Abstract
In a mouse model of multistage carcinogenesis elicited by the SV40 large T-antigen (Tag) oncogene in pancreatic beta cells, the gene for insulin-like growth factor IGF2 is focally up-regulated and functionally implicated in tumour development. The IGF2 gene is differentially regulated in normal tissues: the paternal allele is transiently expressed during embryogenesis, whereas the maternal allele is genomically imprinted and inactive. Crossbred mice carrying the Tag oncogene and a disruption of either the paternal or maternal allele of IGF2 reveal that both alleles are co-activated early during tumour development, and that each contributes to malignant hyperproliferation and consequent tumour volume.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alleles
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Animals
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Base Sequence
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Cell Transformation, Neoplastic / genetics*
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Gene Expression Regulation, Neoplastic
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Genomic Imprinting*
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Genotype
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Insulin-Like Growth Factor II / biosynthesis
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Insulin-Like Growth Factor II / genetics*
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Islets of Langerhans / cytology
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Islets of Langerhans / metabolism
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Islets of Langerhans / pathology
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Mice
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Mice, Inbred Strains
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Mice, Knockout
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Mice, Transgenic
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Molecular Sequence Data
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Muscle Proteins / biosynthesis
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Muscle Proteins / genetics
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Pancreatic Neoplasms / genetics
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Pancreatic Neoplasms / pathology*
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Phenotype
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RNA, Long Noncoding
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RNA, Messenger / biosynthesis
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RNA, Untranslated*
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Up-Regulation
Substances
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H19 long non-coding RNA
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Muscle Proteins
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RNA, Long Noncoding
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RNA, Messenger
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RNA, Untranslated
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Insulin-Like Growth Factor II