ArticleBiomarker research2026
A gene signature derived from leukemia associated macrophages provides a compelling risk stratification for human AML patients.
Article in Biomarker research, 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
In a mouse model of FGFR1-driven leukemia, we demonstrated a role for circulating non-conventional monocyte-derived macrophages in the peripheral blood, which suppressed T-cell function and promoted leukemogenesis. A single cell RNA sequencing (scRNA-Seq) analysis of these leukemia-associated macrophages (LAMs) identified LAM-specific dysregulation of gene expression associated with leukemogenesis. Based on the top markers identified in these LAMs, we generated a LAM score based on the expression levels of a 32 gene signature. This scoring system was then applied to the transcriptomic data from a cohort of 838 newly diagnosed patients treated on Alliance/CALGB protocols, who were similarly treated with intensive cytarabine/daunorubicin-based chemotherapy on the CALGB/Alliance for the Clinical Trials in Oncology protocol. Patients were subclassified as those with high and low LAM scores. Patients with a high LAM score had shorter overall survival, disease-free survival and event-free survival compared to those with a low LAM score. We also noted a strong association of FLT3-ITD, RUNX1 and TP53 mutations with high LAM scores. Applying the LAM score to the current European Leukemia Network risk group criteria, independent prognostic implications and a refined prognostic significance of each subgroup were provided, indicating the value of including immune microenvironment data into AML risk stratification.
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