F how a standard marrow works to suppress early cancer. As leukemia develops the cross-talk among AML and its microenvironment alters the MSCs to promote a survival signal favouring AML growth. Future operate involves the capacity of AML-derived EVs to alter the phenotype of normal marrow towards a pro-leuekmic phenotype. Employing mathematical models to quantify and eventually predict these changes makes it possible for for precise therapeutic intervention. Funding: This perform was funded by NIH [T32 Grant].PF02.Endocytosis and intracellular trafficking of prostate Acid Phosphatase Proteins Formulation cancer exosomes Alex Cocks1; Hope Roberts-Dalton1; Philip Lewis1; Jason P. Webber2; Rachel Errington2; Peter Watson1; Arwyn Jones1; Aled ClaytonCardiff University, Cardiff, UK; 2Tissue Microenvironment Group, Division of Cancer and Genetics, College of Medicine, Cardiff University, Cardiff, UKBackground: Prostate cancer exosomes interact with fibroblasts within the tumour microenvironment to stimulate myofibroblast differentiation, producing a stroma that supports tumour development. We propose that uptake of prostate cancer exosomes and delivery of their cargo for the fibroblast is expected to generate this illness promoting phenotype. The microscopy tactics offered enable us to identify the fate of your exosome following uptake. Understanding the uptake kinetics of exosomes and their intracellular trafficking might deliver insights into how exosomes induce myofibroblast differentiation, and how they may very well be manipulated therapeutically. Techniques: A novel thiol based labelling strategy was carried out to allow visualization and quantification of exosomes taken up by fibroblasts, by fluorescence microscopy and flow cytometry respectively. The endocytic routes applied by exosomes to obtain entry to fibroblasts was determined utilising siRNA mediated knockdowns of endocyticFriday, 04 Mayregulators, and intracellular trafficking of the exosomes was monitored by time-lapse microscopy. Final results: Fluorescent thiol labelling enables visualization of exosomes, but does not have an effect on the exosome function with respect to myofibroblast differentiation. Exosomes are taken up by fibroblasts through Clathrin mediated endocytosis and targeted traffic towards lysosomes. Modulation of exosome uptake by way of interference using the exosome surface is ongoing. Summary/Conclusion: Endocytosis of exosomes is often perturbed by targeting regulators of endocytosis, as well as proteins around the exosome surface revealing that uptake of exosomes by fibroblasts may be modulated. Utilising diverse microscopy methods clarifies the fate on the exosome within the fibroblast. The influence of uptake inhibition on the capability for fibroblasts to differentiate into pro-tumoural myofibroblasts is at present getting examined. Funding: This project is funded by Tenovus Cancer CarePF02.Lysosomal inhibition in triple-negative breast cancer cells alters exosome composition and function Jing Xu1; Shane Colborne1; Elham MMP-11 Proteins manufacturer Hosseini-Beheshti2; Emma Guns3; Gregg Morin4; Sharon Gorski1Canada’s Michael Smith Genome Sciences Centre, Vancouver, Canada; Vancouver Prostate Centre, Sydney, Australia; 3Vancouver Prostate Centre, Vancouver, Canada; 4Canada’s Michael Smith Genome Sciences Centre, Vancouver, CanadaBackground: Viruses are capable of manipulating host endosomal-exosomal pathways which can aid in tumourigenesis. Human papilloma virus (HPV) encoded proteins can alter the production and cargo of extracellular vesicles (EVs) secreted by cervical cancer cells. Even so, the ext.