Despite advances, over half of AML patients relapse or become refractory to chemotherapy. TREM1 (CD354), a regulator of tumor inflammation and immune evasion in solid cancers, remains poorly characterized in AML, especially in underrepresented populations like Egyptians. We aimed to evaluate TREM1 expression in de novo AML, its association with high-risk features (FLT3-ITD, CD123), and its prognostic impact on treatment response and survival. In this prospective case-control study, TREM1 expression was quantified via flow cytometry (APC-conjugated anti-CD354) in 50 newly diagnosed AML patients and 50 matched controls. Patients were risk-stratified per ELN 2022 guidelines and treated with standard induction chemotherapy. TREM1 levels (CD45dim/SSC-low blasts) were correlated with molecular markers (FLT3-ITD, NPM1, cytogenetics), immunophenotypic profiles (CD2/CD7/CD19/CD56/CD123), and clinical outcomes (remission, survival). Statistical analyses included ROC-derived thresholds, Kaplan-Meier survival, and multivariate regression (SPSS v20.0). Key findings revealed significant TREM1 overexpression in AML blasts (median 21% IQR: 12.8–43%) compared to controls (15% 13–18%; p = 0.01). Elevated TREM1 expression (> 21%) robustly predicted adverse prognosis (70% sensitivity, 75% specificity; AUC = 0.70, p = 0.04), chemotherapy resistance (non-complete remission: 77.8% sensitivity, 87% specificity; AUC = 0.80, p 21%) may enhance risk stratification, while its immunomodulatory function underscores its potential as a therapeutic target. Future studies should validate these findings in larger, multiethnic cohorts and explore the mechanistic links between TREM1 and AML pathogenesis.
Mansor et al. (Thu,) studied this question.