TP53 and neoplasm: Moreover, exosome-mediated transfer of these migratory characteristics to fibroblasts was opposed by CRISPR-mediated disruption of Rab35 or PODXL (Supplementary Figure 4b) or overexpression of PODXL-GFP in H1299-p53R273H donor cells (Supplementary Figure 5d), indicating that control of PODXL levels in tumour cells is required for the transfer of mutant p53’s migratory phenotype to fibroblasts (Fig. 5b).