The role of type 1 interferon signaling in the pathogenesis of aggressive fibromatosis.
Published: 2007
Language: eng
Number of pages: 100
ISBN-13: 9780494273753
Description: Aggressive fibromatosis (also called desmoid tumor) is a benign locally invasive soft tissue tumor of mesenchymal origin. This difficult to treat tumor is characterized by increased levels of beta-catenin mediated Tcf-dependent transcriptional activation due to mutations in components of the canonical WNT signaling pathway. We found that type 1 interferon signaling is activated and associated response genes upregulated in human and murine aggressive fibromatosis tumors and that their expression is regulated by beta-catenin. We hypothesized that type 1 interferon signaling promotes tumor formation in aggressive fibromatosis and when mice deficient for the type 1 interferon receptor (Ifnar 1 -/-) were crossed with mice predisposed to aggressive fibromatosis tumor formation (Apc/Apc1638N), a significant decrease in tumor formation was observed compared to littermate controls. In addition, we found that Ifnar 1 -/- mice have fewer numbers of mesenchymal progenitor cells compared to littermate controls. This suggests that type 1 interferon signaling may play a role in regulating the pool of mesenchymal progenitor cells and in turn presents a potential mechanism by which this pathway affects tumorigenesis in aggressive fibromatosis.
Notes: Source: Masters Abstracts International, Volume: 45-06, page: 3036.

Thesis (M.Sc.)--University of Toronto, 2007.

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