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Entopic overexpression of Ascl2 does not accelerate tumourigenesis in ApcMin mice

Reed, Karen Ruth ORCID:, Tunster, Simon James ORCID:, Young, Madeleine, Carrico, Adam Stephen, John, Rosalind Margaret ORCID: and Clarke, Alan Richard ORCID: 2012. Entopic overexpression of Ascl2 does not accelerate tumourigenesis in ApcMin mice. Gut 61 (10) , pp. 1435-1438. 10.1136/gutjnl-2011-300842

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Objective. Expression of the Wnt target gene ASCL2 is elevated in 78% of intestinal neoplasia datasets (Oncomine), suggesting a role for deregulated ASCL2 in the aetiology of intestinal tumourigenesis. Furthermore, ectopic expression of Ascl2 has previously been shown to lead to hyperplasia in the mouse. However, elevated levels of ASCL2 does not have an impact on the overall survival or recurrence-free survival rates in colorectal cancer patients. Here the authors use a novel mouse model to analyse the role of Ascl2 in intestinal tumourigenesis and address the controversy surrounding the relevance of this gene to the aetiology of colorectal cancer. Design. The authors have generated a mouse possessing a transgene carrying the Ascl2 gene together with its endogenous promoter and regulatory regions, thereby elevating Ascl2 expression in an authentic manner. The authors have further intercrossed these Ascl2 overexpressers to the classic ApcMin model, to study the consequence of elevated Ascl2 expression in intestinal tumourigenesis. Results. Here the authors genetically demonstrate that elevated expression of Ascl2 in a Wnt signalling dependent manner specifically in the stem cell compartment of the intestine neither increases tumour formation nor diminishes survival in a well established intestinal tumour model, the Apcmin mouse. Conclusion. The authors conclude that ectopic expression of Ascl2 is more important in the aetiology of neoplasia than overexpression of Ascl2.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
European Cancer Stem Cell Research Institute (ECSCRI)
Subjects: R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Publisher: BMJ Publishing Group
ISSN: 0017-5749
Last Modified: 06 Jan 2023 02:06

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