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The epidermal growth factor receptor (EGFR) is found in 40–80% of non-small cell lung cancers (NSCLC). Somatic mutations of the tyrosine kinase domain of EGFR have been reported in patients with NSCLC who had clinical responses to treatment with tyrosine kinase inhibitors targeted against EGFR. However, little is known about the early pathogenesis of lung adencarcinomas and whether EGFR mutations are involved in this process.
The authors obtained surgically resected tissue specimens from 20 patients with adenocarcinomas and one with adenosquamous carcinoma, all with EGFR gene mutations. Most patients were women and never or former smokers. They also obtained tissue specimens from 16 patients with adenocarcinomas without EGFR mutation as a control group. Microdissection was done to obtain multiple foci of normal epithelium within the tumour and from adjacent normal lung tissue. DNA was extracted from cells obtained from these foci and analysed for EGFR mutation (axons 19 and 21).
Nine of the 21 patients with mutant lung adenocarcinomas (43%) were found to have identical EGFR mutations in normal epithelium foci within the tumour. However, none of the 16 patients in the control group (without tumour EGFR mutations) had mutations in the normal respiratory epithelium. Interestingly, EGFR mutations in normal respiratory epithelium were more frequent within the tumour (43%) than in adjacent sites (24%).
The findings of EGFR mutations in histologically normal epithelium have not been reported before and provide a new insight into the possible mechanisms involved in initiation of peripheral airway tumours such as lung adenocarcinoma. This may provide a future target for detection or treatment.
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