EVs from mutant p53-expressing carcinoma cells generate pro-invasive/migratory niches in metastatic target organs (such as the lung), by influencing deposition of fibrillar ECM components, such as fibronectin and collagen.5 However, brain ECM is composed primarily of proteo- and glycosamino-glycans and is largely devoid of fibrillar proteins.30 We, therefore, used a panel of lectins and reagents recognizing carbohydrate moieties (such as HABP and anti-chondroitin sulfate) to screen for EV-driven alterations to glycan/polysaccharide species in ECM deposited by astrocytes. Here, TP53 is linked to carcinoma.