Multiplicity of EGFR and KRAS mutations in non-small cell lung cancer (NSCLC) patients treated with tyrosine kinase inhibitors
Jazyk angličtina Země Řecko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
20592359
PII: 30/5/1667
Knihovny.cz E-zdroje
- MeSH
- erbB receptory genetika MeSH
- geny ras * MeSH
- inhibitory proteinkinas farmakologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- modely genetické MeSH
- mutace MeSH
- nádory plic genetika MeSH
- nemalobuněčný karcinom plic genetika MeSH
- prognóza MeSH
- Ras proteiny genetika MeSH
- senioři MeSH
- tyrosinkinasy antagonisté a inhibitory MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- erbB receptory MeSH
- inhibitory proteinkinas MeSH
- Ras proteiny MeSH
- tyrosinkinasy MeSH
BACKGROUND: Concurrent presence of EGFR and KRAS mutations in non-small cell lung cancer (NSCLC) patients is relatively rare and their appearance is believed to be mutually exclusive. Tumours harbouring KRAS mutation are perceived as not being capable of response to tyrosine kinase inhibitor (TKI) therapy. PATIENTS AND METHODS: This paper presents 5 case reports of patients with tumours harbouring multiple EGFR and/or KRAS mutations. There were 3 patients with EGFR mutations (2 x exon 19 deletions, 1 x L858R) combined with KRAS mutations (2 x Gly12Asp, 1 x Gly12Val), 1 patient with two EGFR mutations (exon 19 deletion + L858R) and 1 patient with two KRAS mutations (Ala11Pro + Gly12Val). RESULTS: All EGFR(+)/KRAS(+) patients had initially showed positive response to TKI treatment. The EGFR(+)/EGFR(+) patient has exhibited strong rash and good response with the best survival, while the KRAS(+)/KRAS(+) patient did not respond to TKI therapy. CONCLUSION: EGFR(+)/KRAS(+) combination does not necessarily pose a negative prediction. This is probably due to the multiclonal character of the tumour displaying partial response in the EGFR(+) subpopulation.