This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schiffman, M. H. Articles by Wilkins, T. D. Search for Related Content PubMed PubMed Citation Articles by Schiffman, M. H. Articles by Wilkins, T. D.

Case-Control Study of Colorectal Cancer and Fecal Mutagenicity¹

Epidemiology and Biostatistics Program, Division of Cancer Etiology [M. H. S., R. N. H., R. W., H. P.] and Division of Cancer Treatment [G. B.], National Cancer Institute, Bethesda, Maryland 20892; Program Resources, Inc., National Cancer Institute, Frederick Cancer Research Facility, Frederick, Maryland 21701 [A. W. A.]; Department of Anaerobic Microbiology, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061 [R. L. V., T. D. W.]; George Washington University Hospital, Washington, DC 20037 [L. S.]; Walter Reed Army Medical Center, Washington, DC 20307 [J. D.]; National Naval Medical Center, Bethesda, Maryland 20814 [A. R.]; Westat, Inc., Rockville, Maryland 20850 [J. R.]; Lipid Nutrition Laboratory, United States Department of Agriculture, Beltsville, Maryland 20705 [P. P. N.]; and Minneapolis Medical Research Foundation, Minneapolis, Minnesota 55404 [S. S.]

Fecal mutagenicity was measured in 68 patients with colorectal cancer and in 114 controls, using Salmonella tester strains TA98 and TA100 with and without S9 activation. Samples were also tested for fecapentaenes by high-performance liquid chromatography, to permit the separation of fecapentaene and non-fecapentaene mutagenicity. Overall, no significant case-control differences in fecal mutagenicity were observed. However, when samples containing high concentrations of fecapentaenes were excluded, non-fecapentaene TA98 mutagenicity was observed in eight cases (12%) and only four controls (4%), resulting in an estimated relative risk of 4.4 (95% confidence interval = 1.0–21.1). The association of colorectal cancer risk with non-fecapentaene TA98 mutagenicity could not be explained as an artifact of diagnostic workup or gastrointestinal bleeding among the cases. Smoking could also be excluded as a source of the TA98 mutagenicity seen, but possible dietary origins are still being explored.

¹ This work was supported in part by National Cancer Institute Contract FOD-0653.

² To whom requests for reprints should be addressed, at Epidemiology and Biostatistics Program, National Cancer Institute, NIH, Executive Plaza North, Room 443, Bethesda, MD 20892.

³ Deceased.

Received 11/ 4/88. Revised 2/14/89. Accepted 3/13/89.

This article has been cited by other articles:

				M. M. Huycke and H. R. Gaskins Commensal Bacteria, Redox Stress, and Colorectal Cancer: Mechanisms and Models Experimental Biology and Medicine, July 1, 2004; 229(7): 586 - 597. [Abstract] [Full Text] [PDF]