Embryonic stem cell factor FOXD3 (Genesis) defects in gastrointestinal stromal tumors

Gastrointestinal stromal tumors (GIST) are mesenchymal neoplasms, believed to originate from the interstitial cells of <i>Cajal</i> (ICC), often caused by overexpression of tyrosine kinase receptors (TKR) KIT or PDGFRA. FOXD3 suppresses KIT expression in human cells; its inactivation led to an increase in ICCs in zebrafish, as well as mice, providing evidence for a functional link between <i>FOXD3</i> defects and KIT overexpression leading to GIST formation.1- MassArray data on different FOXD3 amplicons. Raw data used in FOXD3 methylation analysis of GIST and paraganglioma samples presented in figure 1C.2- Protein quantification in Paraganglioma (PGL) and GIST samples. Measurements of band densitometry to analyze FOXD3 expression in PGL and GIST samples presented in figure 2A.3- Luciferase assay to determine FOXD3 activation. Raw data of Luciferase assay performed to study protein activation in different FOXD3 variants. Data is presented in fig 3A.4- Measurements of band densitometry to analyze FOXD3 and c-Kit protein expression in HEK and NTERA-2 cells after FOXD3 siRNA assay. Raw data used in the HEK293 and NTERA-2 Protein quantification analysis in the fig 3B.5- Positive c-kit cells quantification after c-kit immunostaining in inner circular muscularis and outer longitudinal muscularis of interstitial cells of Cajal of wild type and FOXD3+/- mice. Data is presented in figure 5B. Raw data of muscle thickness measurement of the ileum of wild type and FOXD3+/- mice. Data is presented in figure 5C.