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J.C.M. Ho



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    MINI 23 - Lung Cancer Risk: Genetic Susceptibility and Airway Biology (ID 135)

    • Event: WCLC 2015
    • Type: Mini Oral
    • Track: Screening and Early Detection
    • Presentations: 1
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      MINI23.05 - A Case-Control Study on the Genetic Risks for Development of Lung Adenocarcinoma in Never-Smoking Hong Kong Population (ID 1003)

      16:45 - 18:15  |  Author(s): J.C.M. Ho

      • Abstract
      • Presentation
      • Slides

      Background:
      Lung cancer with different molecular profile behaves in different ways in terms of etiology, clinical characteristics, and prognosis. It implies that fighting against lung cancer should be moving forward in the direction of modifying the screening strategies on genetically-defined high risk groups, initiating early chemoprevention trials on selected high-risk subjects, and developing personalized cancer treatments. Lung adenocarcinoma in never-smokers, more often harboring epidermal growth factor receptor (EGFR) mutations especially in Asians, has a remarkable therapeutic response to specific tyrosine kinase inhibitors. Most single nucleotide polymorphisms (SNPs) identified by candidate gene and genome-wide association studies are of genes involved in carcinogen metabolic pathway, DNA repair pathway, inflammatory pathway and tumor suppressor pathway. Conflicting results are likely due to heterogeneity of the study population and lack of focus on specific molecular subgroups (e.g. EGFR-mutants). We therefore embark on the current study to identify susceptibility genes in a molecularly-defined (EGFR-mutated) subgroup of never-smoking lung adenocarcinoma in Hong Kong population.

      Methods:
      Eligible patients with confirmed primary lung adenocarcinoma were recruited from Queen Mary Hospital, Hong Kong. Voluntary healthy controls were recruited from blood donors in Hong Kong Red Cross. 10mL venous blood samples were taken from both cases and controls for DNA extraction and SNP assays. 51 SNPs of 14 genes involved in four different pathways were tested using MassARRAY. A structured questionnaire including the information of environmental exposures at home and workplace, family history of lung cancer and other cancer for all subjects, and clinical characteristics (cell type, EGFR mutation status, staging and treatment etc.) for lung cancer patients were administered to cases and controls. Using SNPstats package, logistic regression analysis adjusted for age and gender was performed to evaluate the association between the studied SNPs and lung cancer development.

      Results:
      From September 2006 to February 2015, a total of 614 lung cancer patients regardless of histological type and smoking status were recruited. Out of which, 267 never-smoking lung adenocarcinoma patients (72% females, mean age 61.6+/-12.6 years) were regarded as cases in the study. From July 2013 to August 2014, a total of 453 healthy controls (40% females, mean age 53.8+/- 8.3 years) were recruited. Most cases (69%) were at advanced stage with chemotherapy treatment (67.8%). Higher proportion of cases (41.7% at home; 35.4% at workplace) than controls (24.9% at home; 26.9% at workplace) had been exposed to second-hand smoke. Genetic analysis was restricted to 184 pairs of age and gender well-matched cases and controls. Two of the 51 SNPs showed a significant association with lung adenocarcinoma, which were rs2069840 of IL-6 gene in inflammatory pathway (OR: 5.80; 96%CI: 1.60-20.99) and rs1106087 of XPC gene in DNA repair pathway (OR: 3.72; 95%CI: 1.40-9.83).

      Conclusion:
      Our results suggest that IL-6 rs2069840 and XPC rs1106087 are susceptibility genes for development of EGFR-driven lung adenocarcinoma in never-smoking Hong Kong population.

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