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- W3141524818 endingPage "108944" @default.
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- W3141524818 abstract "Inhibitors of cyclin-dependent kinases 4 and 6 (CDK4/6i) delay progression of metastatic breast cancer. However, complete responses are uncommon and tumors eventually relapse. Here, we show that CDK4/6i can enhance efficacy of T cell-based therapies, such as adoptive T cell transfer or T cell-activating antibodies anti-OX40/anti-4-1BB, in murine breast cancer models. This effect is driven by the induction of chemokines CCL5, CXCL9, and CXCL10 in CDK4/6i-treated tumor cells facilitating recruitment of activated CD8+ T cells, but not Tregs, into the tumor. Mechanistically, chemokine induction is associated with metabolic stress that CDK4/6i treatment induces in breast cancer cells. Despite the cell cycle arrest, CDK4/6i-treated cells retain high metabolic activity driven by deregulated PI3K/mTOR pathway. This causes cell hypertrophy and increases mitochondrial content/activity associated with oxidative stress and inflammatory stress response. Our findings uncover a link between tumor metabolic vulnerabilities and anti-tumor immunity and support further development of CDK4/6i and immunotherapy combinations." @default.
- W3141524818 created "2021-04-13" @default.
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- W3141524818 date "2021-04-01" @default.
- W3141524818 modified "2023-10-17" @default.
- W3141524818 title "Metabolic modulation by CDK4/6 inhibitor promotes chemokine-mediated recruitment of T cells into mammary tumors" @default.
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- W3141524818 doi "https://doi.org/10.1016/j.celrep.2021.108944" @default.
- W3141524818 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8383195" @default.
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