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. 2015 Mar 19;10(3):e0120852. doi: 10.1371/journal.pone.0120852

Table 3. Univariate analysis of genetic alterations and clinical characteristics.

EGFR * KRAS * HER2 * BRAF * ALK **
Characteristics n (%) P value n (%) P value n (%) P value n (%) P value n (%) P value
Age (years) 0.501 0.200 0.502 0.777 0.002
 ≤ 65 536 (55.0) 45 (4.6) 22 (2.3) 6 (0.6) 25 (14.0)
 > 65 451 (56.6) 48 (6.0) 14 (1.8) 6 (0.8) 4 (3.4)
Gender <0.001 <0.001 0.312 0.781 0.331
 Male 367 (44.7) 76 (9.3) 20 (2.4) 5 (0.6) 12 (8.0)
 Female 620 (65.2) 17 (1.8) 16 (1.7) 7 (0.7) 17 (11.7)
Smoking status <0.001 <0.001 1.000 1.000 0.167
 Non-smokers 753 (63.9) 20 (1.7) 24 (2.0) 8 (0.7) 21 (11.9)
 Current/former smokers 234 (39.5) 73 (12.3) 12 (2.0) 4 (0.7) 8 (6.8)
Stage, n (%) # 0.187 1.000 0.015 0.754 0.837
 I-IIIa 298 (58.2) 27 (5.3) 4 (0.8) 4 (0.9) 10 (10.4)
 IIIb-IV 682 (54.6) 66 (5.3) 32 (2.6) 8 (0.6) 19 (9.6)

EGFR, epidermal growth factor receptor; ALK, anaplastic lymphoma kinase.

*Cohort 1 (1772 patients with lung adenocarcinoma) testing of EGFR, KRAS, HER2 and BRAF mutations.

**Cohort 2 (295 patients with EGFR-wild type lung adenocarcinoma) testing of EML4-ALK translocation.

#Exclude 12 patients of cohort 1 and 1 patients of cohort 2 with incomplete data on tumor staging For KRAS mutations, a significantly higher mutation rate was noted in male then in female patients (9.3 vs. 1.8%, P < 0.001) and in smokers then in non-smokers (12.3 vs. 1.7%, P < 0.001). Neither age nor tumor stage were correlated with KRAS mutation. For HER2 mutations, patients with more advanced diseases were associated with a higher mutation rate (2.6% in stage IIIb-IV vs. 0.8% in stage I-IIIa, P = 0.015). For BRAF mutation, there was no significant association between patient characteristics and the mutation rate.