期刊
MUTAGENESIS
卷 26, 期 5, 页码 657-666出版社
OXFORD UNIV PRESS
DOI: 10.1093/mutage/ger030
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资金
- European Commission (SANCO)
- Deutsche Krebshilfe
- Deutsches Krebsforschungszentrum
- German Federal Ministry of Education and Research
- Danish Cancer Society
- Spanish Ministry of Health
- Spanish Regional Government of Andalucia
- Spanish Regional Government of Asturias
- Spanish Regional Government of Basque Country
- Spanish Regional Government of Murcia
- Spanish Regional Government of Navarra
- ISCIII of the Spanish Ministry of Health [RETICC DR06/0020]
- Cancer Research UK
- Medical Research Council, United Kingdom
- Greek Ministry of Health
- Greek Ministry of Education
- Italian Association for Research on Cancer (AIRC)
- Italian National Research Council, Milan, Italy
- Fondazione-Istituto Banco Napoli, Italy
- Compagnia di San Paolo, Italy
- Sicilian Governement, Italy
- World Cancer Research Fund
- Dutch Ministry of Public Health, Welfare and Sports
- Swedish Cancer Society
- Swedish Scientific Council
- Regional Government of Skane and Vasterbotten, Sweden
- Norwegian Cancer Society
- Research Council of Norway
- French League against Cancer (LNCC)
- National Institute for Health and Medical Research (INSERM), France
- Mutuelle Generale de l'Education Nationale (MGEN), France
- 3M Co, France
- Gustave Roussy Institute (IGR), France
- General Councils of France
- Greek Ministry of Health and Social Solidarity
- Hellenic Health Foundation
- Stavros Niarchos Foundation
- Medical Research Council [G1000143, MC_U106179471, G0401527, G0801056B] Funding Source: researchfish
The single-nucleotide polymorphisms (SNPs) rs402710 (5p15.33), rs16969968 and rs8034191 (15q25.1) have been consistently identified by genome-wide association studies (GWAS) as significant predictors of lung cancer risk, while rs4324798 (6p22.1) was previously found to influence survival time in small-cell lung cancer (SCLC) patients. Using the same population of one of the original GWAS, we investigated whether the selected SNPs and 31 others (also identified in GWAS) influence survival time, assuming an additive model. The effect of each polymorphism on all cause survival was estimated in 1094 lung cancer patients, and lung cancer-specific survival in 763 patients, using Cox regression adjusted for a priori confounders and competing causes of death where appropriate. Overall, after 1558 person-years of post-diagnostic follow-up, 874 deaths occurred from all causes, including 690 from lung cancer. In the lung cancer-specific survival analysis (1102 person-years), only rs7452888 (6q27) and rs2710994 (7p15.3) modified survival, with adjusted hazard ratios of 1.19 (P = 0.009) and 1.32 (P = 0.011) respectively, taking competing risks into account. Some weak associations were identified in subgroup analysis for rs16969968 and rs8034191 (15q25.1) and rs4324798 (6p22.1) and survival in never-smokers, as well as for rs402710 in current smokers and SCLC patients. In conclusion, rs402710 (5p15.33), rs16969968 and rs8034191 (both 15q25.1) and rs4324798 (6p22.1) were found to be unrelated to survival times in this large cohort of lung cancer patients, regardless of whether the cause of death was from lung cancer or not. However, rs7452888 (6q27) was identified as a possible candidate SNP to influence lung cancer survival, while stratified analysis hinted at a possible role for rs8034191, rs16969968 (15q25.1) and rs4324798 (6p22.1) in influencing survival time in lung cancer patients who were never-smokers, based on a small sample.
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