Anisms in leukemic B-cells that could alter the phagocytic capacity of macrophages upon CIT. Solutions: The proteomic profile of handle and TP53deficient leukemic B-cells, untreated or treated with mafosfamide, was analysed by mass spectrometry. EVs had been isolated from control and TP53-deficient leukemic B cells by differential ultracentrifugation and their proteomic content was evaluated by mass spectrometry. Validation of protein expression was performed by Western Blot and flow VCAM-1/CD106 Proteins custom synthesis cytometry. The measurements of exosomes concentration and size distribution had been performed by NanoSight NS300 and ZetaView. Outcomes: 244 of 5785 proteins had been observed to be drastically different amongst TP53-deficient and handle leukemic B-cells, with 159 independent of mafosfamide remedy, 147 associated to mafosfamide and 86 modifications shared in between DMSO and mafosfamide therapy. Enrichment analysis for GO terms showed that TP53-deficient leukemic B-cells exhibited mostly altered expression of proteins linked with EVs. We confirmed that TP53-deficient leukemic Bcells developed greater concentration of EVs and that the EV-protein content differed from control leukemic B-cells. Notably, 1239 of 2663 proteins had been significantly various among TP53-deficient and handle leukemic B-cells, 68 were exclusively detected within the control-derived EVs and 128 proteins were only located within the TP53-deficient-related EVs Summary/Conclusion: The loss of TP53 drastically modifies the proteomic profile of leukemic B-cells and influences the protein expression of leukemic Bcells upon mafosfamide remedy. In particular, the loss of TP53 regulates the EV-related protein expression and EV production in leukemic B-cellsISEV2019 ABSTRACT BOOKPF02: EVS within the Central and Posted inUncategorized