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Carcinogenesis Advance Access published online on September 14, 2006
Carcinogenesis, doi:10.1093/carcin/bgl154
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received May 19, 2006
Revised August 8, 2006
Accepted August 18, 2006

CANCER PREVENTION

Inhibition of chronic ulcerative colitis associated adenocarcinoma development in mice by inositol compounds

Jie Liao 1, Darren N. Seril 2, Allison L. Yang 1, Gary G. Lu 2, and Guang-Yu Yang 1 *

1 Department of Pathology, Northwestern University, Feinberg School of Medicine, 303 East Chicago Avenue, Chicago, IL 60611
2 Department of Chemical Biology, Rutgers University, Piscataway, NJ 08854

* To whom correspondence should be addressed.
Guang-Yu Yang, E-mail: g-yang{at}northwestern.edu


  Abstract

Chronic inflammation is a well recognized risk factor for cancer and patients with long-standing ulcerative colitis (UC) are at an increased risk for colorectal carcinoma development. In order to prevent ulcerative colitis (UC) associated carcinogenesis, we tested the effects of inositol compounds (including inositol and hexaphosphate inositol) on UC-associated carcinogenesis in our novel mouse model. Female C57BL/6 mice were subjected to long-term, cyclic dextran sulfate sodium (DSS) treatment and fed a 2-fold iron-enriched diet. The inositol compounds were administered via the drinking fluid. In the DSS-plus-2 fold iron positive control group, colorectal adenocarcinoma incidence was 70.6% (24/34 mice) after 15 cycles of DSS treatment (1 DSS cycle = 7 day DSS treatment period followed by a 10 day recovery period). Tumor multiplicity was 1.26 ± 1.05 and tumor volume was 21.4 ± 5.2 mm3. Adding 1% inositol, tumor incidence was statistically significantly reduced (42%, 9 of 21 mice with tumors), as was tumor multiplicity (0.5 ± 0.7), and tumor volume (4.2 ± 1.9 mm3). Administration of hexaphosphate inositol noticeably reduced tumor incidence (50%, 12 mice with tumors out of 24 total), tumor multiplicity (0.8 ± 0.9) and tumor volume (12.3 ± 4.1 mm3); however, the results were not statistically significant (p>0.05). Further mechanistic studies showed that the inhibition of UC-associated carcinogenesis by inositol compounds might relate to their function on the modulation of macrophage mediated inflammation, nitro-oxidative stress, and cell proliferation in UC-associated carcinogenesis. This study indicates that inositol compounds may have the potential to serve as preventive agents for chronic inflammation-carcinogenesis.

Keywords: ulcerative colitis; colorectal carcinoma; carcinogenesis; inflammation; inositol; hexaphosphate inositol.
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