Non‑small cell lung cancer with EGFR mutations

05/2018

Prof. MUDr. Jana Skřičková, CSc.1, Mgr. Blanka Robešová, Ph.D.2, MUDr. Ondřej Venclíček1, MUDr. Bohdan Kadlec, Ph.D.1, MUDr. Marcela Tomíšková1, MUDr. Lenka Jakubíková, Ph.D.1, MUDr. Jana Špeldová1, MUDr. Zdeněk Merta, CSc.1

1) Klinika nemocí plicních a tuberkulózy LF MU a FN, Brno

2) Interní hematologická a onkologická klinika, Centrum molekulární biologie a genové terapie LF MU a FN, Brno

 

SUMMARY

In the case of non-small cell lung cancer (NSCLC), the existence of somatic mutations in the epidermal growth factor receptor (EGFR) gene and their effect on the sensitivity to the treatment of tyrosine kinase inhibitors (TKI) is known. Mutations occur in the tyrosine kinase domain between EGFR exon 18 and 21, predominantly point deletions and deletions, eventually insertions. In exons 19 and 21, 80-90% of known activating mutations of EGFR are concentrated. The so-called activation mutations include the G719X point mutation in exon 18, the L858R and L861Q point mutations in exon 21 and the deletion in exon 19. Among so-called resistant mutations are the insertions in exon 20, the T790M and S768I point mutations in exon 20, and the D761Y mutation in exon 19. The mutation rate of the EGFR gene in the Caucasian population is 10%. In NSCLC patients experiencing activation mutations for EGFR, the most effective treatment is with tyrosine kinase inhibitors. In our paper, we investigate the activation and resistance mutations of the EGFR gene and provide an overview of the results of first, second and third generation of TKI treatment.

 

KEY WORDS

non-small cell lung cancer, activated EGFR mutation, mutation T790M, tyrosine kinase inhibitors

 

 

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