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 Cajal (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 FOXD3 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.