RGD Reference Report - Detecting pathway-based gene-gene and gene-environment interactions in pancreatic cancer. - Rat Genome Database

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Detecting pathway-based gene-gene and gene-environment interactions in pancreatic cancer.

Authors: Duell, EJ  Bracci, PM  Moore, JH  Burk, RD  Kelsey, KT  Holly, EA 
Citation: Duell EJ, etal., Cancer Epidemiol Biomarkers Prev. 2008 Jun;17(6):1470-9.
RGD ID: 2317130
Pubmed: PMID:18559563   (View Abstract at PubMed)
PMCID: PMC4410856   (View Article at PubMed Central)
DOI: DOI:10.1158/1055-9965.EPI-07-2797   (Journal Full-text)

Data mining and data reduction methods to detect interactions in epidemiologic data are being developed and tested. In these analyses, multifactor dimensionality reduction, focused interaction testing framework, and traditional logistic regression models were used to identify potential interactions with up to three factors. These techniques were used in a population-based case-control study of pancreatic cancer from the San Francisco Bay Area (308 cases, 964 controls). From 7 biochemical pathways, along with tobacco smoking, 26 polymorphisms in 20 genes were included in these analyses. Combinations of genetic markers and cigarette smoking were identified as potential risk factors for pancreatic cancer, including genes in base excision repair (OGG1), nucleotide excision repair (XPD, XPA, XPC), and double-strand break repair (XRCC3). XPD.751, XPD.312, and cigarette smoking were the best single-factor predictors of pancreatic cancer risk, whereas XRCC3.241*smoking and OGG1.326*XPC.PAT were the best two-factor predictors. There was some evidence for a three-factor combination of OGG1.326*XPD.751*smoking, but the covariate-adjusted relative-risk estimates lacked precision. Multifactor dimensionality reduction and focused interaction testing framework showed little concordance, whereas logistic regression allowed for covariate adjustment and model confirmation. Our data suggest that multiple common alleles from DNA repair pathways in combination with cigarette smoking may increase the risk for pancreatic cancer, and that multiple approaches to data screening and analysis are necessary to identify potentially new risk factor combinations.



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Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
OGG1Humanpancreatic cancer  IAGP DNA:polymorphism: :rs1052133 (human)RGD 
Ogg1Ratpancreatic cancer  ISOOGG1 (Homo sapiens)DNA:polymorphism: :rs1052133 (human)RGD 
Ogg1Mousepancreatic cancer  ISOOGG1 (Homo sapiens)DNA:polymorphism: :rs1052133 (human)RGD 
XPCHumanpancreatic cancer  IAGP DNA:polymorphism:intron:AF076952 (human)RGD 
XRCC3Humanpancreatic cancer  IAGP DNA:SNP:cd:rs861539 (human)RGD 
XpcRatpancreatic cancer  ISOXPC (Homo sapiens)DNA:polymorphism:intron:AF076952 (human)RGD 
XpcMousepancreatic cancer  ISOXPC (Homo sapiens)DNA:polymorphism:intron:AF076952 (human)RGD 
Xrcc3Ratpancreatic cancer  ISOXRCC3 (Homo sapiens)DNA:SNP:cd:rs861539 (human)RGD 
Xrcc3Mousepancreatic cancer  ISOXRCC3 (Homo sapiens)DNA:SNP:cd:rs861539 (human)RGD 
1 to 9 of 9 rows


Genes (Rattus norvegicus)
Ogg1  (8-oxoguanine DNA glycosylase) Xpc  (XPC complex subunit, DNA damage recognition and repair factor) Xrcc3  (X-ray repair cross complementing 3)

Genes (Mus musculus)
Ogg1  (8-oxoguanine DNA-glycosylase 1) Xpc  (xeroderma pigmentosum, complementation group C) Xrcc3  (X-ray repair complementing defective repair in Chinese hamster cells 3)

Genes (Homo sapiens)
OGG1  (8-oxoguanine DNA glycosylase) XPC  (XPC complex subunit, DNA damage recognition and repair factor) XRCC3  (X-ray repair cross complementing 3)