96080-114

Different EGFR/KRAS mutation spectrums in lung cancer between never smokers and heavy smokers.

Category: 
Tumor Biology
Session Type and Session Title: 
General Poster Session, Tumor Biology
Abstract Number: 

10548

Citation: 

J Clin Oncol 30, 2012 (suppl; abstr 10548)

Author(s): 

Kazuya Takamochi, Shiaki Oh, Kenji Suzuki; Juntendo University School of Medicine, Tokyo, Japan


Abstracts that were granted an exception in accordance with ASCO's Conflict of Interest Policy are designated with a caret symbol (^).

Abstract Disclosures

Abstract: 

Background: EGFR mutations are more commonly found in lung adenocarcinomas in never smokers, while KRAS mutations are more frequently present in those in heavy smokers. Although the incidence is low, EGFR mutations are also found in tumors in heavy smokers and KRAS mutations also occur in tumors in never smokers. Therefore, there may be different biological characteristics in EGFR/ KRAS mutated lung cancers according to the smoking status. Methods: This was a retrospective review of 382 patients with surgically resected lung cancers between February 2009 and March 2011. The clinicopathological factors (age, gender, histology, serum CEA level, pathological nodal status, lymphatic permeation, and blood vessel invasion) and EGFR/KRAS mutation spectrums were compared between never smokers (pack-year = 0, n = 161) and heavy smokers (pack-year > 20, n = 167). Results: EGFR mutations were detected in 88 (55%) never smokers and in 33 (20%) heavy smokers. In contrast, K-ras mutations were detected in 7 (4%) never smokers and in 31 (19%) heavy smokers. Both EGFR and KRAS mutations were more frequently observed in female never smokers and in male heavy smokers. The spectrum of both EGFR and KRAS mutation differed according to the smoking status. Minor EGFR mutations other than exon 21 L858R and exon 19 deletions that are activating mutations indicating the efficacy of EGFR tyrosine kinase inhibitors (TKIs) were more frequently found in heavy smokers than in never smokers. G→A transitions were more common KRAS mutations in never smokers and G→T transversions that are thought to be related to exposure to the polycyclic aromatic hydrocarbons found in cigarette smoke were more common KRAS mutations in heavy smokers. Conclusions: The EGFR/KRAS mutation spectrums in lung cancer were quite different in never smokers and heavy smokers. Further study is needed to evaluate the relationship between the efficacy of such molecular targeting agents as EGFR TKIs and the EGFR/KRAS mutation spectrums.