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2016 ; 5
(7
): e1151591
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Ranitidine modifies myeloid cell populations and inhibits breast tumor
development and spread in mice
#MMPMID27622015
Vila-Leahey A
; Oldford SA
; Marignani PA
; Wang J
; Haidl ID
; Marshall JS
Oncoimmunology
2016[Jul]; 5
(7
): e1151591
PMID27622015
show ga
Histamine receptor 2 (H2) antagonists are widely used clinically for the control
of gastrointestinal symptoms, but also impact immune function. They have been
reported to reduce tumor growth in established colon and lung cancer models.
Histamine has also been reported to modify populations of myeloid-derived
suppressor cells (MDSCs). We have examined the impact of the widely used H2
antagonist ranitidine, on both myeloid cell populations and tumor development and
spread, in three distinct models of breast cancer that highlight different stages
of cancer progression. Oral ranitidine treatment significantly decreased the
monocytic MDSC population in the spleen and bone marrow both alone and in the
context of an orthotopic breast tumor model. H2 antagonists ranitidine and
famotidine, but not H1 or H4 antagonists, significantly inhibited lung metastasis
in the 4T1 model. In the E0771 model, ranitidine decreased primary tumor growth
while omeprazole treatment had no impact on tumor development. Gemcitabine
treatment prevented the tumor growth inhibition associated with ranitidine
treatment. In keeping with ranitidine-induced changes in myeloid cell populations
in non-tumor-bearing mice, ranitidine also delayed the onset of spontaneous tumor
development, and decreased the number of tumors that developed in LKB1(-/-)/NIC
mice. These results indicate that ranitidine alters monocyte populations
associated with MDSC activity, and subsequently impacts breast tumor development
and outcome. Ranitidine has potential as an adjuvant therapy or preventative
agent in breast cancer and provides a novel and safe approach to the long-term
reduction of tumor-associated immune suppression.
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