EGFR and KRAS mutation coexistence in lung adenocarcinomas
Lung cancer is one of the most common causes of cancer deaths. The development of EGFR targeted therapies, including monoclonal antibodies and tyrosine kinase inhibitors have generated an interest in the molecular characterization of these tumours. KRAS mutations are associated with resistance to EGFR TKIs. EGFR and KRAS mutations have been considered as mutually exclusive.
This paper presents three bronchial-pulmonary carcinomas, two adenocarcinomas and one pleomorphic sarcomatoid carcinoma, harboring EGFR and KRAS mutations.
Case 1 corresponded to an adenocarcinoma with EGFR exon 21 mutation (L858R) and KRAS codon 12 point mutation (G12V); case 2, aÂ mucinous adenocarcinoma expressed coexistence of EGFR exon 21 mutation (L858R) and KRAS codon 12 point mutation (G12V); and case 3 a sarcomatoid carcinoma with EGFR exon 19 deletion â€“ del 9bp and KRAS codon 12 point mutation (G12C - cysteine).
Based on our experience and on the literature, we conclude that EGFR and KRAS mutations can indeed coexist in the same bronchial-pulmonary carcinoma, either in the same histological type or in different patterns. The biological implications of this coexistence are still poorly understood mainly because these cases are not frequent or currently searched. It is therefore necessary to study larger series of cases with the two mutations to better understand the biological, clinical and therapeutic implications.
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