Fig. 7: Chemotherapy with anthracyclines induces ATP release in the tumor microenvironment.

P2X7RA expressed by AML blasts in the presence of high ATP concentration mediates the opening of a large nonselective pore facilitating intracellular uptake of anticancer drugs that induce cell death. On the other hand, the increase of ATP allows the proliferation of P2X7RB expressing blasts, unable to form the cytotoxic pore but still able to activate the channel function of the receptor that protect cells from chemotherapy-dependent death and favors the relapse of AML.