Inactivation of H19, an imprinted and putative tumor repressor gene, is a preneoplastic event during Wilms' tumorigenesis

Cancer Research

Volumn 57, Issue 20, 1997, Pages 4469-4473

  Cui, Hengmi ^a   Hedborg, Fredrik ^a,b   He, Liangmei ^a   Nordenskjöld, Agneta ^c   Sandstedt, Bengt ^c   Pfeifer Ohlsson, Susan ^a,b   Ohlsson, Rolf ^a  

^a UPPSALA UNIVERSITY   (Sweden)

^b UPPSALA UNIVERSITY HOSPITAL   (Sweden)

^c KAROLINSKA UNIVERSITY HOSPITAL   (Sweden)

Author keywords

[No Author keywords available]

Indexed keywords

ALLELE; ARTICLE; GENE LOCUS; GENE REPRESSION; HUMAN; HUMAN TISSUE; NEPHROBLASTOMA; PRIORITY JOURNAL; REPRESSOR GENE; TUMOR SUPPRESSOR GENE;

ALLELES; ANIMALS; CHROMOSOMES, HUMAN, PAIR 11; FEMALE; GENE EXPRESSION REGULATION, NEOPLASTIC; GENES, TUMOR SUPPRESSOR; GENOMIC IMPRINTING; GENOTYPE; HUMANS; IN SITU HYBRIDIZATION; INSULIN-LIKE GROWTH FACTOR II; KIDNEY; KIDNEY NEOPLASMS; LOSS OF HETEROZYGOSITY; MALE; MICE; MODELS, BIOLOGICAL; MUSCLE PROTEINS; PRECANCEROUS CONDITIONS; RNA, UNTRANSLATED; WILMS TUMOR;

EID: 0030760633     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (18)

1. Bove, K. E., and McAdams, A. J. The nephroblastomatosis complex and its relationship to Wilms' tumor, Perspect. Pediatr. Pathol., 3: 185-223, 1976.
2. Reeve, A. E. Role of genomic imprinting in Wilms' tumour and overgrowth disorders. Med. Pediatr. Oncol., 27: 470-475: 1996.
3. Stewart, C. E., and Rotwein, P. Growth, differentiation, and survival: multiple physiological functions for insulin-like growth factors. Physiol. Rev., 76: 1005-1026, 1996.
4. Franklin, G. C., Adam, G. I. R., and Ohlsson, R. Genomic imprinting and mammalian development. Placenta, 17: 3-14, 1996.
5. Leighton, P. A., Ingram, R. S., Eggenschwiler, J., Efstratiadis, A., and Tilghman, S. Disruption of imprinting caused by deletion of the H19 gene region in mice. Nature (Lond.), 375: 34-39, 1995.
6. Leighton, P., Saam, J., Ingram, R., Stewart, C. and Tilghman, S. An enhancer deletion affects both H19 and 1gf2 expression. Genes Dev., 9: 2079-2089, 1995.
7. Moulton, T., Chung, W-Y., Yuan, L., Hensle, T., Waber, P., Nisen, P., and Tycko, B. Genomic imprinting and Wilms' tumor. Med. Pediatr. Oncol., 27: 476-483, 1996.
8. Brannan, C., Dees, E., Ingram, R., and Tilghman, S. The product of the H19 gene may function as an RNA. Mol. Cell. Biol., 10: 28-36, 1990.
9. Hao, Y., Crenshaw, T., Moulton, T., Newcomb, E., and Tycko, B. Tumour-suppressor activity of H19 RNA. Nature (Lond.), 365: 764-767, 1993.
10. Adam, G., Cui, H., Miller, S., Flam, F., and Ohlsson, R. Allele-specific in situ hybridization (ASISH) analysis: a novel technique which resolves differential allelic usage of H19 within the same cell lineage during human placental development. Development (Camb.), 122: 839-847, 1996.
11. Ogawa, O., Becroft, D. M., Morrison, I. M., Eccles, M. R., Skeen, J. E., Mauger, D. C., and Reeve, A. E. Constitutional relaxation of insulin-like growth factor II gene imprinting associated with Wilms' tumor and gigantism. Nat. Genet., 5: 408-412, 1993.
12. Hedborg, F., Holmgren, L., Sandstedt, B., and Ohlsson, R. The cell type-specific IGF2 expression during early human development correlates to the pattern of overgrowth and neoplasia in the Beckwith-Wiedemann syndrome. Am. J. Pathol., 145: 802-817, 1994.
13. Ohlsson, R., Hedborg, F., Holmgren, L., Walsh, C., and Ekström, T. J. Overlapping patterns of IGF2 and H19 expression during human development: biallelic IGF2 expression correlates with a lack of H19 expression. Development (Camb.), 120: 361-368, 1994.
14. Ekblom, P., and Weller, A. Ontogeny of tubulointerstitial cells. Kidney Int., 39: 394-400, 1991.
15. Beckwith, B., Kiviat, N., and Bonadio, J. Nephrogenic rests, nephroblastomatosis, and the pathogenesis of Wilms' tumor. Pediatr. Pathol., 10: 1-36, 1990.
16. Nordenskjöld, A., Friedman, E., Sandstedt, B., Söderhäll, S., and Anvret, M. Constitutional and somatic mutations in the WT1 gene in Wilms' tumor patients. Int J Cancer. 63: 516-522, 1995.
17. Nordenskjöld, A., Friedman, E., and Anvret, M. WT1 mutations in patients with Denys-Drash syndrome: a novel mutation in exon 8 and paternal allele origin. Hum. Genet., 93: 115-120, 1994.
18. Okamoto, K., Morison, I. M., Taniguchi, T., and Reeve, A. E. Epigenetic changes at the insulin-like growth factor II/H19 locus in developing kidney is an early event in Wilms' tumorigenesis. Proc. Natl. Acad. Sci. USA, 94: 5367-5371, 1997.