Significance of CXCL12/CXCR4 Ligand/Receptor Axis in Various Aspects of Acute Myeloid Leukemia

被引:23
作者
Yazdani, Zinat [1 ]
Mousavi, Zahra [2 ]
Moradabadi, Alireza [1 ]
Hassanshahi, Gholamhossein [1 ,3 ]
机构
[1] Kerman Univ Med Sci, Dept Hematol & Blood Banking, Kerman, Iran
[2] Iranshahr Univ Med Sci, Dept Hematol & Med Lab Sci, Iranshahr, Iran
[3] Rafsanjan Univ Med Sci, Inst Basic Med Sci Res, Mol Med Res Ctr, Rafsanjan, Iran
关键词
SDF-1; alpha; CXCL12; CXCR4; chemokine axis; AML; 3'A GENETIC-VARIATION; DOWN-REGULATION; FACTOR-I; CXCR4; ANTAGONIST; INHIBITION; DISEASE; MICROENVIRONMENT; INFILTRATION; PATHOGENESIS;
D O I
10.2147/CMAR.S234883
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Acute myeloid leukemia (AML) is defined as an aggressive disorder which is described by accumulation of immature malignant cells into the bone marrow. Chemokine-receptor 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 bonemarrowmicroenvironment. 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 inAMLin a non-cell autonomousmanner. 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 ofmalignant 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.
引用
收藏
页码:2155 / 2165
页数:11
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