Abstract
The identification of a role for CYP4F2-dependent metabolism in driving immune evasion in non-small cell lung cancer reveals a strategy to improve the efficacy of immunotherapy by inhibiting CYP4F2. See related article by Van Ginderachter, p. 3882.
©2022 American Association for Cancer Research.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Arachidonic Acid / metabolism
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Carcinoma, Non-Small-Cell Lung*
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Catalysis
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Cytochrome P450 Family 4* / metabolism
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Humans
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Hydroxyeicosatetraenoic Acids / metabolism
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Immunosuppression Therapy
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Lung Neoplasms*
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Stromal Cells / metabolism
Substances
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Arachidonic Acid
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CYP4F2 protein, human
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Cytochrome P450 Family 4
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Hydroxyeicosatetraenoic Acids