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G.D. Gamble



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    MO11 - Screening and Epidemiology (ID 131)

    • Event: WCLC 2013
    • Type: Mini Oral Abstract Session
    • Track: Imaging, Staging & Screening
    • Presentations: 1
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      MO11.04 - Lung Cancer risk mediated through susceptibility to COPD: preliminary results from a sub-analysis of the NLST (ID 1540)

      16:15 - 17:45  |  Author(s): G.D. Gamble

      • Abstract
      • Presentation
      • Slides

      Background
      Introduction: Based on a 20% reduction in lung cancer deaths in the CT screening arm of the National Lung Screening Trial (NLST), yearly CT screening for lung cancer is now widely recommended. Recently, a multivariate risk model for lung cancer (LC), be used to identify smokers at greatest risk, has been proposed to better select smokers for CT ([#]Tammemagi et al. JNCI 2011;103:1058).This risk model includes age smoking history, history of COPD, BMI, recent CXR and educational level. This model has been validated in the NLST where recent CXR and educational level was omitted due to the unavailability of this data. In this sub-study of the NLST, we examine the role of the known clinical risk factors for lung cancer and whether they mediate risk for lung cancer via risk for COPD. To test this we compared risk factors between LC cases and controls after stratifying cancer-free screening participants (controls) by spirometry-defined COPD.

      Methods
      Using a sub-group of the NLST (drawn for validation of a gene-based risk stratification tool), we compared known risk factors for LC (recently validated in the PLCO[#] study) in 345 screen-detected lung cancer cases and 1482 randomly selected cancer free screening controls stratified by COPD (pre-bronchodilator GOLD 1-4). These variables included age, pack years, family history of LC (FHx), self-reported COPD and BMI.

      Results
      When the LC risk variables were compared between LC cases (N=345) and the cancer-free screening controls, stratified from baseline data into controls with COPD (N=489) and without COPD (n=993) (see Table1), we found the following; age and pack years but not FHx were significantly higher in those with COPD and LC compared to cancer-free controls with no COPD, self reported COPD was 2 fold higher in COPD controls and LC cases compared to controls without COPD, and BMI was significantly lower in the LC cases and those with COPD compared to cancer-free controls with no COPD. Figure 1

      Conclusion
      These data from the NLST suggest the risk of LC is strongly mediated by variables underlying risk of COPD (age, pack years and BMI). [#]Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO)

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    O05 - Cancer Control (ID 130)

    • Event: WCLC 2013
    • Type: Oral Abstract Session
    • Track: Prevention & Epidemiology
    • Presentations: 1
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      O05.07 - COPD-based eligibility increases lung cancer detection rate and lowers over-diagnosis in CT screening studies (ID 1721)

      10:30 - 12:00  |  Author(s): G.D. Gamble

      • Abstract
      • Presentation
      • Slides

      Background
      Based on a 20% reduction in lung cancer deaths in the CT screening arm of the National Lung Screening Trial (NLST), yearly CT screening for lung cancer is now widely recommended. Eligibility for the NLST was based on age and smoking history only. However, we and others propose that multivariate risk models of lung cancer that incorporate variables for chronic obstructive pulmonary disease (COPD), improve risk prediction for lung cancer. The aim of this study was to examine recently published CT screening studies for lung cancer and the effect of having COPD on outcome.

      Methods
      We searched the literature for CT screening studies of lung cancer where spirometry had been done at baseline to assess the effects of spirometry-defined COPD on outcomes. We identified six studies where there was published data reporting spirometry results in lung cancer screening studies. Using this data we objectively measured outcomes stratified or pre-selected on spirometry-defined COPD.

      Results
      By comparing outcomes in these single arm and randomized studies we found the following lung cancer detection rates were between 1.5 to 6 fold higher in current and former smokers eligible for screening with spirometry-defined COPD compared to those with no airflow limitation or normal lungs (Table 1). Only 15% of those screened had advanced stage COPD (GOLD 3-4) The proportion of eligible current or former smokers with COPD had less indolent lung cancers with long doubling times (Table 2), and Survival after surgical resection of early stage CT-detected lung cancers was no different between those with or without COPD at baseline screening. Figure 1 Figure 2

      Conclusion
      We conclude that a COPD-centric approach to lung cancer screening offers a more efficient means of identifying lung cancer (higher lung cancer detection rate), with less over-diagnosis and comparable outcomes to screening those without COPD.

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    O06 - Cancer Control and Epidemiology I (ID 135)

    • Event: WCLC 2013
    • Type: Oral Abstract Session
    • Track: Prevention & Epidemiology
    • Presentations: 1
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      O06.02 - Statin Use and Reduced Lung Cancer-Related Mortality (ID 1535)

      10:30 - 12:00  |  Author(s): G.D. Gamble

      • Abstract
      • Presentation
      • Slides

      Background
      Lung cancer results from the combined effects of smoking exposure and genetic predisposition. Recent studies have shown that susceptibility to chronic obstructive pulmonary disease (COPD) is also relevant to a predisposition to lung cancer. The latter may be mediated in part through exaggerated systemic inflammation secondary to smoking exposure and the innate response to smoking in genetically susceptible people. Recently a large population based study reported that statin therapy was associated with a reduction in mortality from cancer (Nielsen et al. Statin Use and Reduced Cancer-Related Mortality, NEJM 2012; 367: 1792-1802). The aim of this study was to examine the cancer specific effect of statins on mortality.

      Methods
      Using the raw data from the Nielsen study, we calculated the estimated number of lives saved from statin therapy use according to type of cancer and then estimated the absolute numbers of lives saved.

      Results
      When we examined the raw data showing hazard ratios according to statin use in each of the cancers described, we found that except for lymphoma, the mortality reductions were significant for smoking related cancers (lung, pharynx, oesophagus, urinary) and obesity-related cancers (colon, prostate, breast - see Figure 1). When we calculated the number of lives saved according to specific cancer type, we found that of all lives saved, 43% could be attributed to a reduction in lung cancer deaths (Table 1). Importantly, mortality for many of these cancers (lung, colon, breast and prostate) has been associated, in large prospective studies, to elevation of the C-reactive protein, a marker of systemic inflammation. Figure 1Figure 2

      Conclusion
      We conclude that the reduction in cancer mortality attributed to statin therapy by Nielsen et al. is seen almost exclusively in cancers where smoking and/or systemic inflammation is thought to be of significant pathogenic importance. Significantly, the single largest reduction can be attributed to lung cancer where both smoking and systemic inflammation are strongly implicated. We suggest that a reduction in systemic inflammation by statins may be one mechanism underlying the reduction in mortality reported by Nielsen and colleagues.

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