Crizotinib

Crizotinib Reactions 1680, p101 - 2 Dec 2017 Development of acquired resistance due to acquired PIK3CA gene mutation: case report An elderly woman in her 60s [specific age at the time of reaction onset not stated] developed acquired resistance to crizotinib due to acquired PIK3CA gene mutation during treatment for lung adenocarcinoma [dosage and outcome not stated]. The woman was diagnosed with stage IIIB lung adenocarcinoma, on 13 April 2015. Subsequently, she received chemotherapy with various drugs including pemetrexed, carboplatin and bevacizumab. A CT scan revealed progression of the pulmonary lesions, on 20 November 2015. A next generation sequencing was performed on her blood sample, which demonstrated CD74-ROS1 fusion, a variant of the ROS1 translocation, and C176F and G245S mutation in TP53 gene. She was started on oral crizotinib, on 20 January 2016. A repeated CT scan showed a partial response of her pulmonary lesions, on 03 March 2016. However, she experienced chest tightness and shortness of breath, in June 2016. A CT scan performed on 08 July 2016 demonstrated rapid progression of the pulmonary lesions indicative of an acquired resistance to crizotinib. A subsequent next generation sequencing was performed on her blood samples, which revealed a novel point mutation of L531P type of the PIK3CA gene. The novel point mutation of the PIK3CA gene activated the mTOR signalling pathway. Considering this activation, the woman was treated with everolimus. However, disease progression was substantially significant by this time. She eventually died due to circulatory failure on 16 August 2016. Author comment: "The patient reported herein was diagnosed with lung adenocarcinoma and harbored a ROS1 rearrangement. She initially showed a response to crizotinib treatment, but the disease ultimately progressed. We identified an acquired mutation in her blood that led to mTOR pathway activation, which conferred resistance to Xu C-W, et al. Patient harboring a novel PIK3CA point mutation after acquired resistance to crizotinib in an adenocarcinoma with ROS1 rearrangement: A case report and literature review. Thoracic Cancer 8: 714-719, No. 6, Nov 2017. Available from: URL: http://doi.org/10.1111/1759-7714.12496 - China 803285262 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

Crizotinib

Reactions Weekly , Volume 1680 (1) – Dec 2, 2017
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Publisher
Springer International Publishing
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/s40278-017-39032-8
Publisher site
See Article on Publisher Site

Abstract

Reactions 1680, p101 - 2 Dec 2017 Development of acquired resistance due to acquired PIK3CA gene mutation: case report An elderly woman in her 60s [specific age at the time of reaction onset not stated] developed acquired resistance to crizotinib due to acquired PIK3CA gene mutation during treatment for lung adenocarcinoma [dosage and outcome not stated]. The woman was diagnosed with stage IIIB lung adenocarcinoma, on 13 April 2015. Subsequently, she received chemotherapy with various drugs including pemetrexed, carboplatin and bevacizumab. A CT scan revealed progression of the pulmonary lesions, on 20 November 2015. A next generation sequencing was performed on her blood sample, which demonstrated CD74-ROS1 fusion, a variant of the ROS1 translocation, and C176F and G245S mutation in TP53 gene. She was started on oral crizotinib, on 20 January 2016. A repeated CT scan showed a partial response of her pulmonary lesions, on 03 March 2016. However, she experienced chest tightness and shortness of breath, in June 2016. A CT scan performed on 08 July 2016 demonstrated rapid progression of the pulmonary lesions indicative of an acquired resistance to crizotinib. A subsequent next generation sequencing was performed on her blood samples, which revealed a novel point mutation of L531P type of the PIK3CA gene. The novel point mutation of the PIK3CA gene activated the mTOR signalling pathway. Considering this activation, the woman was treated with everolimus. However, disease progression was substantially significant by this time. She eventually died due to circulatory failure on 16 August 2016. Author comment: "The patient reported herein was diagnosed with lung adenocarcinoma and harbored a ROS1 rearrangement. She initially showed a response to crizotinib treatment, but the disease ultimately progressed. We identified an acquired mutation in her blood that led to mTOR pathway activation, which conferred resistance to Xu C-W, et al. Patient harboring a novel PIK3CA point mutation after acquired resistance to crizotinib in an adenocarcinoma with ROS1 rearrangement: A case report and literature review. Thoracic Cancer 8: 714-719, No. 6, Nov 2017. Available from: URL: http://doi.org/10.1111/1759-7714.12496 - China 803285262 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

References

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