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Wei Xian



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    Lunch & Poster Display session (ID 58)

    • Event: ELCC 2019
    • Type: Poster Display session
    • Track:
    • Presentations: 3
    • Moderators:
    • Coordinates: 4/11/2019, 12:30 - 13:00, Hall 1
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      48P - Education and lung cancer: A Mendelian randomisation study (ID 189)

      12:30 - 13:00  |  Author(s): Wei Xian

      • Abstract
      • Slides

      Background

      Education has been shown to be inversely associated with the incidence of lung cancer at several conventional observational studies. However, this association may be biased owing to the methodological limitations of traditional observational study-confounding, reverse causation, and measurement error. Therefore, we aimed to investigate whether more years spent in education is causally associated with risk of lung cancer through a two sample mendelian randomisation study.

      a9ded1e5ce5d75814730bb4caaf49419 Methods

      The main analysis used publicly available genetic summary data from two large consortiums (International Lung Cancer Consortium (ILCCO) and Social Science Genetic Association Consortium (SSGAC)). Genetic variants used as instrumental variables for lung cancer and years of education were derived from two large genome wide association studies: ILCCO and SSGAC, respectively. Finally, genetic data from three additional consortia (TAG, GLGC, GIANT) were analyzed to investigate whether longer education can causally alter the common lung cancer risk factors. The exposure was the genetic predisposition to higher levels of education, measured by 73 SNPs from SSGAC. The primary outcome was the risk of lung cancer (11348 events in ILCCO). Secondary outcomes based on different histologic subtypes were also examined.

      20c51b5f4e9aeb5334c90ff072e6f928 Results

      Genetic predisposition towards 3.6 years of additional education was associated with a 52% lower risk of lung (odds ratio 0.48, 95% confidence interval 0.34 to 0.66; p = 1.02 × 10−5). Sensitivity analyses were consistent with a causal interpretation in which major bias from genetic pleiotropy was unlikely. The Mendelian randomisation assumptions did not seem to be violated. Genetic predisposition towards longer education was additionally associated with less smoking, lower body mass index, and a favorable blood lipid profile.

      Mendelian randomisation estimates of the associations between education attainment and risk of lung cancer overall and histologic types

      OutcomeIVW method
      MR-Egger
      Weighted median method
      OR (95% CI)P valueOR (95% CI)P valueOR (95% CI)P value
      Lung cancer overall0.48 (0.34-0.66)1.02e-05*0.61 (0.12-3.17)0.560.52 (0.35-0.77)1.08e-03*
      Adenocarcinoma0.64 (0.41-1.00)4.97e-02*0.89 (0.09-8.48)0.920.59 (0.32-1.08)8.94e-02
      Squamous cell carcinoma0.41 (0.27-0.62)2.57e-05*0.32 (0.04-2.63)0.290.55 (0.30-1.01)5.24e-02

      : P value < 0.05; IVW: inverse-variance weighted; OR: odds ratio; CI: confidence interval.

      fd69c5cf902969e6fb71d043085ddee6 Conclusions

      Our present mendelian randomisation study provided strong evidence to support that higher education attainment plays a causal role in lowering the risk of lung cancer. Furthermore, more work is needed to elucidate the potential mechanisms which mediate the association between education and lung cancer.

      b651e8a99c4375feb982b7c2cad376e9 Legal entity responsible for the study

      The authors.

      213f68309caaa4ccc14d5f99789640ad Funding

      National Key R&D Program of China (Grant No. 2016YFC0905500, 2016YFC0905503).

      682889d0a1d3b50267a69346a750433d Disclosure

      All authors have declared no conflicts of interest.

      cffcb1a185b2d7d5c44e9dc785b6bb25

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      49P - A Mendelian randomization study of the effects of Crohn&#x02019;s disease on lung cancer (ID 299)

      12:30 - 13:00  |  Author(s): Wei Xian

      • Abstract
      • Slides

      Background

      Crohn’s disease is associated with increased lung cancer risk in observational studies, but the causality of this association is uncertain. Here we conducted a two-sample Mendelian randomisation (MR) study to examine whether Crohn’s disease is causally related to lung cancer.

      a9ded1e5ce5d75814730bb4caaf49419 Methods

      We used the summary data of the International Inflammatory Bowel Disease Genetics Consortium (IIBDGC, 5,956 cases and 14,927 controls; European ancestry) and International Lung Cancer Consortium (ILCCO, 11348 lung cancer cases and 15861 controls; European ancestry). 52 single nucleotide polymorphisms (SNPs) associated with Crohn’s disease were used as instrumental variables in the MR analysis. We utilized various MR methods (inverse-variance weighting (IVW), MR Egger, weighted median regression) to explore the causality. To investigate whether the effect of Crohn’s disease is associated with the histology of lung cancer, we also performed similar analyses on two different histologic subtypes of lung cancer (adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC).

      20c51b5f4e9aeb5334c90ff072e6f928 Results

      Crohn’s disease was not significantly associated with risk of lung cancer (odds ratio [OR], 1.01; 95% confidence interval [CI], 0.97-1.04; p = 0.76, IVW method). Weighted median (OR, 1.03; 95% CI, 0.98-1.07; p = 0.26) and MR Egger analysis (OR, 1.03; 95% CI, 0.95-1.11; p = 0.49) showed similar effect estimates of Crohn’s disease on lung cancer. The MR-Egger regression analysis showed that there was no evidence for the presence of horizontal pleiotropy (intercept β=-0.005, p = 0.532). Our leave-one-out analysis revealed that no single SNP strongly drove the overall effect of Crohn’s disease on lung cancer. The similar causal trend was observed in both LUAD and LUSC (LUAD, OR 0.99, 95% CI 0.94-1.04, p = 0.67, IVW method; LUSC, OR 0.98, 95% CI 0.94-1.03, p = 0.47, IVW method).

      fd69c5cf902969e6fb71d043085ddee6 Conclusions

      Our findings indicated that Crohn’s disease might not be causally associated with lung cancer, although patients with Crohn’s disease were at increased lung cancer risk in observational studies. Our study suggested there might be other risk factors associated with lung cancer in patients Crohn’s disease, which needs to be confirmed in the further study.

      b651e8a99c4375feb982b7c2cad376e9 Legal entity responsible for the study

      The authors.

      213f68309caaa4ccc14d5f99789640ad Funding

      National Key R&D Program of China (2016YFC0905500).

      682889d0a1d3b50267a69346a750433d Disclosure

      All authors have declared no conflicts of interest.

      cffcb1a185b2d7d5c44e9dc785b6bb25

      Only Active Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login or select "Add to Cart" and proceed to checkout.

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      60P - Nomogram for patients with stage I small cell lung cancer: A competing risk analysis (ID 277)

      12:30 - 13:00  |  Author(s): Wei Xian

      • Abstract
      • Slides

      Background

      Small-cell lung cancer (SCLC), accounting for about 15% of all lung cancers, is a subtype of lung cancer with poor prognosis. It has a 5-year survival rate of 7% and kills an estimated 250,000 people worldwide annually. Although many studies have estimated the prognosis of SCLC, most of them were conducted without considering competing risks. This study aimed to evaluate the probability of cause-specific death for patients with stage I small cell lung cancer (SCLC) with a competing risk analysis.

      a9ded1e5ce5d75814730bb4caaf49419 Methods

      We identified patients with stage I SCLC between 2004 and 2010 in the Surveillance Epidemiology, and End Results (SEER) database. We calculated the cumulative incidence function (CIF) for all the SCLC patients, and the differences in CIF between subgroups were estimated by Gray’s test. Proportional subdistribution hazard model was constructed to predict cancer-specific death for patients with stage I SCLC. We also built a competing risk nomogram based on Fine and Gray’s model to predict the 3-year, the 5-year prognosis of SCLC patients. We evaluated the model performance by the c-index and calibration plot using a bootstrap cross-validation method with 200 resamples. All statistical analyses and visualization were performed on R statistical software version 3.4.4 (Institute for Statistics and Mathematics, Vienna, Austria). Statistical significance was set as a 2-sided p < 0.05.

      20c51b5f4e9aeb5334c90ff072e6f928 Results

      We identified 864 stage I SCLC patients. The 5-year cumulative incidence of cause-specific death for stage I SCLC was 56.2% and 13.7% for other causes of death. Predictive factors for the prognosis of stage I SCLC included age, surgery, chemotherapy, and radiotherapy (Table). Fine and Gray competing risk regression model indicated that age at diagnosis, surgery treatment, and radiotherapy could be independent predictive factors of SCLC cause-specific death. Those who were diagnosed with SCLC at an older age were more like to die of lung cancer, with a subdistribution hazard ratios (sdHR) of 1.02 (95% CI, 1.012-1.03). Patients without treatment were at an elevated risk of SCLC cause-specific death except for chemotherapy, with an sdHR of 2.85 (95% CI, 2.29-3.54) and 1.89 (95% CI, 1.53-2.33) for patients without surgery and radiotherapy, respectively. No statistical significance was detected between chemotherapy and SCLC cause-specific death. The competing risk nomogram based on the Fine and Gray’s model was established to predict the 3-year and 5-year cause-specific death. The c-index for SCLC cause-specific mortality model was 0.66, and the calibration curves suggested that the nomogram was well-calibrated.

      fd69c5cf902969e6fb71d043085ddee6 Conclusions

      In the study, we performed a competing risk analysis in patients with stage I SCLC based on the SEER database. We discovered independent predictive factors of death due to SCLC and built a nomogram to calculate the 3- and 5-year cause-specific mortality. The competing risk nomogram might be a convenient tool to evaluate crude mortalities of stage I SCLC, and help clinicians to choose appropriate treatment strategies.

      b651e8a99c4375feb982b7c2cad376e9 Legal entity responsible for the study

      The authors.

      213f68309caaa4ccc14d5f99789640ad Funding

      National Key R&D Program of China (2016YFC0905500).

      682889d0a1d3b50267a69346a750433d Disclosure

      All authors have declared no conflicts of interest.

      Five-year cumulative incidences of death among patients with stage I SCLC

      CharacteristicsN (%)Event (%)Cause-specific death
      Death from other causes
      5 year (%) (95% CI)p5 year (%) (95% CI)p
      Total86468056.2 (52.9-59.5)13.7 (11.5-16.1)
      Age (years)<0.0010.127
      <65257 (29.7)178 (26.2)48.5 (42.2-54.4)12.5 (8.8-16.9)
      65+607 (70.3)502 (42.9)59.5 (55.5-63.3)14.2 (11.6-17.1)
      Sex0.2030.373
      Male407 (47.1)332 (52.9)59.2 (54.2-63.8)15.4 (12.0-19.1)
      Female457 (52.9)348 (40.8)53.6 (48.9-58.1)12.3 (9.5-15.5)
      Race0.0960.096
      White772 (89.4)609 (89.6)55.8 (52.2-59.2)14.4 (12.0-17.0)
      Black68 (7.9)49 (7.2)58.2 (45.3-69.0)6.0 (1.9-13.5)
      Others/Unknown24 (2.8)22 (3.2)65.2 (41.0-81.5)13.0 (3.0-30.6)
      Surgery< 0.0010.548
      Yes305 (35.3)187 (27.5)39.2 (33.7-44.6)11.5 (8.2-15.4)
      No559 (64.7)493 (72.5)65.6 (61.5-69.3)14.9 (12.1-18.0)
      Chemotherapy< 0.0010.719
      Yes567 (65.6)433 (63.7)53.1 (48.9-57.1)13.1 (10.4-16.0)
      No297 (34.4)247 (36.3)62.3 (56.5-67.5)15.0 (11.1-19.3)
      Radiotherapy0.0040.035
      Yes399 (46.2)313 (46.0)52.2 (47.1-56.9)15.1 (11.8-18.8)
      No465 (53.8)367 (54.0)59.8 (55.1-64.1)12.6 (9.7-15.8)

      SCLC: Small cell lung cancer; CI: confidence interval

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