American Association for Cancer Research
Browse
19406207capr110243-sup-table_3_pdf_47k.pdf (52.45 kB)

Supplementary Table 3 from Genetic Variants Associated with the Risk of Chronic Obstructive Pulmonary Disease with and without Lung Cancer

Download (52.45 kB)
journal contribution
posted on 2023-04-03, 19:27 authored by Mariza de Andrade, Yan Li, Randolph S. Marks, Claude Deschamps, Paul D. Scanlon, Curtis L. Olswold, Ruoxiang Jiang, Stephen J. Swensen, Zhifu Sun, Julie M. Cunningham, Jason A. Wampfler, Andrew H. Limper, David E. Midthun, Ping Yang

PDF file - 47K

History

ARTICLE ABSTRACT

Chronic obstructive pulmonary disease (COPD) is a strong risk factor for lung cancer. Published studies about variations of genes encoding glutathione metabolism, DNA repair, and inflammatory response pathways in susceptibility to COPD were inconclusive. We evaluated 470 single-nucleotide polymorphisms (SNP) from 56 genes of these three pathways in 620 cases and 893 controls to identify susceptibility markers for COPD risk, using existing resources. We assessed SNP- and gene-level effects adjusting for sex, age, and smoking status. Differential genetic effects on disease risk with and without lung cancer were also assessed; cumulative risk models were established. Twenty-one SNPs were found to be significantly associated with risk of COPD (P < 0.01); gene-based analyses confirmed two genes (GCLC and GSS) and identified three additional genes (GSTO2, ERCC1, and RRM1). Carrying 12 high-risk alleles may increase risk by 2.7-fold; eight SNPs altered COPD risk without lung cancer by 3.1-fold and 4 SNPs altered the risk with lung cancer by 2.3-fold. Our findings indicate that multiple genetic variations in the three selected pathways contribute to COPD risk through GCLC, GSS, GSTO2, ERCC1, and RRM1 genes. Functional studies are needed to elucidate the mechanisms of these genes in the development of COPD, lung cancer, or both. Cancer Prev Res; 5(3); 365–73. ©2011 AACR.

Usage metrics

    Cancer Prevention Research

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC