PDGFRβ signaling cooperates with β-catenin to modulate c-Abl and biologic behavior of desmoid-type fibromatosis.
Jia HuMeera R HameedNarasimhan P AgaramKarissa A WhitingLi-Xuan QinAnthony M VillanoRachael B O'ConnorJulian M RozenbergSonia CohenKatherine PrendergastSara KryeziuRichard L WhiteMitchell C PosnerNicholas D SocciMrinal M GounderSamuel SingerAimee M CragoPublished in: Clinical cancer research : an official journal of the American Association for Cancer Research (2023)
The β-catenin transcriptional target ABL1 is necessary for proliferation and maintenance of HIF1α in desmoid cells. Regulation of c-Abl activity by PDGF signaling and targeted therapies modulates desmoid cell proliferation, thereby suggesting a reason for variable biologic behavior between tumors, a mechanism for sorafenib activity in desmoids, and markers predictive of outcome in patients.
Keyphrases
- cell proliferation
- tyrosine kinase
- rheumatoid arthritis
- end stage renal disease
- chronic myeloid leukemia
- epithelial mesenchymal transition
- induced apoptosis
- newly diagnosed
- ejection fraction
- signaling pathway
- chronic kidney disease
- prognostic factors
- gene expression
- peritoneal dialysis
- transcription factor
- cell cycle
- pi k akt
- oxidative stress
- smooth muscle
- cell death
- vascular smooth muscle cells
- heat stress