Activity of EGFR TKIs in Caucasian Patients With NSCLC Harboring Potentially Sensitive Uncommon EGFR Mutations.


Journal

Clinical lung cancer
ISSN: 1938-0690
Titre abrégé: Clin Lung Cancer
Pays: United States
ID NLM: 100893225

Informations de publication

Date de publication:
03 2019
Historique:
received: 21 09 2018
revised: 30 10 2018
accepted: 11 11 2018
pubmed: 20 12 2018
medline: 27 6 2019
entrez: 20 12 2018
Statut: ppublish

Résumé

Molecular characterization of non-small-cell lung cancer (NSCLC), defined predictive and druggable mutations that greatly modified patient prognoses. The most frequent driver mutations detected in NSCLC are epidermal growth factor receptor (EGFR) mutations, accounting for approximately 90% of exon 19 deletions and exon 21 point mutations. The other EGFR mutations are classified as uncommon or nonclassical and include exon 18 point mutations, exon 20 insertions, and combined mutations, which present different sensitivity to tyrosine kinase inhibitor (TKI) targeting. We collected data from EGFR TKI-naive patients with metastatic NSCLC, harboring EGFR exon 18 mutations and EGFR combined mutations treated with first- or second-generation EGFR TKIs. Efficacy end points were evaluated considering the activity of EGFR TKIs in exon 18 versus double-mutation EGFR groups. Eighty-eight patients harboring uncommon EGFR mutations were evaluated in our analysis, and subdivided into 2 group: complex mutations (cohort A = 46 patients) and double mutations in exon 18 (cohort B = 42 patients). The results showed a median progression-free survival of 8.3 versus 12.3 months (hazard ratio [HR], 0.65; P = .06) and a median overall survival of 17.0 versus 31.0 months (HR, 0.62, P = .04) favoring the EGFR combination group. Within the combination group, no detrimental effect was associated with exon 20 mutations. Our study confirmed that EGFR exon 18 and combination mutations might be considered potentially sensitive uncommon mutations, with a similar survival compared with the well known common EGFR mutations. Comparative analysis showed that patients with complex mutations achieved longer survival compared with the exon 18 group, without correlation with the presence of exon 20 mutations.

Sections du résumé

BACKGROUND
Molecular characterization of non-small-cell lung cancer (NSCLC), defined predictive and druggable mutations that greatly modified patient prognoses. The most frequent driver mutations detected in NSCLC are epidermal growth factor receptor (EGFR) mutations, accounting for approximately 90% of exon 19 deletions and exon 21 point mutations. The other EGFR mutations are classified as uncommon or nonclassical and include exon 18 point mutations, exon 20 insertions, and combined mutations, which present different sensitivity to tyrosine kinase inhibitor (TKI) targeting.
PATIENTS AND METHODS
We collected data from EGFR TKI-naive patients with metastatic NSCLC, harboring EGFR exon 18 mutations and EGFR combined mutations treated with first- or second-generation EGFR TKIs. Efficacy end points were evaluated considering the activity of EGFR TKIs in exon 18 versus double-mutation EGFR groups.
RESULTS
Eighty-eight patients harboring uncommon EGFR mutations were evaluated in our analysis, and subdivided into 2 group: complex mutations (cohort A = 46 patients) and double mutations in exon 18 (cohort B = 42 patients). The results showed a median progression-free survival of 8.3 versus 12.3 months (hazard ratio [HR], 0.65; P = .06) and a median overall survival of 17.0 versus 31.0 months (HR, 0.62, P = .04) favoring the EGFR combination group. Within the combination group, no detrimental effect was associated with exon 20 mutations.
CONCLUSION
Our study confirmed that EGFR exon 18 and combination mutations might be considered potentially sensitive uncommon mutations, with a similar survival compared with the well known common EGFR mutations. Comparative analysis showed that patients with complex mutations achieved longer survival compared with the exon 18 group, without correlation with the presence of exon 20 mutations.

Identifiants

pubmed: 30563752
pii: S1525-7304(18)30301-2
doi: 10.1016/j.cllc.2018.11.005
pii:
doi:

Substances chimiques

Antineoplastic Agents 0
Protein Kinase Inhibitors 0
EGFR protein, human EC 2.7.10.1
ErbB Receptors EC 2.7.10.1

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

e186-e194

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2018 Elsevier Inc. All rights reserved.

Auteurs

Antonio Passaro (A)

Division of Thoracic Oncology, IEO, European Institute of Oncology IRCCS, Milan, Italy. Electronic address: antonio.passaro@ieo.it.

Arsela Prelaj (A)

Division of Thoracic Oncology, IRCCS, Istituto Nazionale Tumori, Milan, Italy.

Laura Bonanno (L)

Medical Oncology 2, Istituto Oncologico Veneto IRCCS, Padova, Italy.

Marcello Tiseo (M)

Medical Oncology Unit, University Hospital of Parma, Parma, Italy.

Alessandro Tuzi (A)

Medical Oncology, ASST-Settelaghi, Varese, Varese, Italy.

Claudia Proto (C)

Division of Thoracic Oncology, IRCCS, Istituto Nazionale Tumori, Milan, Italy.

Rita Chiari (R)

Medical Oncology, Santa Maria della Misericordia Hospital, AOU di Perugia, Perugia, Italy.

Danilo Rocco (D)

Department of Oncology, AORN Vincenzo Monaldi, Naples, Italy.

Carlo Genova (C)

Lung Cancer Unit, IRCCS AOU San Martino-IST, Genova, Italy.

Claudio Sini (C)

Medical Oncology, Olbia Hospital, Olbia, Italy.

Diego Cortinovis (D)

Medical Oncology Unit, San Gerardo Hospital, Monza, Italy.

Sara Pilotto (S)

Medical Oncology, University of Verona, AOUI Verona, Verona, Italy.

Lorenza Landi (L)

Onco-Hematology Department, AUSL Romagna, Ravenna, Italy.

Chiara Bennati (C)

Onco-Hematology Department, AUSL Romagna, Ravenna, Italy.

Andrea Camerini (A)

Medical Oncology, Versilia Hospital and Istituto Toscano Tumori, Lido di Camaiore, Italy.

Luca Toschi (L)

Medical Oncology, Humanitas Research Hospital, Rozzano, Italy.

Carlo Putzu (C)

Oncology Unit, Department of Clinical and Experimental Medicine, University of Sassari, Sassari, Italy.

Giulio Cerea (G)

Department of Oncology and Hemato-Oncology, Niguarda Cancer Center, Milan, Italy.

Gianluca Spitaleri (G)

Division of Thoracic Oncology, IEO, European Institute of Oncology IRCCS, Milan, Italy.

Federico Cappuzzo (F)

Onco-Hematology Department, AUSL Romagna, Ravenna, Italy.

Filippo de Marinis (F)

Division of Thoracic Oncology, IEO, European Institute of Oncology IRCCS, Milan, Italy.

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Classifications MeSH