Grant Number:	1R01CA127219-01A1 Interpret this number
Primary Investigator:	Spitz, Margaret
Organization:	University Of Tx Md Anderson Can Ctr
Project Title:	Inflammation Genes and Lung Cancer Risk
Fiscal Year:	2008

DESCRIPTION (provided by applicant): There is accumulating evidence that chronic injury and inflammation in the respiratory tract, such as that caused by cigarette smoking, predispose to lung cancer. We therefore propose to conduct an in depth pathway-based analysis of gene variants in the inflammatory pathway using test and validation sets of cases and controls. This proposal builds on a well-annotated specimen repository of lung cancer cases and controls enrolled in an ongoing risk factor study (CA55769, Spitz, PI). Cases are frequency-matched to controls on age, gender, ethnicity and smoking status recruited from a multi-specialty physician practice. Data collected include smoking history, dietary intake, cancer family history, specific occupational exposures (e.g., asbestos, dust), and previous medical history including chronic obstructive airway disease, asthma and hay fever. Genomic DNA and rich candidate genotype and phenotype data are available. Aim 1: To identify novel genetic variants influencing lung cancer risk in a test set of 1500 cases with non-small cell lung cancer and 1500 matched controls (all Caucasian), using the Illumina iSelect Infinium chip with 8.5 to 9K SNP's. Aim 2: In a replication set of an additional 1000 cases and 1000 controls, using a GoldenGate assay, we will evaluate the top 1500 SNPs identified from Aim1 as meeting the P<0.1 criterion, or selected by a rational prioritizing approach that incorporates published results, type of SNP, evolutionary biology, physico-chemical properties and haplotype tagging SNPs. Aim 3: To perform fine mapping in the flanking regions of 50 SNPs selected by the same approach as in Aim 2, combining prior information with in silico approaches for predicting functionality. For each of these 50 SNPs, we will select an average of 10 additional SNPs per gene region to regenotype in all 2500 cases and 2500 controls. Aim 4. To extend our epidemiologic risk prediction model by incorporating established epidemiologic risk factor and gene variant data. We will apply machine-learning tools to identify gene-environment and gene-gene interactions. Covariates will include prior emphysema, asthma, hay fever, dust and asbestos exposure, smoking characteristics, family history of cancer, and anti-inflammatory drug use. The International Lung Cancer Consortium will perform external validation in a proposal to be developed. Our approach to comprehensively evaluate variants in a candidate pathway in a large well- powered study will be applicable to a variety of other cancer sites where inflammation plays an important etiologic role, as well as in non-neoplastic diseases with a strong inflammatory component such as emphysema. The public health potential of a useful risk prediction modes for lung cancer is substantial. Public Health Relevance Statement Cigarette smoking results in inflammation in the respiratory tract and there is growing evidence that chronic inflammatory processes predispose to lung cancer. However, the molecular mechanisms underlying the causal nature of this association are unclear. We propose to conduct an in depth analysis of gene variants in the inflammatory pathway as susceptibility factors for lung cancer. This proposal builds upon an existing well annotated specimen repository. We will evaluate gene variants in a test set of lung cancer cases and matched controls and validate the findings in an independent dataset. Finally we will incorporate these findings into an extended risk prediction model for lung cancer.




Rare deleterious germline variants and risk of lung cancer.
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Rare Variants in Known Susceptibility Loci and Their Contribution to Risk of Lung Cancer.
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Susceptibility Loci Of Cnot6 In The General Mrna Degradation Pathway And Lung Cancer Risk-a Re-analysis Of Eight Gwass
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Associations Between Genetic Variants In Mrna Splicing-related Genes And Risk Of Lung Cancer: A Pathway-based Analysis From Published Gwass
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Gene-set meta-analysis of lung cancer identifies pathway related to systemic lupus erythematosus.
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Genetic variant in DNA repair gene GTF2H4 is associated with lung cancer risk: a large-scale analysis of six published GWAS datasets in the TRICL consortium.
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Genetic variations in interleukin-8 and interleukin-10 are associated with pain, depressed mood, and fatigue in lung cancer patients.
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Hierarchical Modeling Identifies Novel Lung Cancer Susceptibility Variants In Inflammation Pathways Among 10,140 Cases And 11,012 Controls
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Pilot study of CYP2B6 genetic variation to explore the contribution of nitrosamine activation to lung carcinogenesis.
Authors: Wassenaar C.A. , Dong Q. , Amos C.I. , Spitz M.R. , Tyndale R.F. .
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Role Of Selected Genetic Variants In Lung Cancer Risk In African Americans
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Use of the cytokinesis-blocked micronucleus assay to detect gender differences and genetic instability in a lung cancer case-control study.
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Associations between dietary intake of choline and betaine and lung cancer risk.
Authors: Ying J. , Rahbar M.H. , Hallman D.M. , Hernandez L.M. , Spitz M.R. , Forman M.R. , Gorlova O.Y. .
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Integrative Cancer Epidemiology--the Next Generation
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Influence of common genetic variation on lung cancer risk: meta-analysis of 14 900 cases and 29 485 controls.
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Genome-wide Gene-environment Interaction Analysis For Asbestos Exposure In Lung Cancer Susceptibility
Authors: Wei S. , Wang L.E. , McHugh M.K. , Han Y. , Xiong M. , Amos C.I. , Spitz M.R. , Wei Q.W. .
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Multistage Analysis Of Variants In The Inflammation Pathway And Lung Cancer Risk In Smokers
Authors: Spitz M.R. , Gorlov I.P. , Dong Q. , Wu X. , Chen W. , Chang D.W. , Etzel C.J. , Caporaso N.E. , Zhao Y. , Christiani D.C. , et al. .
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Cotinine Conundrum--a Step Forward But Questions Remain
Authors: Spitz M.R. , Amos C.I. , Bierut L.J. , Caporaso N.E. .
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Derived SNP alleles are used more frequently than ancestral alleles as risk-associated variants in common human diseases.
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Roles Of Genetic Variants In The Pi3k And Ras/raf Pathways In Susceptibility To Endometrial Cancer And Clinical Outcomes
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