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Peer-reviewedCC BY 4.0Frontiers in Oncology

Malignant remodeling of the bone marrow microenvironment in acute myeloid leukemia: mechanisms and therapeutic implications

  • Wenhao Xu1
  • Qing Han1
  • Changrong Sun1
  • Daqi Li1,2
  1. 1Shandong Second Medical University
  2. 2Jinan Central Hospital
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Abstract

Acute myeloid leukemia (AML) is an aggressive clonal myeloid malignancy characterized by the expansion of differentiation-arrested blasts. Treatment resistance, measurable residual disease, and relapse remain major causes of treatment failure. Experimental and clinical evidence indicates that the bone marrow microenvironment can protect heterogeneous AML-cell populations and can also sustain functionally defined or stem-enriched leukemic stem cell (LSC) populations through partly overlapping but non-identical mechanisms. Under physiological conditions, stromal, vascular, neural, and immune components coordinate hematopoietic stem-cell quiescence, retention, and regeneration. In AML, bulk leukemia cells remodel stromal, vascular, extracellular-matrix, metabolic, and immune compartments, whereas LSC-focused studies specifically implicate niche-dependent homing, quiescence, self-renewal, and persistence. This review therefore distinguishes evidence obtained in bulk AML cells from evidence obtained in functionally defined or stem-enriched LSC populations, compares conserved and disease-specific remodeling programs, and summarizes niche-directed therapeutic strategies.

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Cite

BibTeXRIS
BibTeX
@article{xu2026malignant,
  title = {{Malignant remodeling of the bone marrow microenvironment in acute myeloid leukemia: mechanisms and therapeutic implications}},
  author = {Wenhao Xu and Qing Han and Changrong Sun and Daqi Li},
  journal = {Frontiers in Oncology},
  year = {2026},
  month = oct,
  doi = {10.3389/fonc.2026.1903019},
  url = {https://www.frontiersin.org/articles/10.3389/fonc.2026.1903019/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Malignant remodeling of the bone marrow microenvironment in acute myeloid leukemia: mechanisms and therapeutic implications
AU  - Wenhao Xu
AU  - Qing Han
AU  - Changrong Sun
AU  - Daqi Li
PY  - 2026
DA  - 2026/10/19
JO  - Frontiers in Oncology
DO  - 10.3389/fonc.2026.1903019
UR  - https://www.frontiersin.org/articles/10.3389/fonc.2026.1903019/full
AB  - Acute myeloid leukemia (AML) is an aggressive clonal myeloid malignancy characterized by the expansion of differentiation-arrested blasts. Treatment resistance, measurable residual disease, and relapse remain major causes of treatment failure. Experimental and clinical evidence indicates that the bone marrow microenvironment can protect heterogeneous AML-cell populations and can also sustain functionally defined or stem-enriched leukemic stem cell (LSC) populations through partly overlapping but non-identical mechanisms. Under physiological conditions, stromal, vascular, neural, and immune components coordinate hematopoietic stem-cell quiescence, retention, and regeneration. In AML, bulk leukemia cells remodel stromal, vascular, extracellular-matrix, metabolic, and immune compartments, whereas LSC-focused studies specifically implicate niche-dependent homing, quiescence, self-renewal, and persistence. This review therefore distinguishes evidence obtained in bulk AML cells from evidence obtained in functionally defined or stem-enriched LSC populations, compares conserved and disease-specific remodeling programs, and summarizes niche-directed therapeutic strategies.
SN  - 2234-943X
ER  -