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. • BMAT is a dynamic regulator of tumor persistence in bone • BMAT is dynamically remodeled by tumors and therapies • Adipocyte-rich marrow niches coordinate tumor stress-adaptive programs • Spatially distinct BMAT states may influence risk of progression and relapse • Distinguishing reparative vs tumor-permissive BMAT is critical
Izabela Podgorski (Fri,) studied this question.