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. 2019 Aug 26;11(8):476–490. doi: 10.4252/wjsc.v11.i8.476

Table 2.

Possible molecules and their role in acute myeloid leukemia stem cells-bone marrow microenvironment interaction

Target Source Role Ref.
VLA-4 AML LSCs Homing [37]
CD44 AML LSCs Homing [38,96]
CXCR4 AML LSCs Adhesion [40]
Jagged-1 Osteoblast Proliferation [42]
CXCR2 AML LSCs Proliferation, survival [44]
Parathyroid hormone BMM OB proliferation, LSCs growth [97]
Proangiogenesis factors (VEGF, HGF, BFGF, VEGFR) AML LSCs, BMM Endothelial and LSC proliferation [47,48]
Cytokines (IL-6, IL1β, TNFα, G-CSF, GM-CSF) AML LSCs, BMM Angiogenesis, LSC proliferation [51]
Tie-2 Osteoblast LSCs quiescent [46]
CD36 AML LSCs Energy source provider [56]

AML LSC: Acute myeloid leukemia stem cell; BMM: Bone marrow microenvironment; VLA-4: Very late antigen-4; CXCR4: C-X-C chemokine receptor type 4; CXCR2: C-X-C chemokine receptor type 2; VEGF: Vascular endothelial growth factor; HGF: Hepatocyte growth factor; BFGF: Basic fibroblast growth factor; VEGFR: Vascular endothelial growth factor receptor; IL-6: Interleukin-6; IL-1β: Interleukin-1 beta, TNFα: Tumor necrosis factor alpha; G-CSF: Granulocyte-colony stimulating factor; GM-CSF: Granulocyte-monocyte colony stimulating factor.