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Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Inflammation-induced myeloid-derived suppressor cells associated with squamous cell carcinoma of the head and neck.
Head & Neck 2017 Februrary
BACKGROUND: The purpose of this study was to present our assessment of the significance of myeloid-derived suppressor cells (MDSCs) in head and neck squamous cell carcinoma (HNSCC).
METHODS: We examined the percentage of MDSCs in the peripheral blood of patients with HNSCC. The relationship among MDSC recruitment, tumor progression, and cyclooxygenase (COX)-2 inhibition was also evaluated by animal models.
RESULTS: Circulating MDSCs were significantly increased in patients with HNSCC compared with healthy people, and this was associated with the clinical tumor burden. In immunocompetent 4-nitroquinoline-1-oxide (4-NQO)-induced oral tumor and immunocompromised tumor implantation animal models, MDSC recruitment was associated with the duration of 4-NQO treatment and tumor progression. The responsible mechanisms included the suppressive ability of T-cell proliferation and augmenting angiogenesis by MDSC. Blockade of COX-2 attenuated the induction and function of MDSCs and subsequently inhibited tumor growth.
CONCLUSION: The levels of MDSC are linked with tumor progression in HNSCC. Moreover, targeting COX-2 could be a promising strategy for the treatment of HNSCC. © 2016 Wiley Periodicals, Inc. Head Neck 39: 347-355, 2017.
METHODS: We examined the percentage of MDSCs in the peripheral blood of patients with HNSCC. The relationship among MDSC recruitment, tumor progression, and cyclooxygenase (COX)-2 inhibition was also evaluated by animal models.
RESULTS: Circulating MDSCs were significantly increased in patients with HNSCC compared with healthy people, and this was associated with the clinical tumor burden. In immunocompetent 4-nitroquinoline-1-oxide (4-NQO)-induced oral tumor and immunocompromised tumor implantation animal models, MDSC recruitment was associated with the duration of 4-NQO treatment and tumor progression. The responsible mechanisms included the suppressive ability of T-cell proliferation and augmenting angiogenesis by MDSC. Blockade of COX-2 attenuated the induction and function of MDSCs and subsequently inhibited tumor growth.
CONCLUSION: The levels of MDSC are linked with tumor progression in HNSCC. Moreover, targeting COX-2 could be a promising strategy for the treatment of HNSCC. © 2016 Wiley Periodicals, Inc. Head Neck 39: 347-355, 2017.
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