Acute myeloid leukemia (AML) is defined as an aggressive disorder which is described by accumulation of immature malignant cells into the bone marrow. Chemokinereceptor axes are defined as factors involved in AML pathogenesis and prognosis. The chemokine receptor CXCR4 along with its ligand, CXCL12 fit in important players that are actively involved in the cross-talk between leukemia cells and bone marrow microenvironment. Therefore, according to the above introductory comments, in this review article, we have focused on delineating some parts played by CXCL12/CXCR4 axis in various aspects of AML malignancy. Targeting both leukemic and stromal cell interaction is nowadays accepted as a wide and attractive strategy for improving the outcome of treatment in AML in a non-cell autonomous manner. This strategy might be employed in a wide variety of AML patients regardless of their causative mutations. In addition to several potential targets involved in the disruption of malignant leukemic cells from their specific protective niches, compounds which interfere with CXCL12/CXCR4 axis have also been explored in multiple early-phase established clinical trials. Moreover, extensive research programs are exploring novel leading mechanisms for leukemia-stromal interactions that appear to find out novel therapeutic targets within the near future.

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The word of hemoglobinopathy is described for an array of disorders that affecting hemoglobin (Hb) functions. Hb is a molecule with 68 kDa molecular weight, serving as oxygen carrying metalloprotein. Hemoglobinopathy includes a wide range of Hb structural deficits varying from thalassemia to sickle cell disease. Cyto-chemokine network members are pivotally involved in the pathogenesis of hemoglobinopathies, however, the exact role of these mediators in the development of these disorders yet to be well addressed. Cytokines and chemokines are generated by inflamed endothelial cells that promote the expression of their respected receptors and further activate NF-κβ, recruit red blood cells (RBCs) and white blood cells (WBCs) toward the inflamed endothelium. Therefore, due to critical roles played by the cyto-chemokine network in several aspects of hemoglobinopathies pathophysiology including apoptosis of endothelial cells, RBC, WBC and etc.…, in the present review, we focused on the critical parts played by this network in the pathogenesis of hemoglobinopathies.

Background and objectives: Acute myeloid leukemia (AML) is a heterogeneous malignancy caused by various pathological mechanisms. Chemokines are involved in the initiation, progression, migration, survival, treatment and complications of AML. CXCL1 has an indirect effect on the progression of cancer and CXCL10 produced by leukemia cells attracts natural killer cells toward tumor sites to eradicate cancer cells. The present study investigated effects of chemotherapy on serum levels of CXCL1 and CXCL10 in patients with AML.Methods: Throughout this case-control study, blood samples were collected from AML patients with M4/M5 subtype (n=25) before and after the first stage of a chemotherapy regimen (7+3). Serum levels of the chemokines were determined using commercial ELISA kits. Data were analyzed using two-sample and paired T-test in SPSS 22 software.Results: The level of CXCL10 was high in patients but decreased following chemotherapy. After the chemotherapy the patients attained partial remission. However, the level of CXCL1 did not change in the patients. Conclusion:Although chemotherapy could decrease CXCL10 levels and induce partial remission, CXCL1 levels does not change in AML patients with M4/M5 subtype. Based on the results, the employment of CXCL1 and CXCL10 inhibitors in the chemotherapy regimen could prevent relapse in the later stages or even reduce the duration of treatment.