ArticleCell death & disease2026
Branching architecture of tryptophan metabolism determines therapeutic vulnerability in acute myeloid leukemia.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute myeloid leukemia (AML) exhibits metabolic reprogramming that supports immune evasion and treatment resistance. The kynurenine pathway (KP) is a key regulator of tumor-immune interactions, yet its downstream organization and clinical relevance in AML remain unclear. Here, we combined in vitro models with patient serum profiling to determine whether KP branching patterns are associated with treatment response. Extracellular KP metabolites were quantified in AML cell lines (HL-60 and MOLM-14) following induction regimens, and quantified circulating KP metabolites in patient serum samples collected from AML patients before and after induction therapy. Treatment was associated with normalization of tryptophan depletion and kynurenine accumulation in responders, indicating partial restoration of systemic KP homeostasis. Notably, baseline (pre-treatment) samples from patients who were later classified as non-responders exhibited a distinct metabolic phenotype characterized by persistent kynurenine elevation, increased anthranilic and kynurenic acid levels, and enrichment of 3-hydroxykynurenine flux, suggesting preferential engagement of oxidative and immunomodulatory KP branches. Among evaluated metabolic indices, the 3-hydroxykynurenine-to-kynurenine ratio demonstrated the strongest discriminatory capacity for distinguishing response to induction therapy (DA: daunorubicin + cytarabine; DAC: daunorubicin + cytarabine + cladribine), outperforming individual metabolite measurements and highlighting functional pathway flux rather than absolute metabolite abundance as a determinant of clinical outcome.
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