Abstract
Similar to solid tumors, acute leukemia growth induces neo-vascularization (angiogenesis) within the bone marrow (BM) microenvironment. Several studies have shown that acute myeloid leukemia (AML) cells release angiogenic growth factors such as vascular endothelial growth factor (VEGF) within the BM. In turn, AML growth and expansion involves the activation of BM vessels, resulting in a paracrine stimulation of leukemia, similar to what is seen in solid neoplasms. In addition, we and others have shown that subsets of acute leukemias also express VEGF receptors; in these cases, autocrine stimulation of leukemia cells by VEGF may result in proliferation, migration and resistance to chemotherapy.1, 2, 3 Therefore, exposure of the BM microenvironment to increased VEGF levels may in fact contribute toward leukemia expansion via paracrine or autocrine stimulation of subsets of leukemia cells.
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