Document Detail

Diet and colorectal cancer: analysis of a candidate pathway using SNPS, haplotypes, and multi-gene assessment.
MedLine Citation:
PMID:  21999454     Owner:  NLM     Status:  MEDLINE    
There is considerable biologic plausibility to the hypothesis that genetic variability in pathways involved in insulin signaling and energy homeostasis may modulate dietary risk associated with colorectal cancer. We utilized data from 2 population-based case-control studies of colon (n = 1,574 cases, 1,970 controls) and rectal (n = 791 cases, 999 controls) cancer to evaluate genetic variation in candidate SNPs identified from 9 genes in a candidate pathway: PDK1, RP6KA1, RPS6KA2, RPS6KB1, RPS6KB2, PTEN, FRAP1 (mTOR), TSC1, TSC2, Akt1, PIK3CA, and PRKAG2 with dietary intake of total energy, carbohydrates, fat, and fiber. We employed SNP, haplotype, and multiple-gene analysis to evaluate associations. PDK1 interacted with dietary fat for both colon and rectal cancer and with dietary carbohydrates for colon cancer. Statistically significant interaction with dietary carbohydrates and rectal cancer was detected by haplotype analysis of PDK1. Evaluation of dietary interactions with multiple genes in this candidate pathway showed several interactions with pairs of genes: Akt1 and PDK1, PDK1 and PTEN, PDK1 and TSC1, and PRKAG2 and PTEN. Analyses show that genetic variation influences risk of colorectal cancer associated with diet and illustrate the importance of evaluating dietary interactions beyond the level of single SNPs or haplotypes when a biologically relevant candidate pathway is examined.
Martha L Slattery; Abbie Lundgreen; Jennifer S Herrick; Bette J Caan; John D Potter; Roger K Wolff
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-10-14
Journal Detail:
Title:  Nutrition and cancer     Volume:  63     ISSN:  1532-7914     ISO Abbreviation:  Nutr Cancer     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-18     Completed Date:  2012-03-19     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  7905040     Medline TA:  Nutr Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1226-34     Citation Subset:  IM    
Department of Medicine, University of Utah, Salt Lake City, Utah 84108, USA.
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MeSH Terms
AMP-Activated Protein Kinases / genetics,  metabolism
Case-Control Studies
Colorectal Neoplasms / genetics*
Dietary Carbohydrates / administration & dosage
Dietary Fats / administration & dosage
Energy Intake
Genetic Predisposition to Disease
Insulin Resistance / genetics
PTEN Phosphohydrolase / genetics,  metabolism
Phosphatidylinositol 3-Kinases / genetics,  metabolism
Polymorphism, Single Nucleotide*
Protein-Serine-Threonine Kinases / genetics,  metabolism
Proto-Oncogene Proteins c-akt / genetics,  metabolism
Ribosomal Protein S6 Kinases, 70-kDa / genetics,  metabolism
Ribosomal Protein S6 Kinases, 90-kDa / genetics,  metabolism
Signal Transduction
TOR Serine-Threonine Kinases / genetics,  metabolism
Tumor Suppressor Proteins / genetics,  metabolism
Grant Support
Reg. No./Substance:
0/Dietary Carbohydrates; 0/Dietary Fats; 0/Tumor Suppressor Proteins; 0/tuberous sclerosis complex 1 protein; 4JG2LF96VF/tuberous sclerosis complex 2 protein; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC protein, human; EC Serine-Threonine Kinases; EC protein, human; EC Protein Kinases; EC protein, human; EC Kinases; EC Proteins c-akt; EC Protein S6 Kinases, 70-kDa; EC Protein S6 Kinases, 90-kDa; EC protein S6 kinase, 70kD, polypeptide 1; EC protein S6 kinase, 70kD, polypeptide 2; EC protein S6 kinase, 90kDa, polypeptide 3; EC dehydrogenase (acetyl-transferring) kinase; EC protein, human; EC Phosphohydrolase

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