Acquired KRAS mutation and loss of low-level MET amplification after durable response to crizotinib in a patient with lung adenocarcinoma.
Lung Cancer
; 133: 20-22, 2019 07.
Article
in En
| MEDLINE
| ID: mdl-31200822
ABSTRACT
OBJECTIVES:
Resistance to tyrosine kinase inhibitor (TKI) therapy occurs inevitably in lung cancer patients with targetable genetic alterations. MET amplification has found to be an oncogenic driver in lung cancer with several reports showing response to MET TKI especially in cases with high-level amplification. MATERIALS ANDMETHODS:
We report the case of a patient with lung adenocarcinoma harbouring low-level MET amplification and strong MET expression who was treated with crizotinib.RESULTS:
The patient developed a durable response to crizotinib. A KRAS mutation and loss of MET amplification was found in a new lesion at time of progression as a potential mechanism of acquired resistance.CONCLUSION:
MET amplification is a continuous biomarker with responses to MET TKI observed even in patients with low-level amplification. KRAS mutations may act as a resistance mechanism to MET inhibition in MET dependent lung cancer.Key words
Full text:
1
Database:
MEDLINE
Main subject:
Antineoplastic Combined Chemotherapy Protocols
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Proto-Oncogene Proteins p21(ras)
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Proto-Oncogene Proteins c-met
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Adenocarcinoma of Lung
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Crizotinib
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Lung Neoplasms
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Mutation
Limits:
Female
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Humans
/
Middle aged
Language:
En
Year:
2019
Type:
Article