Case report: Acquired resistance to crizotinib from a MET Y1230H mutation in a patient with non-small cell lung cancer and KIF5B-MET fusion

BackgroundThe c-met proto-oncogene (MET) serves as a significant primary oncogenic driver in non-small cell lung cancer (NSCLC) and has the potential to fuse with other genes, such as KIF5B, although it occurs infrequently. Only a limited number of reported cases have examined the clinical efficacy...

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Main Authors: Su-Su Dong, Wen Dong, Ya-Fen Tan, Qiang Xiao, Tian-Li Wang
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-04-01
Series:Frontiers in Oncology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fonc.2024.1370901/full
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author Su-Su Dong
Wen Dong
Ya-Fen Tan
Qiang Xiao
Tian-Li Wang
author_facet Su-Su Dong
Wen Dong
Ya-Fen Tan
Qiang Xiao
Tian-Li Wang
author_sort Su-Su Dong
collection DOAJ
description BackgroundThe c-met proto-oncogene (MET) serves as a significant primary oncogenic driver in non-small cell lung cancer (NSCLC) and has the potential to fuse with other genes, such as KIF5B, although it occurs infrequently. Only a limited number of reported cases have examined the clinical efficacy of crizotinib in patients with KIF5B-MET gene fusion, with no known data regarding acquired resistance to crizotinib and its potential mechanisms. In this report, we present the clinical progression of a female patient diagnosed with NSCLC and harboring a KIF5B-MET gene fusion.Case descriptionThe patient initially exhibited partial response to first-line crizotinib treatment, albeit for a short duration and with limited efficacy. Subsequent disease progression revealed the emergence of a secondary MET mutation, specifically MET Y1230H, leading to acquired resistance to crizotinib.ConclusionThe reporting of this case is imperative for informing clinical practice, given the uncommon occurrence of NSCLC with MET fusion, displaying responsiveness to MET tyrosine kinase inhibitor therapy, as well as the emergence of the secondary Y1230H alteration as a potential resistance mechanism.
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spelling doaj.art-8863a532029a40d392f6d929fc4462312024-04-16T05:01:16ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2024-04-011410.3389/fonc.2024.13709011370901Case report: Acquired resistance to crizotinib from a MET Y1230H mutation in a patient with non-small cell lung cancer and KIF5B-MET fusionSu-Su Dong0Wen Dong1Ya-Fen Tan2Qiang Xiao3Tian-Li Wang4Department of Respiratory Medicine, Changde Hospital, Xiangya School of Medicine, Central South University (the First People’s Hospital of Changde City), Changde, Hunan, ChinaDepartment of Oncology, Changde Hospital, Xiangya School of Medicine, Central South University (the First People’s Hospital of Changde City), Changde, Hunan, ChinaDepartment of Respiratory Medicine, Changde Hospital, Xiangya School of Medicine, Central South University (the First People’s Hospital of Changde City), Changde, Hunan, ChinaDepartment of Respiratory Medicine, Changde Hospital, Xiangya School of Medicine, Central South University (the First People’s Hospital of Changde City), Changde, Hunan, ChinaDepartment of Respiratory Medicine, Changde Hospital, Xiangya School of Medicine, Central South University (the First People’s Hospital of Changde City), Changde, Hunan, ChinaBackgroundThe c-met proto-oncogene (MET) serves as a significant primary oncogenic driver in non-small cell lung cancer (NSCLC) and has the potential to fuse with other genes, such as KIF5B, although it occurs infrequently. Only a limited number of reported cases have examined the clinical efficacy of crizotinib in patients with KIF5B-MET gene fusion, with no known data regarding acquired resistance to crizotinib and its potential mechanisms. In this report, we present the clinical progression of a female patient diagnosed with NSCLC and harboring a KIF5B-MET gene fusion.Case descriptionThe patient initially exhibited partial response to first-line crizotinib treatment, albeit for a short duration and with limited efficacy. Subsequent disease progression revealed the emergence of a secondary MET mutation, specifically MET Y1230H, leading to acquired resistance to crizotinib.ConclusionThe reporting of this case is imperative for informing clinical practice, given the uncommon occurrence of NSCLC with MET fusion, displaying responsiveness to MET tyrosine kinase inhibitor therapy, as well as the emergence of the secondary Y1230H alteration as a potential resistance mechanism.https://www.frontiersin.org/articles/10.3389/fonc.2024.1370901/fullacquired resistanceMET fusionnon-small cell lung cancergene mutationscrizotinib
spellingShingle Su-Su Dong
Wen Dong
Ya-Fen Tan
Qiang Xiao
Tian-Li Wang
Case report: Acquired resistance to crizotinib from a MET Y1230H mutation in a patient with non-small cell lung cancer and KIF5B-MET fusion
Frontiers in Oncology
acquired resistance
MET fusion
non-small cell lung cancer
gene mutations
crizotinib
title Case report: Acquired resistance to crizotinib from a MET Y1230H mutation in a patient with non-small cell lung cancer and KIF5B-MET fusion
title_full Case report: Acquired resistance to crizotinib from a MET Y1230H mutation in a patient with non-small cell lung cancer and KIF5B-MET fusion
title_fullStr Case report: Acquired resistance to crizotinib from a MET Y1230H mutation in a patient with non-small cell lung cancer and KIF5B-MET fusion
title_full_unstemmed Case report: Acquired resistance to crizotinib from a MET Y1230H mutation in a patient with non-small cell lung cancer and KIF5B-MET fusion
title_short Case report: Acquired resistance to crizotinib from a MET Y1230H mutation in a patient with non-small cell lung cancer and KIF5B-MET fusion
title_sort case report acquired resistance to crizotinib from a met y1230h mutation in a patient with non small cell lung cancer and kif5b met fusion
topic acquired resistance
MET fusion
non-small cell lung cancer
gene mutations
crizotinib
url https://www.frontiersin.org/articles/10.3389/fonc.2024.1370901/full
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