Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Jornal Brasileiro de Pneumologia (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1806-37132015000400365 |
Resumo: | AbstractLung cancer is the leading cause of cancer-related deaths worldwide. Promising new therapies have recently emerged from the development of molecular targeted drugs; particularly promising are those blocking the signal transduction machinery of cancer cells. One of the most widely studied cell signaling pathways is that of EGFR, which leads to uncontrolled cell proliferation, increased cell angiogenesis, and greater cell invasiveness. Activating mutations in the EGFR gene (deletions in exon 19 and mutation L858R in exon 21), first described in 2004, have been detected in approximately 10% of all non-squamous non-small cell lung cancer (NSCLC) patients in Western countries and are the most important predictors of a response to EGFR tyrosine-kinase inhibitors (EGFR-TKIs). Studies of the EGFR-TKIs gefitinib, erlotinib, and afatinib, in comparison with platinum-based regimens, as first-line treatments in chemotherapy-naïve patients have shown that the EGFR-TKIs produce gains in progression-free survival and overall response rates, although only in patients whose tumors harbor activating mutations in the EGFR gene. Clinical trials have also shown EGFR-TKIs to be effective as second- and third-line therapies in advanced NSCLC. Here, we review the main aspects of EGFR pathway activation in NSCLC, underscore the importance of correctly identifying activating mutations in the EGFR gene, and discuss the main outcomes of EGFR-TKI treatment in NSCLC. |
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Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancerMolecular targeted therapyReceptor, epidermal growth factorLung neoplasms/drug therapyMutationOncogenesAbstractLung cancer is the leading cause of cancer-related deaths worldwide. Promising new therapies have recently emerged from the development of molecular targeted drugs; particularly promising are those blocking the signal transduction machinery of cancer cells. One of the most widely studied cell signaling pathways is that of EGFR, which leads to uncontrolled cell proliferation, increased cell angiogenesis, and greater cell invasiveness. Activating mutations in the EGFR gene (deletions in exon 19 and mutation L858R in exon 21), first described in 2004, have been detected in approximately 10% of all non-squamous non-small cell lung cancer (NSCLC) patients in Western countries and are the most important predictors of a response to EGFR tyrosine-kinase inhibitors (EGFR-TKIs). Studies of the EGFR-TKIs gefitinib, erlotinib, and afatinib, in comparison with platinum-based regimens, as first-line treatments in chemotherapy-naïve patients have shown that the EGFR-TKIs produce gains in progression-free survival and overall response rates, although only in patients whose tumors harbor activating mutations in the EGFR gene. Clinical trials have also shown EGFR-TKIs to be effective as second- and third-line therapies in advanced NSCLC. Here, we review the main aspects of EGFR pathway activation in NSCLC, underscore the importance of correctly identifying activating mutations in the EGFR gene, and discuss the main outcomes of EGFR-TKI treatment in NSCLC.Sociedade Brasileira de Pneumologia e Tisiologia2015-08-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1806-37132015000400365Jornal Brasileiro de Pneumologia v.41 n.4 2015reponame:Jornal Brasileiro de Pneumologia (Online)instname:Sociedade Brasileira de Pneumologia e Tisiologia (SBPT)instacron:SBPT10.1590/S1806-37132015000004531info:eu-repo/semantics/openAccessLopes,Gabriel LimaVattimo,Edoardo Filippo de QueirozCastro Junior,Gilberto deeng2015-09-14T00:00:00Zoai:scielo:S1806-37132015000400365Revistahttp://www.jornaldepneumologia.com.br/default.aspONGhttps://old.scielo.br/oai/scielo-oai.php||jbp@jbp.org.br|| jpneumo@jornaldepneumologia.com.br1806-37561806-3713opendoar:2015-09-14T00:00Jornal Brasileiro de Pneumologia (Online) - Sociedade Brasileira de Pneumologia e Tisiologia (SBPT)false |
dc.title.none.fl_str_mv |
Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer |
title |
Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer |
spellingShingle |
Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer Lopes,Gabriel Lima Molecular targeted therapy Receptor, epidermal growth factor Lung neoplasms/drug therapy Mutation Oncogenes |
title_short |
Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer |
title_full |
Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer |
title_fullStr |
Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer |
title_full_unstemmed |
Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer |
title_sort |
Identifying activating mutations in the EGFR gene: prognostic and therapeutic implications in non-small cell lung cancer |
author |
Lopes,Gabriel Lima |
author_facet |
Lopes,Gabriel Lima Vattimo,Edoardo Filippo de Queiroz Castro Junior,Gilberto de |
author_role |
author |
author2 |
Vattimo,Edoardo Filippo de Queiroz Castro Junior,Gilberto de |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Lopes,Gabriel Lima Vattimo,Edoardo Filippo de Queiroz Castro Junior,Gilberto de |
dc.subject.por.fl_str_mv |
Molecular targeted therapy Receptor, epidermal growth factor Lung neoplasms/drug therapy Mutation Oncogenes |
topic |
Molecular targeted therapy Receptor, epidermal growth factor Lung neoplasms/drug therapy Mutation Oncogenes |
description |
AbstractLung cancer is the leading cause of cancer-related deaths worldwide. Promising new therapies have recently emerged from the development of molecular targeted drugs; particularly promising are those blocking the signal transduction machinery of cancer cells. One of the most widely studied cell signaling pathways is that of EGFR, which leads to uncontrolled cell proliferation, increased cell angiogenesis, and greater cell invasiveness. Activating mutations in the EGFR gene (deletions in exon 19 and mutation L858R in exon 21), first described in 2004, have been detected in approximately 10% of all non-squamous non-small cell lung cancer (NSCLC) patients in Western countries and are the most important predictors of a response to EGFR tyrosine-kinase inhibitors (EGFR-TKIs). Studies of the EGFR-TKIs gefitinib, erlotinib, and afatinib, in comparison with platinum-based regimens, as first-line treatments in chemotherapy-naïve patients have shown that the EGFR-TKIs produce gains in progression-free survival and overall response rates, although only in patients whose tumors harbor activating mutations in the EGFR gene. Clinical trials have also shown EGFR-TKIs to be effective as second- and third-line therapies in advanced NSCLC. Here, we review the main aspects of EGFR pathway activation in NSCLC, underscore the importance of correctly identifying activating mutations in the EGFR gene, and discuss the main outcomes of EGFR-TKI treatment in NSCLC. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-08-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1806-37132015000400365 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1806-37132015000400365 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S1806-37132015000004531 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Pneumologia e Tisiologia |
publisher.none.fl_str_mv |
Sociedade Brasileira de Pneumologia e Tisiologia |
dc.source.none.fl_str_mv |
Jornal Brasileiro de Pneumologia v.41 n.4 2015 reponame:Jornal Brasileiro de Pneumologia (Online) instname:Sociedade Brasileira de Pneumologia e Tisiologia (SBPT) instacron:SBPT |
instname_str |
Sociedade Brasileira de Pneumologia e Tisiologia (SBPT) |
instacron_str |
SBPT |
institution |
SBPT |
reponame_str |
Jornal Brasileiro de Pneumologia (Online) |
collection |
Jornal Brasileiro de Pneumologia (Online) |
repository.name.fl_str_mv |
Jornal Brasileiro de Pneumologia (Online) - Sociedade Brasileira de Pneumologia e Tisiologia (SBPT) |
repository.mail.fl_str_mv |
||jbp@jbp.org.br|| jpneumo@jornaldepneumologia.com.br |
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1750318346325196800 |