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Genetic Variations in the AGEs/AGER ...
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Yale University., Public Health.
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Genetic Variations in the AGEs/AGER Pathway and Risk of Pancreatic Cancer.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Genetic Variations in the AGEs/AGER Pathway and Risk of Pancreatic Cancer./
作者:
Jia, Guochong.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2017,
面頁冊數:
27 p.
附註:
Source: Masters Abstracts International, Volume: 79-10.
Contained By:
Masters Abstracts International79-10.
標題:
Environmental Health. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10276933
ISBN:
9780355777499
Genetic Variations in the AGEs/AGER Pathway and Risk of Pancreatic Cancer.
Jia, Guochong.
Genetic Variations in the AGEs/AGER Pathway and Risk of Pancreatic Cancer.
- Ann Arbor : ProQuest Dissertations & Theses, 2017 - 27 p.
Source: Masters Abstracts International, Volume: 79-10.
Thesis (M.P.H.)--Yale University, 2017.
This item must not be sold to any third party vendors.
Chronic inflammation is implicated in pancreatic cancer carcinogenesis. Advanced glycation end-products (AGEs) can perpetuate inflammation by binding to the receptor for advanced glycation end products (AGER, also known as RAGE). We hypothesized that genetic variation of the AGEs/AGER pathway affects pancreatic cancer risk by modulating levels of AGEs and soluble RAGE and therefore chronic inflammation. We conducted a two-stage case-control study to examine the association between 96 single nucleotide polymorphisms (SNPs) in 21 genes of the AGEs/AGER pathway and risk of pancreatic cancer. The discovery study was conducted in 672 pancreatic cancer cases and 1361 controls ascertained from the Women's Health Initiative (WHI) Study matched on age at screening (±3 years), ethnicity, study center, study arm, and menopause status. The validation study was conducted in a PANC4 pooled hospital-based case-control study of 1,034 women cases and 989 women controls. Eleven SNPs with raw P values < 0.10 were identified in the discovery stage. However, none of the SNPs was validated in the validation and pooled dataset. An interaction effect was found between the GLO1 SNP rs6932648 and smoking status. In the pooled dataset, the variant T allele of rs6932648 was associated with increased risk of pancreatic cancer among ever smokers (additive OR = 1.26, 95% CI: 1.02-1.55), but not among never smokers (additive OR = 0.94, 95% CI: 0.78-1.14), compared with the C allele. Our study did not support the role of genetic polymorphism of AGEs/RAGE in association with pancreatic cancer. GLO1 genetic polymorphism may be associated with smoking-related cancer.
ISBN: 9780355777499Subjects--Topical Terms:
578282
Environmental Health.
Genetic Variations in the AGEs/AGER Pathway and Risk of Pancreatic Cancer.
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Chronic inflammation is implicated in pancreatic cancer carcinogenesis. Advanced glycation end-products (AGEs) can perpetuate inflammation by binding to the receptor for advanced glycation end products (AGER, also known as RAGE). We hypothesized that genetic variation of the AGEs/AGER pathway affects pancreatic cancer risk by modulating levels of AGEs and soluble RAGE and therefore chronic inflammation. We conducted a two-stage case-control study to examine the association between 96 single nucleotide polymorphisms (SNPs) in 21 genes of the AGEs/AGER pathway and risk of pancreatic cancer. The discovery study was conducted in 672 pancreatic cancer cases and 1361 controls ascertained from the Women's Health Initiative (WHI) Study matched on age at screening (±3 years), ethnicity, study center, study arm, and menopause status. The validation study was conducted in a PANC4 pooled hospital-based case-control study of 1,034 women cases and 989 women controls. Eleven SNPs with raw P values < 0.10 were identified in the discovery stage. However, none of the SNPs was validated in the validation and pooled dataset. An interaction effect was found between the GLO1 SNP rs6932648 and smoking status. In the pooled dataset, the variant T allele of rs6932648 was associated with increased risk of pancreatic cancer among ever smokers (additive OR = 1.26, 95% CI: 1.02-1.55), but not among never smokers (additive OR = 0.94, 95% CI: 0.78-1.14), compared with the C allele. Our study did not support the role of genetic polymorphism of AGEs/RAGE in association with pancreatic cancer. GLO1 genetic polymorphism may be associated with smoking-related cancer.
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