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The diverse diversity.

The human being is genomically similar to a chimpanzee, while phenotypically different.1,2 Most of the differences are due to a relatively small number of changes in gene regulation, implying that small genomic differences may cause significant phenotypic diversities. Simple base-pair deletion at epidermal growth factor receptor (EGFR) exon 19 or single point mutation at EGFR exon 21 has dramatically shifted the treatment paradigm of patients with advanced non-small cell lung cancer. Most patients with the mutation will likely respond to EGFR tyrosine kinase inhibitor (TKI) such as gefitinib or erlotinib and benefit from a prolonged duration of progression-free survival.3–5 EGFR TKI is now considered a standard first-line therapy for patients harboring the EGFR mutation. The key issue is to identify these patients in daily practice, thus population-based incidence rate will be an important guide to oncologists. Helland et al.6 reported in the current issue of Journal of Thoracic Oncology the EGFR mutation rate of 7.5% in Norwegian patients with resectable early-stage non-small cell lung cancer. This represents the first report from northern Europe. Authors chose to study the incidence on resected lung tumor to reduce sample bias. Their decision assures sufficient tumor sample for EGFR mutation analysis, but their result may not be directly comparable with other existing reports on EGFR mutations that were conducted in patients with advanced-stage disease. The truth is that the current clinical indication for EGFR TKI is for patients with stage IV lung cancer with EGFR mutation. We cannot assume the incidence of EGFR mutation in early-stage lung cancer to be representative of patients with advanced-stage disease. Diversity in incidence of EGFR mutation may partly be explained by the diversity in population selection. The highest incidence of EGFR mutation reported in a white population was 35%, in which the study population included only adenocarcinoma and 38% of whom were never smokers.7 In unselected white population, the incidence ranges from 4.5 to 16.6%.8,9 Smoking history of the study population contributes to the incidence. The number of pack years of smoking is in reverse proportion to the frequency of mutations.10 Patients with more than 15 pack-year tobacco consumption has a far lower chance of harboring EGFR mutation. Unfortunately, most of the population-based study only classified patient qualitatively as never, former, or current smoker and failed to include quantitative documentation on tobacco consumption. In the report by Helland et al., previous smoker was defined as having stopped smoking at least 1 year before surgery. This definition would have limited correlation with the chance of harboring EGFR mutation. A patient with 30 pack-year history of tobacco consumption and who quit over 1 year before would have much lower incidence than a patient with 10 pack-year history and quitted for the same duration. Authors included only 15 never smokers in the study population of 240 Norwegians and failed to report the national statistics on never smoker with lung cancer in their country. Expectedly, 8 (53%) of the 15 never smokers were positive for EGFR mutation. If more “never smokers” were included in the study population, the overall incidence would be higher than 7.5%. Therefore, the “apparent” ethnic-based incidence depends on proportion of never smokers in the study population.