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. 2011 Nov 16;3(2):207–213. doi: 10.3892/etm.2011.383

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Figure 4. — Kaplan-Meier analysis of overall survival calculated from patients commencing EGFR-TKI treatment. (A) Patients whose tumors had EGFR-activating mutations. No survival difference was noted in patients who received gefitinib treatment (n=94; censor, 54; median, 26 months) or erlotinib treatment (n=52; censor, 40; median, not reached) (p=0.2728; HR, 0.49; 95% CI, 0.36–1.22). (B) Patients whose tumors did not have EGFR-activating mutations. No survival difference was noted in patients who received gefitinib treatment (n=30; censor, 14; median, 8.6 months) or erlotinib treatment (n=48; censor, 31; median, not reached) (p=0.1104; HR, 0.58; 95% CI, 0.29–1.14). TKI, tyrosine kinase inhibitor; EGFR, epidermal growth factor receptor; HR, hazard ratio.

Figure 4. — Kaplan-Meier analysis of overall survival calculated from patients commencing EGFR-TKI treatment. (A) Patients whose tumors had EGFR-activating mutations. No survival difference was noted in patients who received gefitinib treatment (n=94; censor, 54; median, 26 months) or erlotinib treatment (n=52; censor, 40; median, not reached) (p=0.2728; HR, 0.49; 95% CI, 0.36–1.22). (B) Patients whose tumors did not have EGFR-activating mutations. No survival difference was noted in patients who received gefitinib treatment (n=30; censor, 14; median, 8.6 months) or erlotinib treatment (n=48; censor, 31; median, not reached) (p=0.1104; HR, 0.58; 95% CI, 0.29–1.14). TKI, tyrosine kinase inhibitor; EGFR, epidermal growth factor receptor; HR, hazard ratio.