Fig. 1.

Activating PDGFRA mutations differentially promote malignant phenotypes. a Functional activity of a series of PDGFRA mutations in the transient transfection assay using Ba/F3. The transformation activity of each mutation was tested at least three times. The cell viability in the absence of IL-3 of duplicates was measured 7 days after infection with lentiviral virus carrying PDGFRA WT or mutants and presented relative to that of cells expressing PDGFRA WT (Dunnett’s multiple comparisons test). b The distribution of PDGFRA missense mutations in the GENIE dataset across different domains. Total number of PDGFRA missense mutations per tumor type is shown in the middle of each chart. c Expression of PDGFRA WT and mutants in MCF10A stable cell lines was examined by western blot. d Relative cell proliferation of MCF10A parental and cells stably expressing PDGFRA WT or mutants in the absence of EGF/insulin was measured every 24 h. The cell proliferation of three independent replicates relative to day 0 are presented as mean ± SD (exponential growth equation). e MCF10A parental, PDGFRA WT, and mutant expressing cells were grown 3D in growth factor-reduced Matrigel for 10 days. Bar, 100 μm.The size of 50 spheroids are presented as mean ± SD (Dunnett’s multiple comparisons test). f The cell motility of MCF10A parental, PDGFRA WT, and mutant expressing cells was assessed by Boyden chamber migration assay using 5% serum as chemoattractant for 20 h. The number of migrated cells in five fields of each replicate were quantified and presented as mean ± SD (Dunnett’s multiple comparisons test). **p > 0.01; ***p > 0.001