Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma

Abstract Traditionally, the D1228 E/G/H/N mutation has been thought to cause Type I MET-TKI resistance. We reported a 75-year-old female with non-small cell lung cancer harboring MET exon 14 skipping mutation, who developed acquired MET D1228H mutation induced by capmatinib treatment. Interestingly,...
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Autor*in:	Li, Xiuzhen [verfasserIn] Lu, Yuefei [verfasserIn] Zhao, Jie [verfasserIn] Yu, Yinghui [verfasserIn] Tian, Heshen [verfasserIn] Zhu, Hao [verfasserIn] Li, Wen [verfasserIn] Xia, Yang [verfasserIn] Chen, Laijuan [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	Non-small cell lung cancer MET mutation Tyrosine kinase inhibitor Targeted therapy Drug resistant

Anmerkung:	© The Author(s) 2024

Übergeordnetes Werk:	Enthalten in: Journal of cancer research and clinical oncology - Springer Berlin Heidelberg, 1904, 150(2024), 8 vom: 24. Aug.
Übergeordnetes Werk:	volume:150 ; year:2024 ; number:8 ; day:24 ; month:08

Links:	Volltext

DOI / URN:	10.1007/s00432-024-05920-1

Katalog-ID:	SPR057082790

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spelling	10.1007/s00432-024-05920-1 doi (DE-627)SPR057082790 (SPR)s00432-024-05920-1-e DE-627 ger DE-627 rakwb eng 610 VZ 44.81 bkl Li, Xiuzhen verfasserin aut Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2024 Abstract Traditionally, the D1228 E/G/H/N mutation has been thought to cause Type I MET-TKI resistance. We reported a 75-year-old female with non-small cell lung cancer harboring MET exon 14 skipping mutation, who developed acquired MET D1228H mutation induced by capmatinib treatment. Interestingly, the patient demonstrated marked response to second-line savolitinib treatment with the duration of response of 19 months and several additional metastatic lesions appeared. Pathological assessment of rebiopsy sample showed adenocarcinoma and targeted next-generation sequencing revealed the loss of MET D1228H mutation and presence of MET p.Y1230N mutation. In response, the treatment regimen was amended to include a daily administration of 60 mg of cabozantinib, which resulted in moderate size reduction of the tumours. The switch of resistance mutations indicated that different type Ib MET inhibitors may exhibit distinct mechanisms of resistance. We call for futher studies on resistance based on patient-derived pre-clinical models including patient-derived tumor-like cell clusters, patient-derived organoids, and patient-derived xenografts. Non-small cell lung cancer (dpeaa)DE-He213 MET mutation (dpeaa)DE-He213 Tyrosine kinase inhibitor (dpeaa)DE-He213 Targeted therapy (dpeaa)DE-He213 Drug resistant (dpeaa)DE-He213 Lu, Yuefei verfasserin aut Zhao, Jie verfasserin aut Yu, Yinghui verfasserin aut Tian, Heshen verfasserin aut Zhu, Hao verfasserin aut Li, Wen verfasserin aut Xia, Yang verfasserin aut Chen, Laijuan verfasserin aut Enthalten in Journal of cancer research and clinical oncology Springer Berlin Heidelberg, 1904 150(2024), 8 vom: 24. Aug. (DE-627)253769515 (DE-600)1459285-X 1432-1335 nnns volume:150 year:2024 number:8 day:24 month:08 https://dx.doi.org/10.1007/s00432-024-05920-1 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_267 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.81 VZ AR 150 2024 8 24 08
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author	Li, Xiuzhen
spellingShingle	Li, Xiuzhen ddc 610 bkl 44.81 misc Non-small cell lung cancer misc MET mutation misc Tyrosine kinase inhibitor misc Targeted therapy misc Drug resistant Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma
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topic_title	610 VZ 44.81 bkl Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma Non-small cell lung cancer (dpeaa)DE-He213 MET mutation (dpeaa)DE-He213 Tyrosine kinase inhibitor (dpeaa)DE-He213 Targeted therapy (dpeaa)DE-He213 Drug resistant (dpeaa)DE-He213
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title	Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma
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title_full	Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma
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author_browse	Li, Xiuzhen Lu, Yuefei Zhao, Jie Yu, Yinghui Tian, Heshen Zhu, Hao Li, Wen Xia, Yang Chen, Laijuan
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title_sort	savolitinib conferred sensitivity in a patient with d1228h mutation-induced capmatinib-resistant met exon 14 skipping mutated lung adenocarcinoma
title_auth	Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma
abstract	Abstract Traditionally, the D1228 E/G/H/N mutation has been thought to cause Type I MET-TKI resistance. We reported a 75-year-old female with non-small cell lung cancer harboring MET exon 14 skipping mutation, who developed acquired MET D1228H mutation induced by capmatinib treatment. Interestingly, the patient demonstrated marked response to second-line savolitinib treatment with the duration of response of 19 months and several additional metastatic lesions appeared. Pathological assessment of rebiopsy sample showed adenocarcinoma and targeted next-generation sequencing revealed the loss of MET D1228H mutation and presence of MET p.Y1230N mutation. In response, the treatment regimen was amended to include a daily administration of 60 mg of cabozantinib, which resulted in moderate size reduction of the tumours. The switch of resistance mutations indicated that different type Ib MET inhibitors may exhibit distinct mechanisms of resistance. We call for futher studies on resistance based on patient-derived pre-clinical models including patient-derived tumor-like cell clusters, patient-derived organoids, and patient-derived xenografts. © The Author(s) 2024
abstractGer	Abstract Traditionally, the D1228 E/G/H/N mutation has been thought to cause Type I MET-TKI resistance. We reported a 75-year-old female with non-small cell lung cancer harboring MET exon 14 skipping mutation, who developed acquired MET D1228H mutation induced by capmatinib treatment. Interestingly, the patient demonstrated marked response to second-line savolitinib treatment with the duration of response of 19 months and several additional metastatic lesions appeared. Pathological assessment of rebiopsy sample showed adenocarcinoma and targeted next-generation sequencing revealed the loss of MET D1228H mutation and presence of MET p.Y1230N mutation. In response, the treatment regimen was amended to include a daily administration of 60 mg of cabozantinib, which resulted in moderate size reduction of the tumours. The switch of resistance mutations indicated that different type Ib MET inhibitors may exhibit distinct mechanisms of resistance. We call for futher studies on resistance based on patient-derived pre-clinical models including patient-derived tumor-like cell clusters, patient-derived organoids, and patient-derived xenografts. © The Author(s) 2024
abstract_unstemmed	Abstract Traditionally, the D1228 E/G/H/N mutation has been thought to cause Type I MET-TKI resistance. We reported a 75-year-old female with non-small cell lung cancer harboring MET exon 14 skipping mutation, who developed acquired MET D1228H mutation induced by capmatinib treatment. Interestingly, the patient demonstrated marked response to second-line savolitinib treatment with the duration of response of 19 months and several additional metastatic lesions appeared. Pathological assessment of rebiopsy sample showed adenocarcinoma and targeted next-generation sequencing revealed the loss of MET D1228H mutation and presence of MET p.Y1230N mutation. In response, the treatment regimen was amended to include a daily administration of 60 mg of cabozantinib, which resulted in moderate size reduction of the tumours. The switch of resistance mutations indicated that different type Ib MET inhibitors may exhibit distinct mechanisms of resistance. We call for futher studies on resistance based on patient-derived pre-clinical models including patient-derived tumor-like cell clusters, patient-derived organoids, and patient-derived xenografts. © The Author(s) 2024
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title_short	Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma
url	https://dx.doi.org/10.1007/s00432-024-05920-1
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up_date	2024-09-27T04:50:02.604Z
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Savolitinib conferred sensitivity in a patient with D1228H mutation-induced capmatinib-resistant MET exon 14 skipping mutated lung adenocarcinoma

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