Fas/CD95 deficiency in ApcMin/+ mice increases intestinal tumor burden

Citations of this article
Mendeley users who have this article in their library.


Background: Fas, a member of the tumor necrosis family, is responsible for initiating the apoptotic pathway when bound to its ligand, Fas-L. Defects in the Fas-mediated apoptotic pathway have been reported in colorectal cancer. Methodology/Principal Findings: In the present study, a variant of the Apc Min/+ mouse, a model for the human condition, Familial Adenomatous Polyposis (FAP), was generated with an additional deficiency of Fas (Apc Min/+/Faslpr) by crossbreeding ApcMin/+ mice with Fas deficient (Faslpr) mice. One of the main limitations of the Apc Min/+ mouse model is that it only develops benign polyps. However, ApcMin/+/Faslpr mice presented with a dramatic increase in tumor burden relative to ApcMin/+ mice and invasive lesions at advanced ages. Proliferation and apoptosis markers revealed an increase in cellular proliferation, but negligible changes in apoptosis, while p53 increased at early ages. Fas-L was lower in ApcMin/+/Faslpr mice relative to ApcMin/+ cohorts, which resulted in enhanced inflammation. Conclusions/Significance: This study demonstrated that imposition of a Fas deletion in an ApcMin/+ background results in a more aggressive phenotype of the ApcMin/+ mouse model, with more rapid development of invasive intestinal tumors and a decrease in Fas-L levels. © 2010 Guillen-Ahlers et al.




Guillen-Ahlers, H., Suckow, M. A., Castellino, F. J., & Ploplis, V. A. (2010). Fas/CD95 deficiency in ApcMin/+ mice increases intestinal tumor burden. PLoS ONE, 5(2). https://doi.org/10.1371/journal.pone.0009070

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free