{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Damaschke NA"],"funding":["NCI NIH HHS"],"pagination":["5236-5247"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9741865"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["77(19)"],"pubmed_abstract":["Loss of imprinting (LOI) is an epigenetic event that relaxes an allele-specific restriction on gene expression. One gene that experiences LOI is the paracrine insulin-like growth factor <i>IGF2</i>, which occurs commonly in human prostate tissues during aging and tumorigenesis. However, the relationship between <i>IGF2</i> LOI and prostate tumorigenesis has not been established functionally. In this study, we created a mouse model with CTCF-binding site mutations at the <i>Igf2-H19</i> imprint control region that abolishes CTCF insulator activity, resulting in biallelic <i>Igf2</i> expression that mimics increased levels seen with aging-induced LOI. We found that <i>Igf2</i> LOI increased the prevalence and severity of prostatic intraepithelial neoplasia (PIN), a premalignant lesion. Engin"],"journal":["Cancer research"],"pubmed_title":["Loss of <i>Igf2</i> Gene Imprinting in Murine Prostate Promotes Widespread Neoplastic Growth."],"pmcid":["PMC9741865"],"funding_grant_id":["R01 CA097131"],"pubmed_authors":["Blute ML","Bhusari S","Huang W","Damaschke NA","Avilla M","Zhong W","Jarrard DF","Yang B"],"additional_accession":[]},"is_claimable":false,"name":"Loss of <i>Igf2</i> Gene Imprinting in Murine Prostate Promotes Widespread Neoplastic Growth.","description":"Loss of imprinting (LOI) is an epigenetic event that relaxes an allele-specific restriction on gene expression. One gene that experiences LOI is the paracrine insulin-like growth factor <i>IGF2</i>, which occurs commonly in human prostate tissues during aging and tumorigenesis. However, the relationship between <i>IGF2</i> LOI and prostate tumorigenesis has not been established functionally. In this study, we created a mouse model with CTCF-binding site mutations at the <i>Igf2-H19</i> imprint control region that abolishes CTCF insulator activity, resulting in biallelic <i>Igf2</i> expression that mimics increased levels seen with aging-induced LOI. We found that <i>Igf2</i> LOI increased the prevalence and severity of prostatic intraepithelial neoplasia (PIN), a premalignant lesion. Engin","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Oct","modification":"2025-04-26T02:10:26.108Z","creation":"2025-04-06T10:24:05.273Z"},"accession":"S-EPMC9741865","cross_references":{"pubmed":["28775169"],"doi":["10.1158/0008-5472.can-16-3089","10.1158/0008-5472.CAN-16-3089"]}}