Table 1.

Pathways shifting macrophage polarization in hematological malignancies.

Disease	Mechanism of Action	Results
HL	PI3K-Akt pathway	Leading M1 type macrophage to M2 type
DLBCL	GM-CSF synergistic enhancement effect	Enhancing M1 polarization from M2
DLBL	NSE protein mediates nuclear p50 translocation via IRF/STAT signaling pathway	Promoting M2 polarization and migration ability of macrophage
PTCL	GATA3-dependent mechanism	M2 macrophage differentiation
FL	CSF-1R inhibition by PLX3397	repolarization towards an M1-like phenotype
MM	Inactivation of CCL2-CCR2	Macrophage bone marrow homing, proliferation, and polarization
MM	STAT3 pathway	A Janus kinase (JAK)2 inhibitor was correlated to the pro-tumor effect
MM	Exosome-derived miR-let-7c promotes angiogenesis	Polarizing M2 macrophages in MM microenvironment
MM	CSF1R blockade	Inhibits myeloma-associated macrophage polarizing to M2 type
T-ALL	CXCR4/CXCL12 axis	Inhibiting TAM polarization towards M1 phenotype
AML	Demonstrating an arginase-dependent ability of AML	Suppressive M2-like phenotype in vitro
AML	Expressing Gfi1	Polarizing M1 phenotype macrophage into M2
AML	MOZ Forms an Autoregulatory Feedback Loop with miR-223	Promoting monocyte-to-macrophage development and M1 polarization
AML	Inhibiting CSF1R, in the presence of GM-CSF	Reprogramed MΦ orientation and promoted myeloblast apoptosis
CLL	IFN-γ	Reprogramming tool to polarize NLCs to M1 state
CLL	CSF-1R signaling inhibition	LAMs polarization blocking