PDGFRβ signaling cooperates with β-catenin to modulate c-Abl and biologic behavior of desmoid-type fibromatosis [microarray]

Unsupervised clustering of desmoid tumors and normal mesenchymal tissues was performed using henes associated with HIF1 activity. This accurately distiguished neoplastic tissues from normal controls The study sought to identify genes differentially expressed in desmoid-type fibromatosis as opposed to normal mesenchymal tissues. We noted that beta-catenin, the central driver in desmoid-type fibromatosis, appeared to regulate HIF1 signaling in in vitro studies. Genes associated with HIF1 and angiogenesis pathways were then used to perform unsupervised clustering on desmoid tumors and normal mesenchymal tissues. The genes accurately differentiated neoplastic and normal samples. Gene set enrichment analysis of desmoid cells treated with shRNA to knockdown CTNNB1 suggested that β-catenin altered HIF1 target expression and angiogenesis-related genes. These genes were used to perform unsupervised clustering on desmoid tumors and normal tissue analyzed by Affymetrix U133A 2.0 gene expression arrays.