics

ISSUE

3

VOLUME

7

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng0794-440

DOI

http://dx.doi.org/10.1038/ng0794-440

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045611995

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/7920666


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44 schema:description To test the potential role of H19 as a tumour suppressor gene we have examined its expression and DNA methylation in Wilms' tumours (WTs). In most WTs (18/25), H19 RNA was reduced at least 20–fold from fetal kidney levels. Of the expression–negative tumours ten retained 11p15.5 heterozygosity: in nine of these, H19 DNA was biallelically hypermethylated and in two cases hypermethylation locally restricted to H19 sequences was also present in the non–neoplastic kidney parenchyma. IGF2 mRNA was expressed in most but not all WTs and expression patterns were consistent with IGF2/H19 enhancer competition without obligate inverse coupling. These observations implicate genetic and epigenetic inactivation of H19 in Wilms' tumorigenesis.
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51 DNA methylation
52 H19
53 H19 DNA
54 H19 RNA
55 H19 locus
56 IGF2 mRNA
57 Most Wilms tumors
58 RNA
59 Wilms tumor
60 Wilms tumorigenesis
61 Wilms' tumor patients
62 cases
63 competition
64 coupling
65 epigenetic inactivation
66 epigenetic lesions
67 expression
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69 genes
70 heterozygosity
71 inactivation
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73 kidney levels
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