Lifestyle factors and Ki-ras mutations in colon cancer tumors

Martha L. Slattery, Kristin Anderson, Karen Curtin, Ma Khe-Ni, Donna Schaffer, Sandra Edwards, Wade Samowitz

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72 Scopus citations


Heterogeneity in colon tumors implies that environmental, lifestyle, or genetic factors influence the type of mutations seen in tumors. In this study we evaluate the association between previously identified risk factors for colon cancer and Kirsten-ras (Ki-ras) mutations in tumors. The presence of Ki-ras mutations in codons 12 and 13 were determined in a population-based case-control study of colon cancer. Participants were between 30 and 79 years of age at time of diagnosis and include both men and women. Questionnaire data were used to obtain information on lifestyle factors. Valid study data and Ki-ras mutational status were available from 1428 cases of colon cancer, data from 2410 controls were available for comparative purposes. Participants with Ki-ras mutations were more likely to have proximal rather than distal tumors. Cigarette smoking, use of aspirin and/or NSAIDs, use of vitamin/mineral supplements, and consumption of caffeine were associated with both Ki-ras+ and Ki-ras- tumors; the associations were not confounded by dietary intake or other lifestyle factors. Among men, but not among women, those with low levels of physical activity were more likely to have a tumor with a Ki-ras mutation than one without a Ki-ras mutation. However, among women, those with a larger BMI were more likely to have a Ki-ras mutation in their tumor. Given the limited information available on what causes Ki-ras mutations, the information generated from this study indicates that these factors previously associated with colon cancer work through other disease pathways.

Original languageEnglish (US)
Pages (from-to)73-81
Number of pages9
JournalMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Issue number1-2
StatePublished - Nov 1 2001
Externally publishedYes

Bibliographical note

Funding Information:
This study was funded by CA48998 and CA61757 to Dr. Slattery. This research was supported by the Utah Cancer Registry, which is funded by Contract no. N01-PC-67000 from the National Cancer Institute, with additional support from the Department of Health, State of Utah, Northern California Cancer Registry, and the Sacramento Tumor Registry. We would like to acknowledge the contributions and support of Melanie Nichols, Kristen Gruenthal, Margaret Robinson at the University of Utah DNA Sequencing Core Facility, and Dr. Bette Caan, Dr. John Potter Judy Morse, and Leslie Palmer to the data collection efforts of this study. The contents of this manuscript are solely the responsibility of the authors and do not necessarily represent the official view of the National Cancer Institute.


  • Aspirin
  • Body size
  • Colon cancer
  • Ki-ras mutations
  • NSAIDs
  • Physical activity


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