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Cancer Epidemiol Biomarkers Prev. 2014 Jul;23(7):1432-4. doi: 10.1158/1055-9965.EPI-14-0224. Epub 2014 Apr 22.

Evidence that the lung Adenocarcinoma EML4-ALK fusion gene is not caused by exposure to secondhand tobacco smoke during childhood.

Author information

  • 1Authors' Affiliations: Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland;
  • 2Division of Epidemiology, Department of Health Sciences Research; Division of Preventive Medicine, School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 3Department of Laboratory Medicine and Pathology; Gene Expression Core, Medical Genome Facility, Center for Individualized Medicine, Mayo Clinic, Rochester, Minnesota;
  • 4Department of Laboratory Medicine and Pathology;
  • 5Division of Epidemiology, College of Public Health, Ohio State University, Columbus, Ohio; and.
  • 6Division of Epidemiology, Department of Health Sciences Research;
  • 7Authors' Affiliations: Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland; Curtis_Harris@nih.gov.

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.

IMPACT:

These data suggest that childhood exposure to SHS is not a significant etiologic cause of the EML4-ALK fusion gene in lung cancer.

©2014 American Association for Cancer Research.

PMID:
24755712
[PubMed - in process]
PMCID:
PMC4082445
[Available on 2015/7/1]
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