. Pharmacological inhibition of BACE1 suppresses glioblastoma growth by stimulating macrophage phagocytosis of tumor cells. Nature Cancer, November 8, 2021

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  1. This paper raises the exciting possibility of a second life for BACE inhibitors in glioblastoma treatment.

    Additionally, the paper suggests that BACE1 may have more substrates/functions than anticipated, and that they may not be restricted to neurons, where BACE1 is highly expressed. Whether such additional substrates will be cleaved in a healthy tissue or specifically in the context of disease or inflammation remains to be seen.

    The potential use of BACE inhibitors for glioblastoma should be further investigated. Given the possibility of off-target effects of drugs and shRNAs, I would specifically like to see a confirmation using BACE1-deficient mice. I’d also like to see the test of whether BACE2, which is also inhibited by BACE1-targeted drugs, may also be involved.

    View all comments by Stefan Lichtenthaler

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