ArticleDiscover oncology2026
Integrated FHIT and IDH2 biomarker profiling predicts lethal sensitivity to DCPS inhibition in Acute Myeloid Leukemia and Myelodysplastic syndrome.
Article in Discover oncology, 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
BACKGROUND/
objectivesDevelopment of novel therapies for acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) is hindered by limited biomarkers to identify appropriate target populations and poor translatability of preclinical drug candidates. In this study, we sought to validate Fragile histidine triad diadenosine triphosphate (FHIT) deficiency as a predictive biomarker for decapping scavenger enzyme (DCPS)-targeted therapy in AML and MDS, and to identify clinically accessible proxy biomarkers.
methodsWe analyzed primary AML samples treated with the DCPS small-molecule inhibitor RG3039 to identify additional biomarkers beyond FHIT that predict treatment response. We analyzed a large cohort of clinical and multi-omics AML and MDS datasets to define FHIT-low prevalence and stratify patient populations eligible for DCPS-targeted therapy.
resultsLow FHIT expression predicted effective therapeutic response to DCPS inhibition; however, hydroxyurea pretreatment confounded the predictive value of FHIT. FHIT-low expression occurred in 5–24% of AML patients, with highest prevalence in pediatric populations (24.4%). In MDS, FHIT promoter methylation was present in 35.8% of patients and remained stable during treatment with the hypomethylating agent azacitidine, supporting MDS as a potential therapeutic indication. IDH2 mutation status served as a proxy biomarker for FHIT expression and DCPS sensitivity in AML.
conclusionsFHIT expression levels predict sensitivity to DCPS inhibition and a large proportion of adult and pediatric AML as well as MDS patients are eligible for DCPS-targeted therapy. IDH2 mutation status is a clinically accessible proxy biomarker for predicting FHIT expression levels and sensitivity to DCPS inhibition in AML.
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