Gefitinib

Gefitinib Reactions 1680, p151 - 2 Dec 2017 Development of acquired resistance: case report A patient [age and sex not stated] received gefitinib for lung adenocarcinoma and developed acquired resistance to The patient, who had a history of lung adenocarcinoma, was started on gefitinib [route and dosage not stated]. A cell growth inhibition test was performed with gefitinib and afatinib. The lung adenocarcinoma cell line (G719S-GR) was established from the malignant pleural effusion. The test showed human epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI) resistance in G719S-GR cells with an LC50 of greater than 100µM for either afatinib or gefitinib [time to reaction onset not stated], and indicated that the tumour developed an acquired resistance from the initial treatment with gefitinib. The test result also showed the G719S-GR cells resistant to EGFR-TKI in vitro. The next generation sequencing (NGS) revealed G719S-GR cells harbor EGFR mutations of E709A and G719S along with the amplification of EGFR, MYC, interleukin 7 receptor (IL7R) and fibroblast growth factor receptor 1 (FGFR1) locus. Additionally, the loss of tuberous sclerosis 1 (TSC1), phosphatase and tensin homolog (PTEN) and cyclin-dependent kinase inhibitor 2A (CDKN2A) were observed in G719S-GR cells. The loss PTEN was considered to be the mechanism for the development of acquired resistance to gefitinib. Author comment: "We established a lung adenocarcinoma cell line (G719S-GR) from the malignant pleural effusion of a patient whose tumor developed acquired resistance from initial treatment with gefitinib." Osoegawa A, et al. Acquired resistance to EGFR-TKI in an uncommon G719S EGFR mutation. Cancer Research 77 (Suppl. 13): abstr. 4107, No. 13, Jul 2017. Available from: URL: http://doi.org/10.1158/1538-7445.AM2017-4107 [abstract] - Japan 803284992 0114-9954/17/1680-0001/$14.95 Adis © 2017 Springer International Publishing AG. All rights reserved Reactions 2 Dec 2017 No. 1680 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Reactions Weekly Springer Journals

Gefitinib

Reactions Weekly , Volume 1680 (1) – Dec 2, 2017
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Publisher
Springer Journals
Copyright
Copyright © 2017 by Springer International Publishing AG, part of Springer Nature
Subject
Medicine & Public Health; Drug Safety and Pharmacovigilance; Pharmacology/Toxicology
ISSN
0114-9954
eISSN
1179-2051
D.O.I.
10.1007/s40278-017-39082-3
Publisher site
See Article on Publisher Site

Abstract

Reactions 1680, p151 - 2 Dec 2017 Development of acquired resistance: case report A patient [age and sex not stated] received gefitinib for lung adenocarcinoma and developed acquired resistance to The patient, who had a history of lung adenocarcinoma, was started on gefitinib [route and dosage not stated]. A cell growth inhibition test was performed with gefitinib and afatinib. The lung adenocarcinoma cell line (G719S-GR) was established from the malignant pleural effusion. The test showed human epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI) resistance in G719S-GR cells with an LC50 of greater than 100µM for either afatinib or gefitinib [time to reaction onset not stated], and indicated that the tumour developed an acquired resistance from the initial treatment with gefitinib. The test result also showed the G719S-GR cells resistant to EGFR-TKI in vitro. The next generation sequencing (NGS) revealed G719S-GR cells harbor EGFR mutations of E709A and G719S along with the amplification of EGFR, MYC, interleukin 7 receptor (IL7R) and fibroblast growth factor receptor 1 (FGFR1) locus. Additionally, the loss of tuberous sclerosis 1 (TSC1), phosphatase and tensin homolog (PTEN) and cyclin-dependent kinase inhibitor 2A (CDKN2A) were observed in G719S-GR cells. The loss PTEN was considered to be the mechanism for the development of acquired resistance to gefitinib. Author comment: "We established a lung adenocarcinoma cell line (G719S-GR) from the malignant pleural effusion of a patient whose tumor developed acquired resistance from initial treatment with gefitinib." Osoegawa A, et al. Acquired resistance to EGFR-TKI in an uncommon G719S EGFR mutation. Cancer Research 77 (Suppl. 13): abstr. 4107, No. 13, Jul 2017. Available from: URL: http://doi.org/10.1158/1538-7445.AM2017-4107 [abstract] - Japan 803284992 0114-9954/17/1680-0001/$14.95 Adis © 2017 Springer International Publishing AG. All rights reserved Reactions 2 Dec 2017 No. 1680

Journal

Reactions WeeklySpringer Journals

Published: Dec 2, 2017

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