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Secondary Mutations at I1171 in the ALK

Secondary Mutations at I1171 in the ALK CASE REPORT Secondary Mutations at I1171 in the ALK Gene Confer  Resistance to Both Crizotinib and Alectinib Gouji Toyokawa, MD, PhD, Fumihiko Hirai, MD, PhD, Eiko Inamasu, MD, Tsukihisa Yoshida, MD, Kaname Nosaki, MD, Tomoyoshi Takenaka, MD, PhD, Masafumi Yamaguchi, MD, PhD, Takashi Seto, MD, PhD, Mitsuhiro Takenoyama, MD, PhD, and Yukito Ichinose, MD, PhD he first case was a 27-year-old female nonsmoker who and hepatic metastases, as shown in Figure 2C. However, a Twas diagnosed with advanced adenocarcinoma with bone relapse of the primary lesion and hepatic metastases was seen and brain metastases. A FISH study of a biopsy sample of the approximately 7 months after the administration of alectinib left clavicle detected ALK rearrangement, and the patient was (Figure 2D), and a rebiopsy of the hepatic lesion showed a confirmed to harbor variant 2 of the EML4-ALK fusion gene secondary mutation of the ALK gene at codon 1171 (I1171N; by reverse transcription-polymerase chain reaction (RT-PCR) Figure 2E). In both cases, bypass track resistance through the and direct sequencing (Figure 1A). After the failure of first-line activation of an alternative driver oncogene, such as EGFR or chemotherapy with cisplatin plus pemetrexed (Figure 1B), the KRAS, was not identified. patient was enrolled in a phase III study comparing crizotinib Various mechanisms which http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Thoracic Oncology Wolters Kluwer Health

Secondary Mutations at I1171 in the ALK

Journal of Thoracic Oncology , Volume 9 (12) – Dec 1, 2014

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Copyright
Copyright © 2014 by the International Association for the Study of Lung Cancer
ISSN
1556-0864

Abstract

CASE REPORT Secondary Mutations at I1171 in the ALK Gene Confer  Resistance to Both Crizotinib and Alectinib Gouji Toyokawa, MD, PhD, Fumihiko Hirai, MD, PhD, Eiko Inamasu, MD, Tsukihisa Yoshida, MD, Kaname Nosaki, MD, Tomoyoshi Takenaka, MD, PhD, Masafumi Yamaguchi, MD, PhD, Takashi Seto, MD, PhD, Mitsuhiro Takenoyama, MD, PhD, and Yukito Ichinose, MD, PhD he first case was a 27-year-old female nonsmoker who and hepatic metastases, as shown in Figure 2C. However, a Twas diagnosed with advanced adenocarcinoma with bone relapse of the primary lesion and hepatic metastases was seen and brain metastases. A FISH study of a biopsy sample of the approximately 7 months after the administration of alectinib left clavicle detected ALK rearrangement, and the patient was (Figure 2D), and a rebiopsy of the hepatic lesion showed a confirmed to harbor variant 2 of the EML4-ALK fusion gene secondary mutation of the ALK gene at codon 1171 (I1171N; by reverse transcription-polymerase chain reaction (RT-PCR) Figure 2E). In both cases, bypass track resistance through the and direct sequencing (Figure 1A). After the failure of first-line activation of an alternative driver oncogene, such as EGFR or chemotherapy with cisplatin plus pemetrexed (Figure 1B), the KRAS, was not identified. patient was enrolled in a phase III study comparing crizotinib Various mechanisms which

Journal

Journal of Thoracic OncologyWolters Kluwer Health

Published: Dec 1, 2014

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