Tags

Type your tag names separated by a space and hit enter

Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC or KRAS genes.
Cancer Causes Control 2007; 18(8):865-79CC

Abstract

OBJECTIVE

To investigate baseline fat intake and the risk of colon and rectal tumors lacking MLH1 (mutL homolog 1, colon cancer, nonpolyposis type 2) repair gene expression and harboring mutations in the APC (adenomatous polyposis coli) tumor suppressor gene and in the KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) oncogene.

METHODS

After 7.3 years of follow-up of the Netherlands Cohort Study (n = 120,852), adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) were computed, based on 401 colon and 130 rectal cancer patients.

RESULTS

Total, saturated and monounsaturated fat were not associated with the risk of colon or rectal cancer, or different molecular subgroups. There was also no association between polyunsaturated fat and the risk of overall or subgroups of rectal cancer. Linoleic acid, the most abundant polyunsaturated fatty acid in the diet, was associated with increased risk of colon tumors with only a KRAS mutation and no additional truncating APC mutation or lack of MLH1 expression (RR = 1.41, 95% CI 1.18-1.69 for one standard deviation (i.e., 7.5 g/day) increase in intake, p-trend over the quartiles of intake <0.001). Linoleic acid intake was not associated with risk of colon tumors without any of the gene defects, or with tumors harboring aberrations in either MLH1 or APC.

CONCLUSION

Linoleic acid intake is associated with colon tumors with an aberrant KRAS gene, but an intact APC gene and MLH1 expression, suggesting a unique etiology of tumors with specific genetic aberrations.

Authors+Show Affiliations

Department of Epidemiology, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands mp.weijenberg@epid.unimaas.nlNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17636402

Citation

Weijenberg, Matty P., et al. "Dietary Fat and Risk of Colon and Rectal Cancer With Aberrant MLH1 Expression, APC or KRAS Genes." Cancer Causes & Control : CCC, vol. 18, no. 8, 2007, pp. 865-79.
Weijenberg MP, Lüchtenborg M, de Goeij AF, et al. Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC or KRAS genes. Cancer Causes Control. 2007;18(8):865-79.
Weijenberg, M. P., Lüchtenborg, M., de Goeij, A. F., Brink, M., van Muijen, G. N., de Bruïne, A. P., ... van den Brandt, P. A. (2007). Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC or KRAS genes. Cancer Causes & Control : CCC, 18(8), pp. 865-79.
Weijenberg MP, et al. Dietary Fat and Risk of Colon and Rectal Cancer With Aberrant MLH1 Expression, APC or KRAS Genes. Cancer Causes Control. 2007;18(8):865-79. PubMed PMID: 17636402.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC or KRAS genes. AU - Weijenberg,Matty P, AU - Lüchtenborg,Margreet, AU - de Goeij,Anton F P M, AU - Brink,Mirian, AU - van Muijen,Goos N P, AU - de Bruïne,Adriaan P, AU - Goldbohm,R Alexandra, AU - van den Brandt,Piet A, Y1 - 2007/07/18/ PY - 2006/06/07/received PY - 2007/06/20/accepted PY - 2007/7/20/pubmed PY - 2007/10/10/medline PY - 2007/7/20/entrez SP - 865 EP - 79 JF - Cancer causes & control : CCC JO - Cancer Causes Control VL - 18 IS - 8 N2 - OBJECTIVE: To investigate baseline fat intake and the risk of colon and rectal tumors lacking MLH1 (mutL homolog 1, colon cancer, nonpolyposis type 2) repair gene expression and harboring mutations in the APC (adenomatous polyposis coli) tumor suppressor gene and in the KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) oncogene. METHODS: After 7.3 years of follow-up of the Netherlands Cohort Study (n = 120,852), adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) were computed, based on 401 colon and 130 rectal cancer patients. RESULTS: Total, saturated and monounsaturated fat were not associated with the risk of colon or rectal cancer, or different molecular subgroups. There was also no association between polyunsaturated fat and the risk of overall or subgroups of rectal cancer. Linoleic acid, the most abundant polyunsaturated fatty acid in the diet, was associated with increased risk of colon tumors with only a KRAS mutation and no additional truncating APC mutation or lack of MLH1 expression (RR = 1.41, 95% CI 1.18-1.69 for one standard deviation (i.e., 7.5 g/day) increase in intake, p-trend over the quartiles of intake <0.001). Linoleic acid intake was not associated with risk of colon tumors without any of the gene defects, or with tumors harboring aberrations in either MLH1 or APC. CONCLUSION: Linoleic acid intake is associated with colon tumors with an aberrant KRAS gene, but an intact APC gene and MLH1 expression, suggesting a unique etiology of tumors with specific genetic aberrations. SN - 0957-5243 UR - https://www.unboundmedicine.com/medline/citation/17636402/Dietary_fat_and_risk_of_colon_and_rectal_cancer_with_aberrant_MLH1_expression_APC_or_KRAS_genes_ L2 - https://doi.org/10.1007/s10552-007-9032-6 DB - PRIME DP - Unbound Medicine ER -