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- W4309438093 abstract "Anti-PD(L)1 immunotherapy recently arises as an effective treatment against triple-negative breast cancer (TNBC) but is only applicable to a small portion of TNBC patients due to the low PD-L1 expression and the immunosuppressive tumor microenvironment (TME). To address these challenges, a multifunctional drug-like copolymer that possesses the auto-changeable upper critical solution temperature and the capacity of scavenging reduced nicotinamide adenine dinucleotide phosphate (NADPH) inside tumor cells is synthesized and employed to develop a hypoxia-targeted and BMS202 (small molecule antagonist of PD-1/PD-L1 interactions)-loaded nanomedicine (BMS202@HZP NPs), combining the anti-PD-L1 therapy and the low-dose radiotherapy (LDRT) against TNBC. In addition to the controlled release of BMS202 in the hypoxic TNBC, BMS202@HZP NPs benefit the LDRT by upregulating the pentose phosphate pathway (PPP, the primary cellular source for NADPH) of TME whereas scavenging the NADPH inside tumor cells. As a result, the BMS202@HZP NPs-mediated LDRT upregulate the PD-L1 expression of tumor to promote anti-PD-L1 therapy response while reprogramming the immunometabolism of TME to alleviate its immunosuppression. This innovative nanomedicine-mediated radio-immunometabolism regulation provides a promising strategy to reinforce the anti-PD-L1 therapy against TNBC." @default.
- W4309438093 created "2022-11-27" @default.
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- W4309438093 date "2022-11-20" @default.
- W4309438093 modified "2023-10-16" @default.
- W4309438093 title "NADPH Selective Depletion Nanomedicine‐Mediated Radio‐Immunometabolism Regulation for Strengthening Anti‐PDL1 Therapy against TNBC" @default.
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- W4309438093 doi "https://doi.org/10.1002/advs.202203788" @default.
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