Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
1600072
Reference Type
Journal Article
Subtype
Review
Title
Lung cancer in never smokers--a review
Author(s)
Couraud, S; Zalcman, G; Milleron, B; Morin, F; Souquet, PJ
Year
2012
Is Peer Reviewed?
Yes
Journal
European Journal of Cancer
ISSN:
0959-8049
EISSN:
1879-0852
Volume
48
Issue
9
Page Numbers
1299-1311
Language
English
PMID
22464348
DOI
10.1016/j.ejca.2012.03.007
Web of Science Id
WOS:000304243300006
Abstract
An estimated 10-25% of lung cancers worldwide occur in never smokers, i.e. individuals having smoked less than 100 cigarettes in their lifetime. Lung cancer in never smokers (LCINS) is more frequent in women, although large geographic variations are found. Histologically, adenocarcinomas predominate. The mere existence of LCINS suggests that risk factors other than smoking must be present. Exposure to environmental tobacco smoke (particularly in women) and exposure to workplace carcinogens (particularly in men) are the two most important alternative risk factors. However, a history of either is absent in more than a third of LCINS. The large proportion of women in LCINS suggest a hormonal element that may interact with other identified factors such as hereditary risks, a history of respiratory infections or disease, exposure to air pollution, cooking and heating fumes, or exposure to ionising radiation. The study of genomic polymorphisms finds constitutive DNA variations across subjects according to their smoking status, particularly in genes coding for enzymes that participate in the metabolism of certain carcinogens, in those coding for DNA repair enzymes, or in genes associated with tobacco addiction, or inflammatory processes. The type of molecular mutation in p53 or KRAS varies with smoking status. EGFR mutations are more frequent in never smokers, as are EML4-ALK fusions. The mutually exclusive nature of certain mutations is a strong argument in favour of separate genetic paths to cancer for ever smokers and never smokers. In the present paper we review current clinical and molecular aspects of LCINS.
Keywords
Lung cancer; Never smoker; Pollution; Biomarkers; Genetic polymorphism; Genome wide association study
Tags
•
LitSearch-NOx (2024)
Forward Citation Search
Exposure
Results
Confounding
PubMed
Other
•
Mouse Lung Tumor Workshop 2014
Cited
Key Reference
Session 1 – Epidemiology and Human Pathophysiology
Human Lung Cancer
Mechanisms
Human Pathophysiology
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity