Your browser doesn't support javascript.
loading
Non-small-cell lung cancer harbouring mutations in the EGFR kinase domain
Rosell, R; Morán, T; Carcereny, E; Quiroga, V; Molina, M. A; Costa, C; Benlloch, S; Tarón, M.
Afiliação
  • Rosell, R; Hospital Germans Trias i Pujol. Badalona. Spain
  • Morán, T; Hospital Germans Trias i Pujol. Badalona. Spain
  • Carcereny, E; Hospital Germans Trias i Pujol. Badalona. Spain
  • Quiroga, V; Hospital Germans Trias i Pujol. Badalona. Spain
  • Molina, M. A; USP Dexeus University Institute. Barcelona. Spain
  • Costa, C; USP Dexeus University Institute. Barcelona. Spain
  • Benlloch, S; USP Dexeus University Institute. Barcelona. Spain
  • Tarón, M; Hospital Germans Trias i Pujol. Badalona. Spain
Clin. transl. oncol. (Print) ; 12(2): 75-80, feb. 2010. ilus
Artigo em Inglês | IBECS | ID: ibc-123890
Biblioteca responsável: ES1.1
Localização: BNCS
ABSTRACT
Key "driver" mutations have been discovered in specific subgroups of non-small-cell lung cancer (NSCLC) patients. Activating mutations in the form of deletions in exon 19 (del 19) or the missense mutation L858R in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) predict outcome to EGFR tyrosine kinase inhibitors (TKIs) such as gefitinib and erlotinib. Pooled data from several phase II studies show that gefitinib and erlotinib induce responses in over 70% of NSCLC patients harbouring EGFR mutations, with progression-free survival (PFS) ranging from 9 to 13 months and median survival of around 23 months. Two studies in Caucasian and Asian patients have confirmed that these subgroups of patients attain response rates of 70% with erlotinib and ge- fitinib, including complete responses, PFS up to 14 months and median survival up to 27 months. These landmark outcomes have been accompanied by new challenges the additional role of chemotherapy and the management of tumours with the secondary T790M mutation that confers resistance to EGFR TKIs. Mechanisms of resistance to reversible EGFR TKIs should be further clarified and could be related to modifications in DNA repair. The presence of double mutations (T790M plus either L858R or del 19) at the time of diagnosis could be much more frequent than originally thought. The sensitivity to EGFR TKIs could be greatly influenced by the expression of genes involved in the repair of DNA double-strand breaks by homologous recombination and non-homologous end joining (AU)
Assuntos
Buscar no Google
Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Estrutura Terciária de Proteína / Carcinoma Pulmonar de Células não Pequenas / Receptores ErbB / Neoplasias Pulmonares / Mutação / Antineoplásicos Tipo de estudo: Estudo prognóstico Limite: Feminino / Humanos / Masculino País/Região como assunto: Europa Idioma: Inglês Revista: Clin. transl. oncol. (Print) Ano de publicação: 2010 Tipo de documento: Artigo Instituição/País de afiliação: Hospital Germans Trias i Pujol/Spain / USP Dexeus University Institute/Spain
Buscar no Google
Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Estrutura Terciária de Proteína / Carcinoma Pulmonar de Células não Pequenas / Receptores ErbB / Neoplasias Pulmonares / Mutação / Antineoplásicos Tipo de estudo: Estudo prognóstico Limite: Feminino / Humanos / Masculino País/Região como assunto: Europa Idioma: Inglês Revista: Clin. transl. oncol. (Print) Ano de publicação: 2010 Tipo de documento: Artigo Instituição/País de afiliação: Hospital Germans Trias i Pujol/Spain / USP Dexeus University Institute/Spain
...