TY - JOUR
T1 - Insulin-like growth factor-II gene expression in Wilms' tumour and embryonic tissues
AU - Scott, J.
AU - Cowell, J.
AU - Robertson, M. E.
AU - Priestley, L. M.
AU - Wadey, R.
AU - Hopkins, B.
AU - Pritchard, J.
AU - Bell, G. I.
AU - Rall, L. B.
AU - Graham, C. F.
AU - Knott, T. J.
PY - 1985
Y1 - 1985
N2 - Wilms' tumour (nephroblastoma) is an embryonal neoplasm occurring in hereditary and spontaneous forms. Both types show rearrangements of the short arm of chromosome 11. The germ line of children with the rare inherited triad of aniridia, genitourinary abnormality and mental retardation carry a chromosome 11 that has a deletion in its short arm (band 11p13) and these children are at increased risk of developing Wilms' tumour1,2. Neonates with the Beckwith-Wiedemann syndrome, in which there may be duplication of the 11p13-11p15 region, are similarly predisposed3. In the spontaneous form of the tumour a deletion of the Hp14 band in tumour cells, but not in normal cells, has been reported4, and the development of homozygosity for recessive mutations in the 11p region is implicated in the aetiology of Wilms' tumour5-8. In view of these chromosomal rearrangements and because Wilms' tumour is historically indistinguishable from the early stages of kidney development9, we have now examined the expression of genes localized to 11p in Wilms' tumour and human embryonic tissue. In 12 sporadic tumours examined, the expression of the gene coding for insulin-like growth factor-II (IGF-II), localized to the 11p15 region, was markedly increased relative to adult tissues, but was comparable to the level of expression in several fetal tissues including kidney, liver, adrenals and striated muscle. This may reflect the stage of tumour differentiation, but could also contribute to the malignant process, as IGF-II is an embryonal mitogen10-13.
AB - Wilms' tumour (nephroblastoma) is an embryonal neoplasm occurring in hereditary and spontaneous forms. Both types show rearrangements of the short arm of chromosome 11. The germ line of children with the rare inherited triad of aniridia, genitourinary abnormality and mental retardation carry a chromosome 11 that has a deletion in its short arm (band 11p13) and these children are at increased risk of developing Wilms' tumour1,2. Neonates with the Beckwith-Wiedemann syndrome, in which there may be duplication of the 11p13-11p15 region, are similarly predisposed3. In the spontaneous form of the tumour a deletion of the Hp14 band in tumour cells, but not in normal cells, has been reported4, and the development of homozygosity for recessive mutations in the 11p region is implicated in the aetiology of Wilms' tumour5-8. In view of these chromosomal rearrangements and because Wilms' tumour is historically indistinguishable from the early stages of kidney development9, we have now examined the expression of genes localized to 11p in Wilms' tumour and human embryonic tissue. In 12 sporadic tumours examined, the expression of the gene coding for insulin-like growth factor-II (IGF-II), localized to the 11p15 region, was markedly increased relative to adult tissues, but was comparable to the level of expression in several fetal tissues including kidney, liver, adrenals and striated muscle. This may reflect the stage of tumour differentiation, but could also contribute to the malignant process, as IGF-II is an embryonal mitogen10-13.
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U2 - 10.1038/317260a0
DO - 10.1038/317260a0
M3 - Article
C2 - 2995818
AN - SCOPUS:0022414038
SN - 0028-0836
VL - 317
SP - 260
EP - 262
JO - Nature
JF - Nature
IS - 6034
ER -