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Article: Association of Exon 19 and 21 EGFR Mutation Patterns with Treatment Outcome after First-Line Tyrosine Kinase Inhibitor in Metastatic Non–Small-Cell Lung Cancer

TitleAssociation of Exon 19 and 21 EGFR Mutation Patterns with Treatment Outcome after First-Line Tyrosine Kinase Inhibitor in Metastatic Non–Small-Cell Lung Cancer
Authors
KeywordsEpidermal growth factor receptor
Non-small-cell lung cancer
Prognostic factors
Tyrosine kinase inhibitors
Issue Date2013
PublisherLippincott Williams & Wilkins.
Citation
Journal of Thoracic Oncology, 2013, v. 8 n. 9, p. 1148-1155 How to Cite?
AbstractBackground: This study investigated whether there were differential survival outcomes to first-line tyrosine kinase inhibitors (TKI) in patients with metastatic non–small-cell lung cancer harboring different subtypes of exon 19 and exon 21 mutations on epidermal growth factor receptor (EGFR). Methods: Of 452 patients with stage IIIB and IV non–small-cell lung cancer, 192 patients (42.5%) harbored EGFR mutation and 170 (37.5%) received TKI as first-line treatment. EGFR mutation analysis was performed by direct sequencing. Survival and response outcome were compared among different subtypes of exon 19 and exon 21 EGFR mutations in these 170 patients. Results: Patients harboring exon 19 18-nucleotide deletion (delL747_P753insS) had the shortest median progression-free survival (PFS) (6.5 months), followed by those with 15-nucleotide deletion (delE746_A750) (12.4 months) and mixed insertion/substitution mutations (22.3 months; p = 0.012). However, patients who had exon 19 deletions starting on codon E746 had better median PFS (14.2 months) than those starting on L747 (6.5 months; hazard ratio, 0.445; 95% confidence interval [0.219–0.903]; p = 0.021). Besides, exon 21 L858R derived a longer median PFS than L861R/L861Q (11.4 months versus 2.1 months, respectively; hazard ratio, 0.298; 95% confidence interval [0.090–0.980]; p = 0.034). Conclusions: Different subtypes of EGFR exon 19 and 21 mutations exhibited differential survival to first-line TKI therapy. Detailed sequence evaluation of exon 19 deletions may provide important prognostic information on survival outcome after TKI.
Persistent Identifierhttp://hdl.handle.net/10722/191306
ISSN
2019 Impact Factor: 13.357
2015 SCImago Journal Rankings: 2.597
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLee, VHFen_US
dc.contributor.authorTin, PCen_US
dc.contributor.authorChoy, TSen_US
dc.contributor.authorLam, KOen_US
dc.contributor.authorChoi, CWen_US
dc.contributor.authorChung, LPen_US
dc.contributor.authorTsang, JWHen_US
dc.contributor.authorHo, PPYen_US
dc.contributor.authorLeung, DKCen_US
dc.contributor.authorMa, ESKen_US
dc.contributor.authorLiu, J-
dc.contributor.authorShek, TWH-
dc.contributor.authorKwong, DLW-
dc.contributor.authorLeung, TW-
dc.contributor.authorWong, MP-
dc.date.accessioned2013-10-15T06:53:51Z-
dc.date.available2013-10-15T06:53:51Z-
dc.date.issued2013en_US
dc.identifier.citationJournal of Thoracic Oncology, 2013, v. 8 n. 9, p. 1148-1155en_US
dc.identifier.issn1556-0864-
dc.identifier.urihttp://hdl.handle.net/10722/191306-
dc.description.abstractBackground: This study investigated whether there were differential survival outcomes to first-line tyrosine kinase inhibitors (TKI) in patients with metastatic non–small-cell lung cancer harboring different subtypes of exon 19 and exon 21 mutations on epidermal growth factor receptor (EGFR). Methods: Of 452 patients with stage IIIB and IV non–small-cell lung cancer, 192 patients (42.5%) harbored EGFR mutation and 170 (37.5%) received TKI as first-line treatment. EGFR mutation analysis was performed by direct sequencing. Survival and response outcome were compared among different subtypes of exon 19 and exon 21 EGFR mutations in these 170 patients. Results: Patients harboring exon 19 18-nucleotide deletion (delL747_P753insS) had the shortest median progression-free survival (PFS) (6.5 months), followed by those with 15-nucleotide deletion (delE746_A750) (12.4 months) and mixed insertion/substitution mutations (22.3 months; p = 0.012). However, patients who had exon 19 deletions starting on codon E746 had better median PFS (14.2 months) than those starting on L747 (6.5 months; hazard ratio, 0.445; 95% confidence interval [0.219–0.903]; p = 0.021). Besides, exon 21 L858R derived a longer median PFS than L861R/L861Q (11.4 months versus 2.1 months, respectively; hazard ratio, 0.298; 95% confidence interval [0.090–0.980]; p = 0.034). Conclusions: Different subtypes of EGFR exon 19 and 21 mutations exhibited differential survival to first-line TKI therapy. Detailed sequence evaluation of exon 19 deletions may provide important prognostic information on survival outcome after TKI.-
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins.-
dc.relation.ispartofJournal of Thoracic Oncologyen_US
dc.subjectEpidermal growth factor receptor-
dc.subjectNon-small-cell lung cancer-
dc.subjectPrognostic factors-
dc.subjectTyrosine kinase inhibitors-
dc.titleAssociation of Exon 19 and 21 EGFR Mutation Patterns with Treatment Outcome after First-Line Tyrosine Kinase Inhibitor in Metastatic Non–Small-Cell Lung Canceren_US
dc.typeArticleen_US
dc.identifier.emailLee, VHF: vhflee@hku.hken_US
dc.identifier.emailTin, PC: pctin@hku.hken_US
dc.identifier.emailLam, KO: lamkaon@hku.hken_US
dc.identifier.emailTsang, JWH: jwhtsang@hku.hken_US
dc.identifier.emailChoy, TS: choyts@hku.hk-
dc.identifier.emailChoi, CW: hcchoi@hku.hk-
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hk-
dc.identifier.emailLiu, J: jingliue@hku.hk-
dc.identifier.emailShek, TWH: whshek@hkucc.hku.hk-
dc.identifier.emailKwong, DLW: dlwkwong@hku.hk-
dc.identifier.emailLeung, TW: ltw920@hkucc.hku.hk-
dc.identifier.emailWong, MP: mwpik@hku.hk-
dc.identifier.authorityLee, VHF=rp00264en_US
dc.identifier.authorityLam, KO=rp01501en_US
dc.identifier.authorityTsang, JWH=rp00278en_US
dc.identifier.authorityChung, LP=rp00249-
dc.identifier.authorityKwong, DLW=rp00414-
dc.identifier.authorityWong, MP=rp00348-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1097/JTO.0b013e31829f684a-
dc.identifier.pmid23945384-
dc.identifier.scopuseid_2-s2.0-84883378283-
dc.identifier.hkuros226498en_US
dc.identifier.hkuros223514-
dc.identifier.volume8en_US
dc.identifier.issue9-
dc.identifier.spage1148en_US
dc.identifier.epage1155en_US
dc.identifier.isiWOS:000323429100011-
dc.publisher.placeUnited States-

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