Remodeling the marrow fat niche: BMAT in cancer bone metastases and hematological malignancies.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Bone marrow adipose tissue (BMAT) is a dynamic component of the marrow microenvironment that influences tumor persistence, therapy response, and skeletal integrity. Recent work shows that marrow adipocytes function not only as metabolic partners for malignant cells but also as stress-responsive components of bone marrow niche remodeled by tumor progression and cancer therapy. Reciprocal signaling between tumor cells and adipogenic lineage populations alters lipid mobilization, redox balance, and stromal differentiation, creating microenvironments that support tumor cell survival under metabolic and therapeutic stress. Cancer therapies can reprogram adipocyte and stromal populations, generating inflammatory or senescent niches that persist beyond active disease and influence residual tumor behavior. At the same time, adipogenic cells contribute to marrow repair, highlighting the need to distinguish regenerative from tumor-permissive states. Spatial heterogeneity across skeletal sites, and its evolution during treatment, adds an additional layer of complexity to how BMAT regulates tumor behavior in bone. Here, we review recent advances that are redefining the role of BMAT in cancer progression and therapy response.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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