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Understanding this duality is essential as endogenous NO within the tumor microenvironment may protect cancer cells from ferroptotic death, while exogenous, high-dose NO delivery represents a promising therapeutic strategy to forcibly induce it

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In addition, the rise in blood glucose levels of transplanted Insr P1195L/ +/HFD mice on re-feeding was significantly reduced compared with those of un-transplanted Insr P1195L/ +/HFD mice (Fig