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Sensitivity and Resistance of MET Exon 14 Mutations in Lung Cancer to Eight MET Tyrosine Kinase Inhibitors In Vitro

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TLDR
MET-TKIs inhibited the growth of cells with MET exon 14 mutations, and this finding should provide relevant clinical implication for treating patients with lung cancer harboring MET ex on 14 mutations.
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This article is published in Journal of Thoracic Oncology.The article was published on 2019-10-01 and is currently open access. It has received 91 citations till now. The article focuses on the topics: Point mutation & Mutation.

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MET-dependent solid tumours - molecular diagnosis and targeted therapy

TL;DR: The utility of various diagnostic techniques and the roles of different classes of MET-targeted therapies in cancers with MET amplification, mutation and fusion, and MET overexpression are evaluated.
Journal ArticleDOI

KRAS Secondary Mutations That Confer Acquired Resistance to KRAS G12C Inhibitors, Sotorasib and Adagrasib, and Overcoming Strategies: Insights From In Vitro Experiments

TL;DR: In this article, the secondary KRAS mutations were identified in the presence of Nethyl-N-nitrosourea and a combination of the SOS1 inhibitor, BI-3406, and trametinib had potent activity against this resistance.
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Beyond EGFR, ALK and ROS1: Current evidence and future perspectives on newly targetable oncogenic drivers in lung adenocarcinoma.

TL;DR: The clinicopathological features, the emerging targeted therapies and mechanisms of resistance and strategies to overcome them of KRAS, BRAF, MET, RET, HER2 and NTRK-addicted advanced NSCLCs are reviewed.
References
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Journal ArticleDOI

Comprehensive molecular profiling of lung adenocarcinoma: The cancer genome atlas research network

Eric A. Collisson, +318 more
- 01 Jan 2014 - 
TL;DR: In this paper, the authors report molecular profiling of 230 resected lung adnocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses.
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Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors

TL;DR: Detailed genetic and histological analysis of 37 patients with drug-resistant non–small cell lung cancers carrying EGFR mutations provides new insights into the shifting sands of drug resistance evolution in lung cancers and suggests that serial biopsies may be essential in the quest to reverse or even prevent the development ofdrug resistance.

Comprehensive molecular profiling of lung adenocarcinoma

TL;DR: High rates of somatic mutation were seen, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification, and MAPK and PI(3)K pathway activity was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation.
Journal ArticleDOI

Somatic mutations affect key pathways in lung adenocarcinoma

Li Ding, +96 more
- 23 Oct 2008 - 
TL;DR: Somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B are found.
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Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing

TL;DR: Exome and genome sequences and whole-genome sequence analysis revealed frequent structural rearrangements, including in-frame exonic alterations within EGFR and SIK2 kinases, which are attractive targets for biological characterization and therapeutic targeting of lung adenocarcinoma.
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