Virtual Library

 x 
My Library Virtual Library FAQ

Start Your Search

J. Cadranel



Author of

  • +

    O18 - Cancer Control and Epidemiology II (ID 133)

    • Event: WCLC 2013
    • Type: Oral Abstract Session
    • Track: Prevention & Epidemiology
    • Presentations: 1
    • +

      O18.04 - Impact of Passive Smoking on molecular pattern in Never Smokers with Non-Small Cell Lung Cancer: Findings from the BioCAST / IFCT-1002 Study (ID 3305)

      11:00 - 11:10  |  Author(s): J. Cadranel

      • Abstract
      • Presentation
      • Slides

      Background
      EGFR and HER2 mutations are usually associated with never-smokers while KRAS and BRAF mutations are thought to be link with smoking behavior in Non-Small Cell Lung Cancer (NSCLC). Passive smoking exposure is a well-known risk factor for lung cancer. Only EGFR and KRAS mutations were investigated in association with passive smoking and showed conflicting results. We aimed to investigate mutation rate of EGFR, HER2, KRAS, BRAF and ALK in a cohort of never smokers regarding their passive smoke exposure.

      Methods
      The BioCAST / IFCT-1002 study is a prospective cohort of NSCLC patients diagnosed in French never-smokers patients (less than 100 cigarettes in lifetime) between November 2011 and January 2013, Passive smoking exposure was evaluated through standardized questionnaire. We obtained biomarkers mutation results through routine testing. We used Fisher, Chi-square, median test and Mann-Whitney U test for comparisons as appropriate. We used logistic regression to calculate adjusted odds ratio for risk of each mutations.

      Results
      Out of the 384 patients included in the BioCAST database, 334 (87.0%) had available data on passive smoking exposure. Among them, 219 patients (65.6%) were ever exposed to passive smoking in their lifetime. 198 (59.3%) reported a domestic exposure (122 during childhood at least) and 60 (18.0%) a workplace exposure. Result of at least one biomarker mutation was available in 313 patients (93.7%). including 128 EGFR mutations in 297 patients, 8/174 HER2 mutations, 18/256 KRAS mutations, 10/196 BRAF mutations, and 20/171 ALK gene rearrangements. We found no difference in mutation rate according to passive smoke exposure (cf. Table 1). There was no difference when comparing cumulative year of exposure, smoker-year or passive-pack year (as continuous variable) to the mutation rate, for any biomarker. When considered as categorical variable – after division in quartiles – we found also no difference. Results were similar when focusing on domestic (childhood versus adulthood included) and workplace exposure only. Finally, we found no significant increased risk for mutation for any biomarker in logistic regression adjusted for most of other lung cancer risk factors.

      EGFR Mt (n=297) HER2 Mt (n=171) KRAS Mt (n=256) BRAF Mt (n=196) ALK Fusion (n=171)
      % % % % %
      Overall exposure Never 46.5 3.5 6.7 5.9 13.0
      Ever 41.3 5.1 7.2 4.7 11.1
      Domestic exposure Never 45.8 2.9 7.7 6.4 11.1
      Ever 41.3 5.7 6.6 4.2 12.0
      Exposure at workplace Never 43.3 5.5 7.0 5.4 12.2
      Ever 42.3 0 7.0 3.6 8.3
      Total 43.1 4.6 7.0 5.1 11.7
      Exposure in childhood Ever 40.5 3.0 6.5 2.7 14.7
      Only in adulthood 42.6 10.3 6.8 6.7 7.5

      Conclusion
      Although we report the largest and more comprehensive study focusing on this topic, we found no significant difference in the biomarker mutation profile of NSCLC occurring in French never-smokers regarding their exposure to passive smoking as compared with the pattern of mutations described never-smoker patients with any passive smoking.

      Only 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, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.

      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.

  • +

    P2.24 - Poster Session 2 - Supportive Care (ID 157)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Supportive Care
    • Presentations: 1
    • +

      P2.24-038 - Lung cancer and combined pulmonary fibrosis and emphysema syndrome in Western patients: a series of 47 patients (ID 2844)

      09:30 - 09:30  |  Author(s): J. Cadranel

      • Abstract

      Background
      The syndrome of combined pulmonary fibrosis and emphysema (CPFE) is characterized by imaging features consisting of the association of centrilobular and/or paraseptal emphysema and pulmonary fibrosis, associated with subnormal spirometry, contrasting with severe impairment of gas exchange with strong decrease in carbon monoxide diffusing capacity, and hypoxaemia at exercise. Virtually all patients presenting with CPFE are smokers and may be at high-risk to develop lung cancer; limited data have been made available on such association, mostly from Japanese cohorts.

      Methods
      This retrospective multicentre study was conducted by the Groupe d’Etudes et de Recherche sur les Maladies “Orphelines” Pulmonaires (GERM”O”P), a collaborative group of about 200 French physicians dedicated to the study of rare pulmonary diseases. Patients presenting with CPFE syndrome and lung cancer at the referring centers from 2003 to 2012, were included. The clinical, pathological, and therapeutic features, as well as the outcome of patients, were collected and analyzed.

      Results
      A total of 47 patients presenting with lung cancer and CPFE syndrome were identified. All patients but one were men, with a mean age of 68 years. All patients were smokers, with a mean of 47 pack-years. The CPFE syndrome was diagnosed synchronously with lung cancer in 27 (57%) patients. Detection of lung cancer was incidental in 22 (47%) patients. The tumour was diagnosed at an early-stage, i.e. stage I-II, in 55% of cases. A pathological diagnosis of lung cancer was obtained for only 38 (81%) patients. Histological type was squamous cell carcinoma in 17 (36%) patients, adenocarcinoma in 14 (30%) patients, non-small cell lung cancer not otherwise specified in 3 (6%) patients, small cell lung cancer in 3 (6%) patients, and sarcomatoid carcinoma in one (2%) patient. There was no significant relation between tumor histology and location in the lung parenchyma (p=0.32). Overall, 20 of the 47 patients could not receive standard-of-care treatment for lung cancer, as per international recommendations and guidelines; this limitation was considered to be directly related to the CPFE syndrome in 8 (40%) cases. After a mean follow-up of 17 months, 35 patients were dead, and 12 patients were alive. Causes of death included locoregional or systemic tumor progression in 5 (14%) and 17 (49%) patients, respectively, respiratory failure in 8 (23%) patients, treatment-induced toxicity in 4 (11%) patients, and post-operative exacerbation of pulmonary fibrosis in 1 (3%) patient.

      Conclusion
      Lung cancer in patients with CPFE syndrome represents a specific entity characterized by very strong association with tobacco-smoking and male gender, peculiar histological-radiological presentation, poor prognosis due to major limitations and risks to conduct standard-of-care diagnostic and therapeutic interventions in a significant proportion of patients, and possible interest of screening. Lung cancer in CPFE syndrome further represents the most characteristic and severe model of tobacco-related disease.