1998
DOI: 10.1016/s1357-4310(97)01197-0
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Insulin-like growth factor 2 and overgrowth: molecular biology and clinical implications

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Cited by 58 publications
(37 citation statements)
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“…IGF-1 expression is essential to achieve maximal growth in mammals, whereas IGF-2 is thought to be a primary growth factor regulating early development. Loss of IGF-1 or IGF-2 in knock-out mice results in significant loss of body weight [17,18], while over-expression of IGF-1 or IGF-2 causes somatic over-growth in mammals [19,20]. The IGFs bind to IGF receptors, insulin receptor, insulin-related receptor, and possibly other receptors.…”
Section: Insulin-like Growth Factorsmentioning
confidence: 99%
“…IGF-1 expression is essential to achieve maximal growth in mammals, whereas IGF-2 is thought to be a primary growth factor regulating early development. Loss of IGF-1 or IGF-2 in knock-out mice results in significant loss of body weight [17,18], while over-expression of IGF-1 or IGF-2 causes somatic over-growth in mammals [19,20]. The IGFs bind to IGF receptors, insulin receptor, insulin-related receptor, and possibly other receptors.…”
Section: Insulin-like Growth Factorsmentioning
confidence: 99%
“…Normal development requires accurate expression, and many disorders can be attributed to an abnormally high dose of IGF2 caused by loss of imprinting (LOI). BWS is one such disease, characterized by fetal and neonatal overgrowth, and is often accompanied by an increased risk of childhood cancers (reviewed in [58]). BWS patients almost always have mutations in the chromosome 11p15.5 region, a large cluster of imprinted genes that includes IGF2 and p57 KIP2 (Figure 3).…”
Section: Loss Of Igf2 Imprintingmentioning
confidence: 99%
“…Insulin like growth factor II is a mitogen for fetal and placental cells, and it also has an anti-apoptotic function (Baker et al, 1993;Christofori et al, 1994;Morison and Reeve, 1998). A subset of individuals with the BWS of somatic overgrowth show abnormal biallelic expression of IGF2 (''loss of imprinting'') in some tissues (Weksberg et al, 1993;Morison et al, 1996;Morison and Reeve, 1998), while other cases are due to mutations or silencing of a different imprinted gene, p57 KIP2 (see below).…”
Section: Imprinted Genes Expressedmentioning
confidence: 99%
“…A subset of individuals with the BWS of somatic overgrowth show abnormal biallelic expression of IGF2 (''loss of imprinting'') in some tissues (Weksberg et al, 1993;Morison et al, 1996;Morison and Reeve, 1998), while other cases are due to mutations or silencing of a different imprinted gene, p57 KIP2 (see below). The tissues that are most affected in BWS coincide with the normal sites of high IGF2 expression .…”
Section: Imprinted Genes Expressedmentioning
confidence: 99%