Abstract

ABSTRACT Bone marrow microenvironment provides critical regulatory signals for lineage differentiation and maintenance of HSC quiescence, and these signals also contribute to hematological myeloid malignancies. Macrophages exhibit high phenotypic heterogeneity under both physiological and pathological conditions and are mainly divided into proinflammatory M1 and anti-inflammatory M2 macrophages. Furthermore, osteoclasts are multinucleated giant cells that arise by fusion of monocyte/macrophage-like cells, which are commonly known as bone macrophages. Emerging evidence suggests that macrophages and osteoclasts originating from myeloid progenitors lead to two competing differentiation outcomes, and they appear to play an important role in the onset, progression, and bone metastasis of solid cancers. However, little is known about their role in the development of hematological malignancies. In this review, we focus on macrophages and osteoclasts, their role in leukemia, and the potential for targeting these cells in this disease.

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