Loading
Life sciences · Journal article
Frontiers in Oncology · October 12, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Background Acute myeloid leukemia (AML) with monocytic differentiation (FAB M4/M5 subtypes) is a distinct subtype of pediatric AML characterized by aggressive clinical behavior and common extramedullary involvement. Despite therapeutic advances, outcomes remain suboptimal, particularly in resource-limited settings. The study aimed to evaluate the clinical characteristics, treatment outcomes, and prognostic markers in pediatric patients with AML, FAB M4/M5 subtypes. Patients and methods A retrospective cohort study analyzing 193 patients with AML, FAB M4/M5 subtypes diagnosed at the Children’s Cancer Hospital, Egypt-57357 (CCHE-57357) between January 2016 and December 2021. Results The cohort comprised 131 patients with M4 and 62 with M5 morphology. Median follow-up was 62.0 months among survivors and 37.6 months for the entire cohort. Three- and five-year OS were 53.1% and 48.3%; three- and five-year EFS were 48.2% and 45.5%. Five-year CIR was 23.8%. Forty-eight patients (24.9%) died during induction. Multivariate Cox regression identified MRD positivity after first induction (HR 2.868, 95% CI 1.133–7.260, p = 0.026) and monosomy 7 (HR 6.206, 95% CI 2.692–14.306, p < 0.001) as independent adverse prognostic factors. Conversely, inv(16)(p13.1;q22) or t(16;16)(p13.1;q22); CBFB::MYH11 was an independent favorable prognostic factor (HR 0.253, 95% CI 0.108–0.592, p = 0.002). 14 high-risk pediatric AML patients underwent HSCT post-induction; three experienced adverse outcomes, comprising relapses ( n = 2), and acute GVHD ( n = 1). Conclusion Genetic findings and treatment response were associated with outcome, supporting a complete diagnostic assessment. Improving survival requires precise risk stratification, MRD-guided therapy, and robust supportive care.