Journal
CARCINOGENESIS
Volume 29, Issue 4, Pages 880-886Publisher
OXFORD UNIV PRESS
DOI: 10.1093/carcin/bgn040
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Funding
- NCI NIH HHS [T32 CA09592, R01 CA60867, P30 CA68485, R01 CA060867, P30 CA068485, T32 CA009592] Funding Source: Medline
- NEI NIH HHS [P30 EY008126, P30 EY08126] Funding Source: Medline
- NHLBI NIH HHS [1 P01 HL6744-01] Funding Source: Medline
- NIDDK NIH HHS [P30 DK58404, P60 DK020593, P30 DK058404, P60 DK20593] Funding Source: Medline
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Mast cells have been observed in numerous types of tumors; however, their role in carcinogenesis remains poorly understood. The majority of epidemiological evidence suggests a negative association between the presence of mast cells and tumor progression in breast, lung and colonic neoplasms. Intestinal adenomas in the multiple intestinal neoplasia (Min, AP(Min/+)) mouse displayed increased numbers of mast cells and increased abundance of mast cell-associated proteinases as determined by transcriptional profiling with the Hu/Mu ProtIn microarray. To examine the role of mast cells in intestinal tumorigenesis, a mutant mouse line deficient in mast cells, Sash mice (c-ki(W-sh/W-sh)) was crossed with the Min mouse, a genetic model of intestinal neoplasia. The resulting mast cell-deficient Min-Sash mice developed 50% more adenomas than littermate controls and the tumors were 33% larger in Min-Sash mice. Mast cell deficiency did not affect tumor cell proliferation; however, apoptosis was significantly inhibited in mast cell-deficient mice. Mast cells have been shown to act as critical upstream regulators of numerous inflammatory cells. Neutrophil, macrophage and T cell populations were similar between Min and Min-Sash mice; however, eosinophils were significantly less abundant in tumors obtained from Min-Sash animals. These results indicate a protective, antitumor role of mast cells in a genetic model of early-stage intestinal tumorigenesis.
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