What question did this study set out to answer?

This research aims to investigate the role of TREM1 in predicting chemotherapy resistance and prognosis in acute myeloid leukemia (AML), particularly in Egyptian patients.

May 16, 2026Open Access

Overexpression of TREM1 predicts poor prognosis and chemotherapy resistance in Egyptian acute myeloid leukemia associated with FLT3 internal tandem duplication and CD123 expression and stemness signatures

Key Points

This research aims to investigate the role of TREM1 in predicting chemotherapy resistance and prognosis in acute myeloid leukemia (AML), particularly in Egyptian patients.
Evaluated TREM1 expression in 50 newly diagnosed AML patients and 50 controls via flow cytometry.
Correlated TREM1 levels with molecular markers (FLT3-ITD, NPM1), immunophenotypic profiles (CD123), and clinical outcomes including remission and survival.
Conducted statistical analyses using ROC curves, Kaplan-Meier survival, and multivariate regression.
TREM1 expression was significantly higher in AML blasts (median 21%) compared to controls (15%, p = 0.01).
Elevated TREM1 (> 21%) predicted poor prognosis with 70% sensitivity and 75% specificity (AUC = 0.70, p = 0.04).
TREM1/FLT3-ITD co-expression resulted in a 5.4-fold increased mortality risk (p = 0.008).

Abstract

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.

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