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.

Keywords

BiologyCarcinogenesisAlleleGeneGeneticsGenomic imprintingGrowth factorInsulinCancer researchInsulin-like growth factor 2Gene expressionEndocrinologyDNA methylation

MeSH Terms

AllelesAnimalsBase SequenceCell TransformationNeoplasticGene Expression RegulationNeoplasticGenomic ImprintingGenotypeInsulin-Like Growth Factor IIIslets of LangerhansMiceMiceInbred StrainsMiceKnockoutMiceTransgenicMolecular Sequence DataMuscle ProteinsPancreatic NeoplasmsPhenotypeRNALong NoncodingRNAMessengerRNAUntranslatedUp-Regulation

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Publication Info

Year
1995
Type
article
Volume
10
Issue
2
Pages
196-201
Citations
124
Access
Closed

Social Impact

Social media, news, blog, policy document mentions

Citation Metrics

124
OpenAlex
1
Influential
82
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Cite This

Gerhard Christofori, Paul Naik, Douglas Hanahan (1995). Deregulation of both imprinted and expressed alleles of the insulin–like growth factor 2 gene during β–cell tumorigenesis. Nature Genetics , 10 (2) , 196-201. https://doi.org/10.1038/ng0695-196

Identifiers

DOI
10.1038/ng0695-196
PMID
7663515

Data Quality

Data completeness: 81%