title: Evidence that the lung Adenocarcinoma EML4-ALK fusion gene is not caused by exposure to secondhand tobacco smoke during childhood.
abstract: BACKGROUND
  The EML4-ALK fusion gene is more frequently found in younger, never smoking patients with lung cancer. Meanwhile, never smokers exposed to secondhand tobacco smoke (SHS) during childhood are diagnosed at a younger age compared with never smoking patients with lung cancer who are not exposed. We, therefore, hypothesized that SHS, which can induce DNA damage, is associated with the EML4-ALK fusion gene.
  
  
  METHODS
  We compared the frequency of the EML4-ALK fusion gene among 197 never smoker patients with lung cancer with and without a history of exposure to SHS during childhood at Mayo Clinic.
  
  
  RESULTS
  The EML4-ALK fusion gene was detected in 33% of cases from never smokers with a history of SHS exposure during childhood, whereas 47% of never smoking lung cancer cases without a history of childhood SHS exposure tested positive for the fusion gene.
  
  
  CONCLUSIONS
  The EML4-ALK fusion gene is not enriched in tumors from individuals exposed to SHS during childhood.
  
  
  CONCLUSIONS
  These data suggest that childhood exposure to SHS is not a significant etiologic cause of the EML4-ALK fusion gene in lung cancer.
authors.affiliation: Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
authors.forename: Bríd M
authors.initials: BM
authors.lastname: Ryan
authors.affiliation: Division of Preventive Medicine, School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, China.|Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
authors.forename: Yi
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.|Gene Expression Core, Medical Genome Facility, Center for Individualized Medicine, Mayo Clinic, MN USA.
authors.forename: Jin
authors.initials: J
authors.lastname: Jen
authors.affiliation: Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.
authors.forename: Eunhee S
authors.initials: ES
authors.lastname: Yi
authors.affiliation: Division of Epidemiology, College of Public Health, Ohio State University, OH, US.
authors.forename: Susan
authors.initials: S
authors.lastname: Olivo-Marston
authors.affiliation: Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
authors.forename: Ping
authors.initials: P
authors.lastname: Yang
authors.affiliation: Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.
authors.forename: Curtis C
authors.initials: CC
authors.lastname: Harris
mesh_terms: D000230:Adenocarcinoma / Q000209:etiology* / Q000235:genetics; D000328:Adult; D002648:Child; D005260:Female; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008175:Lung Neoplasms / Q000209:etiology* / Q000235:genetics; D008297:Male; D015514:Oncogene Proteins, Fusion / Q000235:genetics*; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
chemical_list: C522504:EML4-ALK fusion protein, human; D015514:Oncogene Proteins, Fusion; D014028:Tobacco Smoke Pollution
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