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2 results on '"MET Y1003 mutation"'

1. Case Report: A 91-Year-Old Patient With Non-Small Cell Lung Cancer Harboring MET Y1003S Point Mutation

Author

Beili Gao and Ran Zeng

Subjects
MET Y1003 mutation, crizotinib, non-small cell lung cancer, next-generation sequencing, case report, Medicine (General), R5-920
Abstract

BackgroundThe Y1003S point mutation in exon 14 of mesenchymal-epithelial transition (MET) is a rare mutation that can lead to oncogenic transformation. Few data are available on the characteristics of this mutation. This report presents an elderly patient with non-small cell lung cancer (NSCLC) and a Y1003S mutation in MET detected by next-generation sequencing (NGS).Case ReportIn October 2020, a 91-year-old male was admitted to the Department of Respiratory and Critical Care Medicine, Ruijin Hospital because of an increased carcinoembryonic antigen. Imaging revealed highly suspicious lesions in the right upper lobe of the lung, right apex, and left upper lobe with traction of the adjacent pleura. The patient was histologically confirmed as having adenocarcinoma and the MET Y1003S mutation was detected by the NGS subsequently. After evaluation, the patient started crizotinib treatment in December 2020. In the first assessment of tumor response, a chest CT scan in January 2021 showed a partial response. The patient experienced a pulmonary embolism and an abnormal liver function during the treatment and recovered after symptomatic treatment. He maintained a partial response in the last available assessment in July 2021, with the right upper lung lesion being 26 × 9 mm.ConclusionThe MET Y1003S mutation was detected in this case, and the patient achieved a partial response using crizotinib. This case highlighted the role of NGS in detecting a rare mutation. Successful remission of complications in such an elderly patient necessitates careful and timely management.

Published
2022
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2. Characterization of 298 Patients with Lung Cancer Harboring MET Exon 14 Skipping Alterations

Author

James Suh, Balazs Halmos, Sai-Hong Ignatius Ou, Gregory P. Kalemkerian, Kurt Leuenberger, Vincent A. Miller, Zachary R. Chalmers, Jeffrey S. Ross, Garrett M. Frampton, Philip J. Stephens, Jonathan H. Goldman, Margaret Rosenzweig, Rachel L. Erlich, Siraj M. Ali, Alexa B. Schrock, Nir Peled, and Patrick M. Forde

Subjects
0301 basic medicine, Oncology, Pulmonary and Respiratory Medicine, medicine.medical_specialty, Splice site mutations, MET Y1003 mutation, 03 medical and health sciences, Exon, 0302 clinical medicine, Internal medicine, medicine, Lung cancer, biology, MET exon 14 skipping, business.industry, Large cell, Not Otherwise Specified, Genomic profiling, medicine.disease, MET Exon 14 Skipping Mutation, Molecular biology, 030104 developmental biology, 030220 oncology & carcinogenesis, biology.protein, Adenocarcinoma, Mdm2, business, Tyrosine kinase, MET exon 14 alterations
Abstract

Background The hepatocyte growth factor receptor gene ( MET ) exon 14 skipping ( METex14 ) has recently been described a potential driver alteration in lung cancer targetable by mesenchymal-to-epithelial transition factor (MET) tyrosine kinase inhibitors (TKIs). Methods Well-validated hybrid capture–based comprehensive genomic profiling was performed at the request of individual treating physicians. Results Of 11,205 lung cancers profiled by comprehensive genomic profiling, 298 (2.7%) carcinomas harbored alterations predicted to cause METex14 , including adenosquamous (8.2%), sarcomatoid (7.7%), histologic subtype not otherwise specified (3.0%), adenocarcinoma (2.9%), squamous cell (2.1%), large cell (0.8%), and SCLC (0.2%). Acinar features were present in 24% of the METex14 samples. Six cases (2%) harbored MET Y1003X mutations affecting binding of the MET-negative regulator, E3 ubiquitin protein ligase. The median age of all patients with METex14 was 73 years (range 43–95) and 60% were female. Concurrent, murine double minute gene ( MDM2 ) amplification, cyclin-dependent kinase 4 gene ( CDK4 ) amplification, and EGFR amplification were observed in 35%, 21%, and 6.4% of patients with METex14 , respectively. KRAS mutation was observed in 3% of cases. Concurrent MET amplification ( MET amp) (median copy number 10) was identified in 15% of METex14 samples. Significant differences in tumor mutational burden and type of the METex14 alterations were observed between the MET amp and non- MET amp samples. Response to MET TKI was observed in both in patients with MET amp and in patients without MET amp METex14 . Conclusion Diverse targetable METex14 alterations were identified in patients with NSCLC across age groups, including elderly patients, and in all major NSCLC histologic subtypes with an overall frequency of 2.7%. These findings support the use of hybrid capture–based molecular profiling across NSCLC subtypes to identify patients who will potentially benefit from MET TKIs.

Published
2016
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