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- W2968476411 endingPage "1926" @default.
- W2968476411 startingPage "1926" @default.
- W2968476411 abstract "Glutathione (GSH) is the predominant low-molecular-weight antioxidant with a ubiquitous distribution inside the cell. The steady-state level of cellular GSH is dependent on the balance between synthesis, hydrolysis, recycling of glutathione disulphide (GSSG) as well as cellular extrusion of reduced, oxidized, or conjugated-forms. The augmented oxidative stress typical of cancer cells is accompanied by an increase of glutathione levels that confers them growth advantage and resistance to a number of chemotherapeutic agents. Targeting glutathione metabolism has been widely investigated for cancer treatment although GSH depletion as single therapeutic strategy has resulted largely ineffective if compared with combinatorial approaches. In this review, we circumstantiate the role of glutathione in tumour development and progression focusing on how interfering with different steps of glutathione metabolism can be exploited for therapeutic purposes. A dedicated section on synthetic lethal interactions with GSH modulators will highlight the promising option of harnessing glutathione metabolism for patient-directed therapy in cancer." @default.
- W2968476411 created "2019-08-22" @default.
- W2968476411 creator A5005428894 @default.
- W2968476411 creator A5007336855 @default.
- W2968476411 creator A5051452016 @default.
- W2968476411 date "2019-08-16" @default.
- W2968476411 modified "2023-10-06" @default.
- W2968476411 title "Targeting Glutathione Metabolism: Partner in Crime in Anticancer Therapy" @default.
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- W2968476411 doi "https://doi.org/10.3390/nu11081926" @default.
- W2968476411 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6724225" @default.
- W2968476411 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31426306" @default.
- W2968476411 hasPublicationYear "2019" @default.
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