Single-cell profiling reveals reprogrammed hierarchy and disrupted immune-stromal ecosystem in
TP53-mutated AML

Acute myeloid leukaemia (AML) is a biologically heterogeneous blood cancer driven by abnormal proliferation of immature myeloid cells. Among its genetic subtypes, TP53-mutated AML is associated with complex cytogenetics, treatment resistance, and poor prognosis. TP53 plays a key role in maintaining genomic stability and regulating cell cycle and apoptosis. Its mutation leads to disrupted hematopoietic differentiation and aggressive disease behaviour. However, the impact of TP53 mutations on the bone marrow cellular ecosystem is not fully understood. Single-cell profiling enables detailed analysis of tumour heterogeneity and the interaction between leukemic cells and the immune-stromal microenvironment. In this study, we use single-cell approaches to explore how TP53 mutations reshape cellular hierarchy and disrupt immune-stromal balance in AML. From a patient education perspective, understanding AML at the molecular level helps improve awareness of disease severity, treatment response variability, and the importance of genetic testing for risk stratification. Clear communication about TP53 mutation status can guide expectations regarding prognosis and therapeutic options.

From a case report writing perspective, detailed clinical documentation combined with molecular and single-cell findings can provide valuable insights into rare or high-risk AML presentations. Such reports help highlight unique disease patterns, treatment challenges, and emerging diagnostic tools that contribute to medical literature and clinical decision-making.