Author(s): Dr. Haggag R
Acute Myeloid Leukemia (AML) is an aggressive hematologic malignancy characterized by accumulation of immature malignant myeloid cells in the bone marrow and blood due to their clonal proliferation without substantial maturation [1]. Angiogenesis is the formation of new vessels from an existing network of vasculature [2]. Irrespective of cellular origin, induction of angiogenesis requires a shift/switch towards activation/upregulation of inducers of angiogenesis over suppression of angiogenic inhibitors (hereafter AI). Some key angiogenic activators include vascular endothelial growth factor A hereafter VEGF (VEGF-A) [3], Matrix Metalloproteinases (MMPs), Placenta Growth Factor (PlGF), Fibroblast Growth Factor (FGF) and Hepatocyte Growth Factor (HGF) [4]. Endogenous inhibitors of angiogenesis include Thrombospondins (THSBs) endostatin, angiostatin and cytokines such as interleukin- 12 [5]. The crucial role of angiogenesis in the growth, persistence, and metastases of solid tumors has been indicated in many studies [6,7]. There is mounting evidence that angiogenesis is also significant in leukemia [8].
