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(A) Passive targeting. Liposomes leave the blood circulation and accumulate in the tumor vicinity via the EPR effect, which relies on the tumor’s defective vasculature and lymphatic drainage system. Then, the drug diffuses out of the liposomes and enters the cancer cells; (B) active targeting. After passive targeting, cancer cells internalize the liposomes via receptor-mediated endocytosis. The latter is induced by the ligand–receptor interactions between cancer cells and liposomes.
