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2017 ; 10
(ä): 1977-1982
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Serum galectin-1 in patients with multiple myeloma: associations with survival,
angiogenesis, and biomarkers of macrophage activation
#MMPMID28435287
Andersen MN
; Ludvigsen M
; Abildgaard N
; Petruskevicius I
; Hjortebjerg R
; Bjerre M
; Honoré B
; Møller HJ
; Andersen NF
Onco Targets Ther
2017[]; 10
(ä): 1977-1982
PMID28435287
show ga
Galectin-1 (Gal-1) is known to regulate cell signaling within the immune system
and may be a target for new anticancer immune therapy. In patients with chronic
lymphocytic leukemia (CLL) and classical Hodgkin lymphoma (cHL), high levels of
Gal-1 within the tumor microenvironment were associated with worse disease state
or poor outcome. Gal-1 can be secreted from cells by an unknown mechanism, and
levels in blood samples were associated with high tumor burden and worse disease
state in cHL and CLL patients. However, serum levels of Gal-1 have never been
investigated in patients with multiple myeloma (MM). We measured serum Gal-1
levels in samples from patients with treatment demanding MM at the time of
diagnosis (n=102) and after treatment (n=24) and examined associations of serum
Gal-1 with clinicopathological information obtained from patient medical records,
as well as data on bone marrow angiogenesis and the macrophage activation
biomarkers soluble CD163 (sCD163) and soluble mannose receptor. Serum Gal-1
levels were not elevated in patients with MM at diagnosis compared with healthy
donors (median values 8.48 vs 11.93 ng/mL, P=0.05), which is in contrast to
results in cHL and CLL. Furthermore, Gal-1 levels did not show association with
bone marrow angiogenesis, clinicopathological parameters, overall survival, or
response to treatment. There was a statically significant association between
Gal-1 and sCD163 levels (R=0.24, P=0.02), but not with soluble mannose receptor
(P=0.92). In conclusion, our results indicate that Gal-1 is not an important
serum biomarker in MM, which is in contrast to data from patients with cHL and
CLL. However, the association with sCD163 is in line with previous data showing
that Gal-1 may be involved in alternative (M2-like) activation of macrophages.
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