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. 2022 Feb 15;13:768606. doi: 10.3389/fimmu.2022.768606

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Copyright © 2022 Saito, Andrade, Bustos and Chammas

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Intracellular and intercellular consequences of altered phosphatidylcholine (PtdCho) metabolism that impacts response to therapy. Increased PtdCho metabolism supports cancer cell accelerated growth by providing the major cellular membrane component. Additionally, PtdCho promotes intracellular events that mediate resistance to therapy, such as DNA repair, lipid droplet synthesis, and autophagy process. PtdCho-derived lipid mediators are prominent drivers of resistance. They are recognized by their cognate receptors present both in cancer cells and immune microenvironment cells, driving cancer cell survival and proliferation and promoting immunosuppression. Created with BioRender.com.