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- W2321206730 abstract "Prostate cancer is the most common non-cutaneous malignant neoplasm in men in Western countries. In humans, prostate cancer progresses from precursor lesions, termed prostatic intraepithelial neoplasia (PIN), to overt carcinoma confined to the prostate, and finally to metastatic disease that often results in lethality. Previous studies in our laboratory have shown that δ-catenin/NPRAP/Neurojungin (gene designation: CTNND2), a primarily neural-enriched protein in the brain of healthy individuals, is overexpressed corresponding to human prostate cancer progression. This finding has led us to investigate the roles of δ-catenin in prostate cancer progression. We utilized a novel transgenic model of mouse prostate cancer with overexpression of human Myc oncogene driven by rat-probasin promoter as the initiating event, which has been proven to mimic human disease conditions. These Myc overexpressing mice were further crossbred with δ-catenin mutant (δ-cat−/−) mice whose exon 9 of δ-catenin gene was disrupted. In this study, we examined the histological differences of mouse prostate in wild type and Myc overexpression with δ-catenin mutant mice (Myc/δ-cat−/−). We observed that morphological alterations characteristic of high grade PIN developed in luminal epithelial cells of transgenic mice by 6 weeks. These changes include an increase of nuclear size, multi-layering, and cribriform formation. Surprisingly, Myc/δ-cat−/- mice at 6 months of age displayed the dramatically increased tumor size and progression from PIN to adenocarcinomas. We also discovered that Myc/δ-cat−/- mice increased in both number of proliferating cells and cells undergoing apoptosis compared with that of wild type animals. However, in Myc/δ-cat−/- mice, proliferative index was greater than apoptotic index by 3.7 fold. Collectively, our findings suggest that mutation of δ-catenin may contribute to tumorigenesis of mouse prostate by enhancing the effects of Myc oncogene resulting in an increase of cell proliferation and thereby promoting prostate tumor growth. Supported by NIHCA111891 and NIHCA165202. Citation Format: Jongdee Nopparat, Jiao Zhang, Yan-Hua Chen, Qun Lu. δ-Catenin/NPRAP/Neurojungin mutation promotes prostate tumorigenesis in mice overexpressing Myc oncogene . [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 308. doi:10.1158/1538-7445.AM2013-308" @default.
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- W2321206730 date "2013-04-15" @default.
- W2321206730 modified "2023-09-27" @default.
- W2321206730 title "Abstract 308: δ-Catenin/NPRAP/Neurojungin mutation promotes prostate tumorigenesis in mice overexpressing Myc oncogene ." @default.
- W2321206730 doi "https://doi.org/10.1158/1538-7445.am2013-308" @default.
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