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Genetic variation in inflammatory genes and survival after lung cancer diagnosis

Tuesday, October 25, 2011 — Poster Session II

Noon – 2:00 p.m.

Natcher Conference Center



* FARE Award Winner


  • C Bodelon
  • J Shi
  • RM Pfeiffer
  • NE Caporaso
  • A Pesatori
  • M Rubagotti
  • MT Landi


Background: Lung cancer is the leading cause of cancer death worldwide. Genetic heterogeneity has been suggested to partially explain the variable response to treatment and clinical outcomes. It is known that inflammatory alterations of the lung microenvironment increase the risk of lung cancer mortality. Conceivably, common genetic variation in inflammatory genes could predispose patients to poor survival. Methods: Nineteen thousand and eighty-two single nucleotide polymorphisms (SNPs) in 970 inflammatory related genes were genotyped in 1,919 lung cancer patients and analyzed in relation to survival. Adjusted hazard ratios (HR) and corresponding 95% confidence intervals (CI) were computed using Cox regression. Results: The T allele of SNP rs228975 in the interleukin 2 receptor beta (IL2RB) gene, involved in the T cell-mediated immune response, increased the risk of mortality in patients diagnosed with adenocarcinoma by 42% (95% CI: 26%-60). Current smokers with the C allele in SNP rs3758338 located in the tumor suppressor gene DBC1 had a reduced risk of lung cancer mortality (HR=0.60, 95% CI: 0.49-0.73). Conclusions: In this first study of the association of inflammatory genes and lung cancer mortality, we found evidence that polymorphisms in IL2RB and DBC1 might contribute to survival. These results could lead to future therapeutic strategies.

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