Genomic imprinting and Wilms' tumor
| Autor: | Wai-Yee Chung, Thomas A. Moulton, Pamela Waber, Benjamin Tycko, Terrence Hensle, Luwa Yuan, Perry Nisen |
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| Rok vydání: | 1996 |
| Předmět: |
Male
Heterozygote Cancer Research RNA Untranslated Saccharomyces cerevisiae Proteins Genotype Tumor suppressor gene Muscle Proteins Growth Biology Wilms Tumor Fungal Proteins Loss of heterozygosity Genomic Imprinting Insulin-Like Growth Factor II medicine Humans Genes Tumor Suppressor Alleles Genetics Chromosomes Human Pair 11 Molecular Motor Proteins Chromosome Mapping Epistasis Genetic Wilms' tumor Oncogenes DNA Methylation medicine.disease Candidate Tumor Suppressor Gene Kidney Neoplasms Gene Expression Regulation Neoplastic Oncology Tumor progression Multigene Family Pediatrics Perinatology and Child Health Chromosomal region DNA methylation Female RNA Long Noncoding Genomic imprinting Microtubule-Associated Proteins Gene Deletion |
| Zdroj: | Medical and Pediatric Oncology. 27:476-483 |
| ISSN: | 1096-911X 0098-1532 |
| DOI: | 10.1002/(sici)1096-911x(199611)27:5<476::aid-mpo15>3.0.co;2-8 |
| Popis: | The selective loss of maternal and reduplication of paternal chromosome 11p15.5 alleles in Wilms' tumors (WTs) points to the existence of a paternally imprinted tumor suppressor gene(s) and/or a maternally imprinted dose-dependent growth-promoting gene(s) in this chromosomal region. Two reciprocally imprinted chromosome 11p15.5 genes, H19, a candidate tumor suppressor gene, and IGF2, a candidate dominant oncogene, have been well-characterized in terms of their imprinting and expression status in WTs. Here we review and extend data indicating that a majority of WTs show a bipaternal epigenotype at these loci, with H19 inactive and IGF2 biallelically active. This can arise either through loss of heterozygosity (LOH) or by a non-LOH pathway involving localized biallelic hypermethylation of H19 DNA. Conversion to this bipaternal endpoint has recently been found to affect not only these two genes, but also at least one other imprinted 11p15.5 gene, KIP2. Since 11p15.5 LOH and biallelic H19 hypermethylation can occur both early and late in tumor progression and since early loss is not associated with bilaterality or multifocality of WTs, these types of lesions appear to be permissive rather than rate-limiting in Wilms' tumorigenesis. |
| Databáze: | OpenAIRE |
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