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Article

Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers

  • Authors:
    • Kazuya Takamochi
    • Shiaki Oh
    • Kenji Suzuki
  • View Affiliations / Copyright

    Affiliations: Department of General Thoracic Surgery, Juntendo University School of Medicine, Bunkyo‑ku, Tokyo 113‑8431, Japan
  • Pages: 1207-1212
    |
    Published online on: August 29, 2013
       https://doi.org/10.3892/ol.2013.1551
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Abstract

Epidermal growth factor receptor (EGFR) mutations are common in lung adenocarcinomas of never smokers, while KRAS mutations are more frequent among heavy smokers. Different clinicopathological and biological characteristics may, therefore, exist in lung adenocarcinoma according to smoking status. In the present study, a retrospective review was performed using 521 patients with surgically resected lung adenocarcinomas. The clinicopathological factors of age, gender, pathological tumor size, nodal status, lymphatic permeation and blood vessel invasion and the EGFR and KRAS mutation spectra were compared between never and heavy smokers. EGFR mutations were detected in 233 (45%) patients, while KRAS mutations were detected in 56 (11%) patients. EGFR‑mutated adenocarcinomas had a higher prevalence of females in the never smokers compared with the heavy smokers (P<0.001). KRAS‑mutated adenocarcinomas had a higher prevalence of females (P<0.001) and showed less frequent vascular invasion (P=0.018) in the never smokers compared with the heavy smokers. Minor EGFR mutations, excluding exon 21 L858R and exon 19 deletions, w­ere more common in heavy smokers than never smokers (P=0.055). KRAS G to A transition was more common in never smokers, while KRAS G to T and G to C transversions were more common in heavy smokers (P=0.036). The clinicopathological characteristics and the spectra of the EGFR and KRAS mutations in lung adenocarcinoma were different between the never and heavy smokers. Further large‑scale studies are required to evaluate the efficacy of molecular targeting agents with consideration to specific EGFR and KRAS mutations.
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Copy and paste a formatted citation
Spandidos Publications style
Takamochi K, Oh S and Suzuki K: Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers. Oncol Lett 6: 1207-1212, 2013.
APA
Takamochi, K., Oh, S., & Suzuki, K. (2013). Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers. Oncology Letters, 6, 1207-1212. https://doi.org/10.3892/ol.2013.1551
MLA
Takamochi, K., Oh, S., Suzuki, K."Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers". Oncology Letters 6.5 (2013): 1207-1212.
Chicago
Takamochi, K., Oh, S., Suzuki, K."Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers". Oncology Letters 6, no. 5 (2013): 1207-1212. https://doi.org/10.3892/ol.2013.1551
Copy and paste a formatted citation
x
Spandidos Publications style
Takamochi K, Oh S and Suzuki K: Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers. Oncol Lett 6: 1207-1212, 2013.
APA
Takamochi, K., Oh, S., & Suzuki, K. (2013). Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers. Oncology Letters, 6, 1207-1212. https://doi.org/10.3892/ol.2013.1551
MLA
Takamochi, K., Oh, S., Suzuki, K."Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers". Oncology Letters 6.5 (2013): 1207-1212.
Chicago
Takamochi, K., Oh, S., Suzuki, K."Differences in EGFR and KRAS mutation spectra in lung adenocarcinoma of never and heavy smokers". Oncology Letters 6, no. 5 (2013): 1207-1212. https://doi.org/10.3892/ol.2013.1551
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