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BIOMARKER:

KIF5B-MET fusion

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Other names: KIF5B, Kinesin Family Member 5B, Conventional Kinesin Heavy Chain, Ubiquitous Kinesin Heavy Chain, Kinesin-1 Heavy Chain, KNS1, UKHC, KNS, Epididymis Secretory Protein Li 61, Kinesin 1 (110-120kD), Kinesin Heavy Chain, HEL-S-61, KINH, DFNB97, AUTS9, RCCP2, C-Met, HGFR, HGF Receptor, Met Proto-Oncogene, HGF/SF Receptor, Proto-Oncogene C-Met, Scatter Factor Receptor, Tyrosine-Protein Kinase Met, Hepatocyte Growth Factor Receptor, MET, MET Proto-Oncogene, Receptor Tyrosine Kinase
Entrez ID:
over1year
Resistance to MET inhibition in MET-dependent NSCLC and therapeutic activity after switching from type I to type II MET inhibitors. (PubMed, Eur J Cancer)
Resistance to MET inhibition is heterogeneous with on- and off-target mechanisms occurring regardless of the initial MET aberration. Switching therapy between different types of kinase inhibitors can lead to repeated responses in cases with second-site mutations. Controlled clinical trials in this setting with larger patient numbers are needed, as evidence to date is limited to preclinical data and case series.
Clinical • Journal
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HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • KIF5B (Kinesin Family Member 5B) • PRKAR1A (Protein Kinase CAMP-Dependent Type I Regulatory Subunit Alpha) • PRKAR2B (Protein Kinase CAMP-Dependent Type II Regulatory Subunit Beta)
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KRAS mutation • HER-2 amplification • MET amplification • MET exon 14 mutation • KIF5B-MET fusion • MET fusion
2years
Journal
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KIF5B (Kinesin Family Member 5B)
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KIF5B-MET fusion • MET fusion