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Lipid metabolism-related genetic pol...
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Gong, Zhihong.
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Lipid metabolism-related genetic polymorphisms, diet, other related environmental factors, and risk of colorectal adenoma.
Record Type:
Language materials, printed : Monograph/item
Title/Author:
Lipid metabolism-related genetic polymorphisms, diet, other related environmental factors, and risk of colorectal adenoma./
Author:
Gong, Zhihong.
Description:
203 p.
Notes:
Chair: James R. Hebert.
Contained By:
Dissertation Abstracts International66-04B.
Subject:
Health Sciences, Nutrition. -
Online resource:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3173159
ISBN:
9780542102004
Lipid metabolism-related genetic polymorphisms, diet, other related environmental factors, and risk of colorectal adenoma.
Gong, Zhihong.
Lipid metabolism-related genetic polymorphisms, diet, other related environmental factors, and risk of colorectal adenoma.
- 203 p.
Chair: James R. Hebert.
Thesis (Ph.D.)--University of South Carolina, 2005.
Cyclooxygenase (COX) and lipoxygenase (LOX) are the two major enzymes that convert arachidonic acid (AA) into various bioactive lipids. Evidence exists that metabolites from AA metabolism play roles in inflammation and colorectal carcinogenesis. PPARgamma is involved in cellular proliferation, lipid metabolism, and inflammation. The overall purpose of this dissertation was to evaluate possible roles of genetic polymorphisms of COX, LOX, and PPARgamma genes, related environmental factors, potential gene-environment interactions among them, and risk of incident, sporadic colorectal adenoma. We investigated the hypotheses using data from a community-, colonoscopy-based case-control study.
ISBN: 9780542102004Subjects--Topical Terms:
1017801
Health Sciences, Nutrition.
Lipid metabolism-related genetic polymorphisms, diet, other related environmental factors, and risk of colorectal adenoma.
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Lipid metabolism-related genetic polymorphisms, diet, other related environmental factors, and risk of colorectal adenoma.
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203 p.
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Chair: James R. Hebert.
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Source: Dissertation Abstracts International, Volume: 66-04, Section: B, page: 2008.
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Thesis (Ph.D.)--University of South Carolina, 2005.
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Cyclooxygenase (COX) and lipoxygenase (LOX) are the two major enzymes that convert arachidonic acid (AA) into various bioactive lipids. Evidence exists that metabolites from AA metabolism play roles in inflammation and colorectal carcinogenesis. PPARgamma is involved in cellular proliferation, lipid metabolism, and inflammation. The overall purpose of this dissertation was to evaluate possible roles of genetic polymorphisms of COX, LOX, and PPARgamma genes, related environmental factors, potential gene-environment interactions among them, and risk of incident, sporadic colorectal adenoma. We investigated the hypotheses using data from a community-, colonoscopy-based case-control study.
520
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We evaluated associations of four important polymorphisms of the COX1 (-842 A > G) and COX2 (-765 G > C, 8473 T > C, 9850 A > G) genes with colorectal adenoma risk. An inverse association between the -765 G > C polymorphism and adenoma risk was observed among those who had multiple polyps. In addition, a statistically significant interaction was observed between the 8473 T > C polymorphism and non-steroidal anti-inflammatory drugs (NSAIDs).
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Similarly, three polymorphisms in the 5-LOX (-1708 G > A, 21 C > T) and 12-LOX (Arg261Gln) genes were the focus in this study. A statistically significant inverse association between the Arg261Gln polymorphism of 12-LOX and colorectal adenoma risk was observed. In addition, a significant interaction between the Arg261Gln polymorphism and NSAID use was observed. There was no statistically significant association found between either polymorphism of the 5-LOX gene and adenoma risk.
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A common polymorphism, the Pro12Ala polymorphism in the PPARgamma gene, was evaluated in this study. Study results, although not statistically significant, were consistent with our priori hypothesis, and suggested that the Ala12 variant was associated with a reduced risk of colorectal adenoma.
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In summary, our results indicated that the polymorphisms of these genes may not substantially influence disease risk by themselves. However, estimated associations of these polymorphisms with colorectal adenoma risk tended to differ depending on other environmental factors, suggesting potential gene-environment interactions. Thus, the effect of an individual polymorphism may be small, but it may interact with other factors to modify susceptibility to the disease. Understanding how these polymorphisms modify risk of colorectal adenoma could help improve risk stratification in the general population, and guide appropriate prevention programs.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3173159
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