Abstract
Researchers have pinpointed metabolic alterations that may allow tumors to evade the IDO1 inhibitor epacadostat. Tumor cells enlisted an alternative pathway to break down tryptophan, the target of IDO1, and increased the activity of pathways that generate NAD+. The metabolic changes also suppressed CD8+ T cells.
©2022 American Association for Cancer Research
2022
American Association for Cancer Research
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