Exploring the role of osteoblast-lineage cells in the evolutionary dynamics of acute myeloid leukemia through a stochastic differential equation model.

Acute myeloid leukemia (AML) is characterized by the uncontrolled proliferation of abnormal myeloid cells in the bone marrow and peripheral blood. In this study, we develop a stochastic differential equation model to capture the dynamic interactions among hematopoietic, osteoblastic, and leukemic cell populations within the bone marrow microenvironment. We calibrate model parameters using clinical data via an optimal control framework. Our study provides a mathematical framework to investigate how leukemic cells may remodel the heterogeneous bone marrow niche through dynamic interactions with osteoblastic lineages. This remodeling process disrupts both the quantity and functional capacity of hematopoietic populations, thereby offering insights into how leukemic-niche interactions may contribute to AML treatment failure. Furthermore, we evaluate the efficacy of combination therapies (traditional chemotherapy with targeted therapy) and compare their therapeutic outcomes. These findings offer a theoretical foundation for optimizing clinical strategies and advancing personalized treatment approaches for AML.