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Epidemiology and Prevention |
Health Research Center, Department of Family and Preventive Medicine, University of Utah, Salt Lake City, Utah 84108 [M. L. S., K. C., K-N. M., S. E.]; University of Minnesota, School of Public Health, Minneapolis, Minnesota 55455-0381 [K. A.]; Departments of Genetics [M. L.] and Pathology [W. S. S.], University of Utah, Salt Lake City, Utah 84108; Fred Hutchinson Cancer Research Center, Seattle, Washington 98104 [J. P.]; and Kaiser Permanente Medical Care Program, Oakland, California 94611-5714 [D. S.]
Ki-ras
mutations are thought to be early events in the carcinogenic process
leading to colon tumors. Dietary factors associated with colon cancer
may be associated with these mutations. Data from a population-based,
multicenter, case-control study of colon cancer were used to determine
whether dietary factors are associated with Ki-ras
mutations. Ki-ras mutations were detected by direct
sequencing of codons 12 and 13 of the Ki-ras gene on
exon 1 from DNA obtained from archival tissue. Ki-ras
data were available for 1428 cases with valid interview data; data from
2410 controls were available for comparison with cases positive and
negative for Ki-ras mutations. Mutations in the
Ki-ras gene were detected in 32% of tumors. Of these
mutations, 32.8% were G
A transitions in the second base of codon 12
(2GA). Other than cruciferous vegetables, there were no nutrients or
foods associated specifically with Ki-ras mutations
[odds ratio (OR) for high intake relative to low intake, 0.7; 95%
confidence interval (CI), 0.5–1.0]. However, evaluation of specific
types of Ki-ras mutations revealed that for each of the
most common types of mutation, dietary associations existed. Dietary
factors involved in DNA methylation pathways were associated with
2GA mutations. Comparison of individuals with and without
Ki-ras mutations revealed that individuals with low
levels of dietary folate (OR, 0.7; 95% CI, 0.4–1.3), vitamin
B6 (OR, 0.5; 95% CI, 0.3–1.0), vitamin B12
(OR, 0.6; 95% CI, 0.3–1.1), and high levels of alcohol (OR, 0.7; 95%
CI, 0.4–1.1) were less likely to have a 2GA mutation. Individuals
with high levels of dietary carbohydrate (OR, 2.0; 95% CI, 0.9–4.4)
and a high glycemic index (OR, 1.9; 95% CI, 0.8–4.6) were more likely
to have a GA transition mutation in the second base of codon 13
(5GA). Individuals with high levels of dietary fat (OR, 1.6; 95%
CI, 0.8–3.2), saturated fat (OR, 1.7; 95% CI, 0.8–3.5), and
monounsaturated fat (OR, 1.9; 95% CI, 1.0–3.7) were more likely to
harbor a 2GT mutation. Low levels of cruciferous vegetable intake
and high levels of processed meat intake also were associated with
fewer 5GA, as reflected by the ORs (OR, 0.4; 95% CI, 0.2–1.0 and
OR, 0.4; 95% CI 0.2–0.8, respectively). These data suggest that diet
may be involved in disease pathways represented by specific
Ki-ras mutations. However, given the limited information
currently available on associations between specific genetic mutations
in colon tumors and diet, these findings also should be viewed as
hypothesis generating.
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