Angiogenesis Status in Patients with Acute Myeloid Leukemia: From Diagnosis to Post-hematopoietic Stem Cell Transplantation

M Mohammadi Najafabadi, K Shamsasenjan, P Akbarzadehalaleh


As already proven in solid tumors, increased angiogenesis leads to increased number of blood vessels, resulting in unfavorable outcomes and resistance to chemotherapy. It was previously thought that angiogenesis plays no role in the pathogenesis of acute myeloid leukemia (AML), due to the fact that AML is a liquid tumor. However, many studies have suggested that increased angiogenesis has important roles in patients with AML, including increased numbers of vessels in bone marrow and pro-angiogenic factors, as well as decreased anti-angiogenic factors. Also a large number of studies demonstrated that a two-way communication is established between leukemic and endothelial cells, as a component of the vessel wall, in the bone marrow of patients with AML. These two cells support the survival and proliferation of each other through a paracrine pathway, resulting in resistance to chemotherapy. In addition, It is well-established that increased angiogenesis is associated with unfavorable prognosis, lower survival rate, resistance to chemotherapy, and relapse. Furthermore, increased angiogenesis affects the response to treatment, hematopoietic stem cell transplantation (HSCT) outcome and graft versus host disease (GVHD) occurrence. In this regard, this review will address vascular endothelial growth factor (VEGF) and angiopoietin (Ang), two of the most important angiogenic factors, in patients with AML before and after HSCT. By increasing our understanding of the role of endothelial cells and angiogenic factors in patients with AML from diagnosis to post-HSCT, new therapeutic strategies can be developed to reduce angiogenesis, improve patients’ survival and reduce complications.


Leukemia, myeloid, acute; Angiogenesis inducing agents; Vascular endothelial growth factor A; Endothelial cells; Hematopoietic stem cell transplantation

Full Text:


Copyright (c)

 pISSN: 2008-6482
 eISSN: 2008-6490


Creative Commons LicenseThis work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License