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    GENE:

    MET (MET proto-oncogene, receptor tyrosine kinase)

    i
    Other names: 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
    1d
    Genomic alterations in circulating tumor DNA (ctDNA) and response to ABBV-400 treatment in patients with advanced solid tumors (AIOM 2024)
    The ADC ABBV-400 comprises the c-Met–targeting antibody telisotuzumab conjugated to a potent topoisomerase 1 inhibitor payload. ABBV-400 showed promising preliminary efficacy, with molecular and radiographic responses in pts with advanced solid tumors with heterogeneous genomic profiles, including pts with high TMB and KRAS mutations.
    Clinical • Tumor mutational burden • Circulating tumor DNA • Metastases
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    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • MET (MET proto-oncogene, receptor tyrosine kinase) • MSI (Microsatellite instability) • LRP1B (LDL Receptor Related Protein 1B) • PTPRT (Protein tyrosine phosphatase receptor type T)
    |
    KRAS mutation • TMB-H • MET overexpression • PTPRT mutation
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    GuardantINFINITY™
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    telisotuzumab adizutecan (ABBV-400) • telisotuzumab (h224G11)
    1d
    Impact of genomic alterations measured in circulating tumor DNA (ctDNA) on clinical response to telisotuzumab vedotin treatment in patients with non-small cell lung cancer (NSCLC) (AIOM 2024)
    METamp occurred more frequently in responders; but Teliso-V activity wasn’t restricted to these pts: most responders weren’t METamplified. Specific genomic alts beyond MET may influence clinical response. The current analysis demonstrated numeric differences between pts with identified drivers who did or didn’t respond to Teliso-V.
    Clinical • Circulating tumor DNA
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    EGFR (Epidermal growth factor receptor) • KRAS (KRAS proto-oncogene GTPase) • MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    KRAS G12C • MET amplification • KRAS G12
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    Labcorp® Plasma Complete™
    |
    telisotuzumab vedotin (ABBV-399)
    1d
    Liquid Biopsy in Next Generation Sequencing (NGS) for tumor molecular profiling in advanced NSCLC in Umbria population: a realworld experience (AIOM 2024)
    Blood-based LB performed by NGS is a non-invasive viable alternative tool for molecular genotyping and identifiy tumor-derived somatic alterations to increase the number of pts elegible to target therapy and guide personalized medicine.
    Clinical • Real-world evidence • Liquid biopsy • Next-generation sequencing • Real-world • Metastases • Biopsy
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    EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase) • RET (Ret Proto-Oncogene)
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    TP53 mutation • BRAF V600E • KRAS mutation • EGFR mutation • KRAS G12C • BRAF V600 • RET fusion • MET exon 14 mutation • KRAS G12 • KRAS exon 4 mutation
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    Oncomine™ Pan-Cancer Cell-Free Assay
    1d
    Molecular characterization of adult non-glioblastoma central nervous system (CNS) tumors to identify potential targettable alterations (AIOM 2024)
    4 pts received TT at recurrence, within clinical trials: one with grade 3 meningioma and ALK rearrangement treated with alectinib, one with PTCH1 mutant medulloblastoma treated with vismodegib, and two with high TMB treated with nivolumab/ipilumumab. The incidence of targettable molecular alterations in adult CNS tumor patients was lower than in GBM. Nevertheless, in a few selected cases TT have the potential to increase treatment options at recurrence and improve outcomes.
    Clinical • Tumor mutational burden • BRCA Biomarker • PD(L)-1 Biomarker • IO biomarker
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    BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • TMB (Tumor Mutational Burden) • MET (MET proto-oncogene, receptor tyrosine kinase) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • FGFR1 (Fibroblast growth factor receptor 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • NF1 (Neurofibromin 1) • POLE (DNA Polymerase Epsilon) • MDM2 (E3 ubiquitin protein ligase) • PTCH1 (Patched 1) • NF2 (Neurofibromin 2) • BRCA (Breast cancer early onset) • NTRK (Neurotrophic receptor tyrosine kinase)
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    BRAF V600E • BRCA2 mutation • BRCA1 mutation • TMB-H • PIK3CA mutation • MET amplification • ALK rearrangement • FGFR1 amplification • POLE mutation • NF1 mutation • MDM2 amplification • RET mutation • PTCH1 mutation • NF2 mutation • ROS1 mutation • BRCA mutation • ALK rearrangement + PIK3CA mutation • PTCH1 rearrangement • NTRK fusion
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    FoundationOne® CDx
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    Opdivo (nivolumab) • Yervoy (ipilimumab) • Alecensa (alectinib) • Erivedge (vismodegib)
    1d
    Enhanced tumoricidal activity of PD-1 antibody-secreting c-Met CAR-T cells against pancreatic cancer cells (PubMed, Nan Fang Yi Ke Da Xue Xue Bao)
    PD-1/c-Met CAR-T cells have higher killing efficiency against pancreatic cancer cells with also higher proliferative activity than c-Met CAR-T cells.
    Journal • CAR T-Cell Therapy • PD(L)-1 Biomarker • IO biomarker
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    PD-L1 (Programmed death ligand 1) • MET (MET proto-oncogene, receptor tyrosine kinase) • TNFA (Tumor Necrosis Factor-Alpha) • IL2 (Interleukin 2)
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    PD-L1 expression • MET expression
    2d
    Targeted RNA Sequencing of Head and Neck Adenoid Cystic Carcinoma Reveals SEC16A::NOTCH1 Fusion and MET Exon 14 Skipping as Potentially Actionable Alterations. (PubMed, Head Neck Pathol)
    The study improved the understanding of AdCC providing the first documentation of tumor clinical behavior associated with MYB::MPDZ and FUS::MYB fusions and reporting potentially actionable SEC16A::NOTCH1 fusion and MET exon 14 skipping mutation. Further research is needed to explore the therapeutic utility of MET inhibition and the efficacy of γ-secretase inhibitors against rare NOTCH1 fusions in AdCC.
    Retrospective data • Journal • IO biomarker
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    MET (MET proto-oncogene, receptor tyrosine kinase) • NOTCH1 (Notch 1) • MYB (MYB Proto-Oncogene, Transcription Factor) • FUS (FUS RNA Binding Protein) • NFIB (Nuclear Factor I B) • MYBL1 (MYB Proto-Oncogene Like 1)
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    MET exon 14 mutation • MET mutation • MET D1010N • MYB-NFIB fusion
    2d
    Targeting c-Met in breast cancer: From mechanisms of chemoresistance to novel therapeutic strategies. (PubMed, Curr Res Pharmacol Drug Discov)
    This review explores the mechanisms by which c-Met contributes to chemoresistance in breast cancer and current challenges in targeting c-Met for breast cancer therapy. It discusses strategies to optimize treatment outcomes, ultimately improving patient prognosis and reducing mortality rates associated with this devastating disease.
    Review • Journal
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    MET (MET proto-oncogene, receptor tyrosine kinase)
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    MET expression
    2d
    Discovery of N-substituted-2-oxoindolin benzoylhydrazines as c-MET/SMO modulators in EGFRi-resistant non-small cell lung cancer. (PubMed, RSC Med Chem)
    To address this unmet medical need, we explored the therapeutic potential of multitargeting agents that simultaneously inhibit two key signalling pathways, the mesenchymal-epithelial transition factor (c-MET) and the G protein-coupled receptor Smoothened (SMO), frequently dysregulated in NSCLC. By employing a combination of in silico drug repurposing and structure-based structure-activity relationship (SAR) studies, we identified and developed novel c-MET/SMO-targeting agents with antiproliferative activity against first- as well as third-generation EGFR-TKI-resistant NSCLC cells suggesting a synergistic effect arising from the simultaneous inhibition of c-MET and SMO.
    Journal
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    MET (MET proto-oncogene, receptor tyrosine kinase)
    3d
    Evaluation of a Novel MET-Targeting Camelid-Derived Antibody in Head and Neck Cancer. (PubMed, Mol Pharm)
    Our preclinical data suggest that the camelid antibody 1E7-Fc could be a potential theranostic agent for HNSCC. Further investigations are warranted to confirm these findings in patients and to evaluate 1E7-Fc as an imaging agent and platform to deliver radionuclide or drug therapy to MET-driven cancers.
    Journal
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    MET (MET proto-oncogene, receptor tyrosine kinase)
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    MET overexpression • MET expression
    3d
    Targeting c-MET for Endoscopic Detection of Dysplastic Lesions Within Barrett's Esophagus Using EMI-137 Fluorescence Imaging. (PubMed, Clin Cancer Res)
    EMI-137 accumulates in dysplastic lesions within BE and in c-MET positive EAC. EMI-137 imaging has potential as a screening and surveillance tool for patients with BE and as a means to detecting dysplasia and EAC.
    Journal
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    MET (MET proto-oncogene, receptor tyrosine kinase) • IL1B (Interleukin 1, beta)
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    MET overexpression • MET expression • MET positive
    3d
    Tumor Cell-Specific Signal Processing Platform Controlled by ATP for Non-invasive Modulation of Cellular Behavior. (PubMed, Nano Lett)
    Upon the dual-aptamer recognition in the upstream input signal circuit (UISC) to discriminate target cancer cells, the membrane-anchored DNA signal processor (DSP) is activated for signal amplification via rolling circle amplification (RCA) followed by the working of an ATP molecular switch for signal conversion, achieving receptor modulation in the downstream output signal circuit (DOSC). Benefiting from the rigid structure of DSP, the protective effect, and spatial confinement effect of RCA products, this TCS-SPP has demonstrated good performance in accurately modulating cellular behavior such as cell migration, invasion, and proliferation, showing great potential for targeted cancer therapy and biomedical engineering applications.
    Journal • Tumor cell
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    MET (MET proto-oncogene, receptor tyrosine kinase)
    3d
    MET amplification correlates with poor prognosis and immunotherapy response as a subtype of melanoma: a multicenter retrospective study. (PubMed, BMC Cancer)
    This database analysis showed that the main type of MET mutation is amplification in malignant melanoma. MET-amplified solid tumors might be considered for targeted therapy, as MET amplification can be regarded as a risk factor affecting the prognosis of patients with tumors treated with immunotherapy.
    Retrospective data • Journal • IO biomarker
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    MET (MET proto-oncogene, receptor tyrosine kinase)
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    MET amplification
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    MSK-IMPACT
    3d
    Systemic therapy for non-clear cell renal cell carcinomas: A systematic review. (PubMed, J Oncol Pharm Pract)
    While combination therapies, including immunotherapies, have shown positive outcomes, immune checkpoint inhibitors like nivolumab and pembrolizumab have demonstrated encouraging antitumor activity. Additionally, targeting the c-MET pathway has proven effective in certain papillary RCC. Further research is warranted to establish optimal treatment strategies and improve outcomes for patients with non-clear cell RCC. Systemic therapy for non-clear cell RCC is complex and evolving. Further research is needed to delineate optimal treatment strategies for different histological subtypes and improve patient outcomes.
    Review • Journal
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    MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    Keytruda (pembrolizumab) • Opdivo (nivolumab) • sunitinib • Torisel (temsirolimus)
    3d
    Erratum: Clonal MET Amplification as a Determinant of Tyrosine Kinase Inhibitor Resistance in Epidermal Growth Factor Receptor-Mutant Non-Small-Cell Lung Cancer. (PubMed, J Clin Oncol)
    No abstract available
    Journal
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    EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase)
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    EGFR mutation • MET amplification
    5d
    Development of a Machine Learning Model for ASPYRE-Lung Blood: A New Assay for Rapid Detection of Actionable Variants from Plasma in NSCLC Patients (AMP 2024)
    These data support further clinical testing using the best performing model and development of ASPYRE-Lung blood for liquid biopsy samples.
    Clinical • Machine learning
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    MET (MET proto-oncogene, receptor tyrosine kinase)
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    MET exon 14 mutation
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    ASPYRE-Lung
    5d
    MET Transcript Quantification by a NanoString-Based Platform Guides Threshold for MET Exon 14 Splice Variant Reporting by Clinical Next-Generation Sequencing (AMP 2024)
    METex14 results by NGS and RNA STEP gene expression demonstrated strong correlation and were 100% concordant for 370 lung cases (25 positive) with a cut-off of ≥100 METex14 SRs for NGS and a METex14 log2 ratio cut-off of ≥4.0 for RNA STEP. Comparison of METex14 results with 2 assays, NGS and RNA STEP, provided practical insight into cutoffs for METex14 reporting with critical implications for clinical therapeutic decisions.
    Clinical • Next-generation sequencing
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    MET (MET proto-oncogene, receptor tyrosine kinase)
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    MET exon 14 mutation
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    TruSight Oncology 500 Assay
    5d
    Validation and Clinical Utility of the Oncomine Comprehensive Assay v3 (OCAv3) for Comprehensive Genomic Profiling of Solid Tumors Using the GeneXus System (AMP 2024)
    The OCAv3 assay on the GeneXus System provides a rapid and reliable method for CGP of solid tumors from FFPE samples, enabling the identification of clinically actionable mutations for personalized oncology. Whereas limitations exist in homopolymer regions and coverage variability through all targets, the assay's turnaround time, low input material requirement, and overall performance when using optimal cut-offs support its adoption in clinical practice.
    Clinical
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    MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    MET exon 14 mutation
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    Oncomine™ Comprehensive Assay v3M
    5d
    Detection of a Novel MET Intronic Insertion in NSCLC, Leading to an Exon 14 Skipping Variant: An Interruption in the Pattern of Deletions (AMP 2024)
    Thus, for variants within the MET gene in patients with NSCLC, particular attention is required to assess for possible intronic variants that may lead to the METex14, especially if only sequencing DNA. The novelty of the intronic variant herein identified is heightened by being a net insertion rather than a deletion, as all reported intronic variants in the Catalogue of Somatic Mutations in Cancer (COSMIC) within this region are deletions. If sequencing DNA and RNA, both the intronic variant and RNA consequence should be used synergistically as evidence for the presence of METex14 skipping variant.
    MET (MET proto-oncogene, receptor tyrosine kinase)
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    MET exon 14 mutation
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    Ion AmpliSeq™ Cancer Hotspot Panel v2
    5d
    Re-verification and Report Ruling Revision of NTRK Fusion Results of Idylla GeneFusion Assay after Manufacturer Algorithm Update (AMP 2024)
    Our standard operating procedure (SOP) was updated to perform orthogonal confirmation testing for stand-alone equivocal NTRK1/2 and equivocal NTRK3 (5' failure), but to ignore equivocal NTRK3 (5' intact) and report as NTRK2/3 indeterminate. Re-verification showed no change to ALK, ROS1, RET, MET ex14, and NTRK1 results. Sensitivity of NTRK2 detection was significantly increased (80% after orthogonal testing).
    ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • NTRK2 (Neurotrophic tyrosine kinase, receptor, type 2) • NTRK (Neurotrophic receptor tyrosine kinase)
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    NTRK1 fusion • NTRK3 fusion • NTRK2 fusion • MET exon 14 mutation • ALK fusion • ROS1 fusion • NTRK fusion
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    Idylla™ GeneFusion Assay
    5d
    Characterization of ESR1-CCDC170 and Other Intra-Chromosomal Gene Fusions in FFPE Samples with Oncomine Precision Assay on Ion Torrent GeneXus System (AMP 2024)
    This report offers a thorough characterization of expected prevalence and expression levels for CSFs and NDFs with an NGS study of a broad scope. We describe ESR1 fusions in a cohort of thousands of breast tumors and show lower median expression levels relative to NDFs such as ALK, ROS1, and RET fusions. Our findings suggest that some CSFs, like ESR1 fusions in breast cancer, may be the result of tandem duplication with upstream partners, and may be subclonal and acquired later in cancer progression.
    ER (Estrogen receptor) • ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • FGFR3 (Fibroblast growth factor receptor 3) • CCDC170(Coiled-Coil Domain Containing 170) • RSPO3 (R-Spondin 3)
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    RET fusion • MET exon 14 mutation • ROS1 fusion • FGFR3 fusion • ER-CCDC170 fusion
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    Oncomine Precision Assay
    8d
    A Phase I Clinical Study Evaluating the Safety, Tolerability, Pharmacokinetic Profiles, and Preliminary Efficacy of SYS6023 in Patients with Advanced Solid Tumors (ChiCTR2400089836)
    P1, N=388, Recruiting, Shanghai Chest Hospital; CSPC Megalith Biopharmaceutical Co., Ltd
    New P1 trial • Metastases
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    KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ER (Estrogen receptor) • ALK (Anaplastic lymphoma kinase) • PGR (Progesterone receptor) • MET (MET proto-oncogene, receptor tyrosine kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • NRG1 (Neuregulin 1) • NTRK (Neurotrophic receptor tyrosine kinase)
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    KRAS mutation • EGFR mutation • KRAS G12C • BRAF mutation • HER-2 amplification • HER-2 negative • BRAF V600 • HER-2 expression • ALK positive • MET amplification • ALK fusion • ERBB3 expression • RET mutation • ROS1 fusion • MET mutation • NRG1 fusion • RET rearrangement • KRAS G12 • KRAS amplification • ER expression • PGR expression • ALK-ROS1 fusion • NRG1 fusion • NTRK fusion
    10d
    ICARUS-LUNG01: Datopotamab Deruxtecan (Dato-DXd, DS-1062a) in Advanced and/or Unresectable Non-Small Cell Lung Cancer (clinicaltrials.gov)
    P2, N=100, Active, not recruiting, Gustave Roussy, Cancer Campus, Grand Paris | Recruiting --> Active, not recruiting | Trial completion date: Nov 2025 --> Mar 2028 | Trial primary completion date: Nov 2022 --> Mar 2025
    Enrollment closed • Trial completion date • Trial primary completion date • Metastases
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    EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK (Neurotrophic receptor tyrosine kinase)
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    EGFR mutation • BRAF mutation • RET mutation • MET mutation • NTRK fusion
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    datopotamab deruxtecan (DS-1062a)
    11d
    Fusion transcriptome landscape in Glioblastoma (SNO 2024)
    Comprehensive molecular profiling reveals that approximately 10% of IDH WT GBMs carry oncogenic fusions that may be therapeutic targets. Broad spectrum of observed fusions underscores the need for novel clinical trial designs to allow efficient enrollment for prospective testing of potential targeted agents.
    EGFR (Epidermal growth factor receptor) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • FGFR3 (Fibroblast growth factor receptor 3) • NTRK2 (Neurotrophic tyrosine kinase, receptor, type 2) • RB1 (RB Transcriptional Corepressor 1) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • TACC3 (Transforming acidic coiled-coil containing protein 3) • CDK4 (Cyclin-dependent kinase 4) • CAPZA2 (Capping Actin Protein Of Muscle Z-Line Subunit Alpha 2) • SEC61G (SEC61 Translocon Subunit Gamma) • PTPRZ1 (Protein Tyrosine Phosphatase Receptor Type Z1)
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    TP53 mutation • EGFR mutation • NTRK1 fusion • NTRK2 fusion • MET amplification • EGFR amplification • ALK fusion • ROS1 fusion • MET mutation • EGFRvIII mutation • FGFR3 fusion • IDH wild-type • EGFR fusion
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    MI Tumor Seek™
    13d
    The potential role of next-generation sequencing in identifying MET amplification and disclosing resistance mechanisms in NSCLC patients with osimertinib resistance. (PubMed, Front Oncol)
    The known resistance mechanisms, including MET amplification, EGFR (C797S, L718Q/R), TP53, CDK4, CDK6, CDKN2A, BRAF, KRAS, NRAS and PIK3CA mutations were also disclosed in our cohort. NGS assay can achieve a high concordance with FISH in MET amplification detection and has advantages in portraying various genetic alterations, which is of worthy in clinical promotion.
    Journal • Next-generation sequencing
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    KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • NRAS (Neuroblastoma RAS viral oncogene homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • NRG1 (Neuregulin 1) • CDK4 (Cyclin-dependent kinase 4) • CDK6 (Cyclin-dependent kinase 6) • CYP3A4 (Cytochrome P450, family 3, subfamily A, polypeptide 4)
    |
    TP53 mutation • EGFR mutation • BRAF mutation • NRAS mutation • PIK3CA mutation • MET amplification • EGFR T790M • EGFR C797S • EGFR L718Q • BRAF amplification • EGFR C797S + MET amplification
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    Tagrisso (osimertinib)
    13d
    Comprehensive liquid biopsy analysis for monitoring NSCLC patients under second-line osimertinib treatment. (PubMed, Front Oncol)
    AXL and PIM-1 expression detected in CTCs during treatment suggesting new possible therapeutic strategies. Our results reveal that comprehensive liquid biopsy analysis can efficiently represent the heterogeneous molecular landscape and provide prominent information on subsequent treatments for NSCLC patients at PD since druggable molecular alterations were detected in CTCs.
    Journal • Liquid biopsy • PD(L)-1 Biomarker • IO biomarker • Biopsy
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    EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • AXL (AXL Receptor Tyrosine Kinase) • B2M (Beta-2-microglobulin) • FOXA1 (Forkhead Box A1) • PIM1 (Pim-1 Proto-Oncogene) • VIM (Vimentin) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • KRT19 (Keratin 19) • RASSF1 (Ras Association Domain Family Member 1) • WIF1 (WNT Inhibitory Factor 1) • BRMS1 (BRMS1 Transcriptional Repressor And Anoikis Regulator)
    |
    PD-L1 expression • BRAF V600E • KRAS mutation • EGFR mutation • KRAS G12C • HER-2 amplification • PIK3CA mutation • BRAF V600 • MET amplification • EGFR T790M • MET mutation • KRAS G12 • EGFR mutation + PIK3CA mutation • HER-2 amplification + PD-L1 expression • VIM expression • HER-2 amplification + MET amplification • RASSF1 methylation
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    Tagrisso (osimertinib)
    14d
    Actionable Structural Variant Detection via RNA-NGS and DNA-NGS in Patients With Advanced Non-Small Cell Lung Cancer. (PubMed, JAMA Netw Open)
    Emerging structural variants (eSVs) were found to have a combined prevalence to be 0.7%, with only 47.5% of eSVs detected by DNA-NGS. In this cohort study, the detection of structural variants via concurrent RNA-NGS and DNA-NGS was higher across multiple NCCN-guideline recommended biomarkers compared with DNA-NGS alone, suggesting that RNA-NGS should be routinely implemented in the care of patients with advanced NSCLC.
    Retrospective data • Journal • Next-generation sequencing • Metastases
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    ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK1 (Neurotrophic tyrosine kinase, receptor, type 1) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • NTRK2 (Neurotrophic tyrosine kinase, receptor, type 2)
    |
    NTRK1 fusion • NTRK3 fusion • NTRK2 fusion • MET exon 14 mutation • ROS1 fusion
    14d
    Tepotinib in Cholangiocarcinoma with MET Amplification: A Case Report. (PubMed, Onco Targets Ther)
    Systemic therapy, such as chemotherapy using gemcitabine and cisplatin, is the first choice for patients with cholangiocarcinoma who were inoperable. The development of precision medicine has expanded the paradigm of targeted therapies to increasingly favorable options in the second line and beyond, and prolong overall survival. Detecting druggable mutations (mutations potentially amenable to treatment with) for identifying a landscape of therapeutic options is imperative for managing cholangiocarcinoma.
    Journal
    |
    MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    MET amplification
    |
    cisplatin • gemcitabine • Tepmetko (tepotinib)
    14d
    KisMET-01: Clinical Study of Antibody-Drug Conjugate MYTX-011 in Subjects With Non-Small Cell Lung Cancer (clinicaltrials.gov)
    P1, N=250, Recruiting, Mythic Therapeutics | N=150 --> 250
    Enrollment change
    |
    MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    MET amplification • MET exon 14 mutation • MET mutation
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    MYTX-011
    14d
    Multinucleated tumor cells and micropapillary morphology appear to be predictors of poor prognosis in renal cell carcinoma with papillary and oncocytic features. (PubMed, Hum Pathol)
    RCC-PO are cytogenetically heterogeneous with overlapping features of various renal neoplasms. Micropapillary features and MTC appear to be independent predictors of poor outcomes in these tumors.
    Journal • Tumor cell
    |
    ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • TFE3 (Transcription Factor Binding To IGHM Enhancer 3) • FLCN (Folliculin) • CTSK (Cathepsin K)
    17d
    Targeting c-Met in Cancer Therapy: Unravelling Structure-Activity Relationships and Docking Insights for Enhanced Anticancer Drug Design. (PubMed, Curr Top Med Chem)
    Furthermore, the integration of computational methodologies with experimental approaches has accelerated the discovery and optimization of c-Met inhibitors, fostering the advancement of promising candidates for clinical applications. Overall, this review underscores the pivotal role of SAR and molecular docking studies in advancing our understanding of c-Met inhibition and guiding the rational design of next-generation anticancer agents targeting this pathway.
    Journal
    |
    MET (MET proto-oncogene, receptor tyrosine kinase)
    17d
    Targeting the MET gene: unveiling therapeutic opportunities in immunotherapy within the tumor immune microenvironment of non-small cell lung cancer. (PubMed, Ther Adv Med Oncol)
    MET mutations can reshape the tumor immune microenvironment of NSCLC by reducing tumor immunogenicity, inducing exhaustion in immune-activated cells, and promoting immune evasion, which are crucial for modulating treatment responses. Furthermore, we emphasize the promising synergy of immunotherapy with emerging treatments and the challenges and opportunities in refining these approaches to improve patient outcomes.
    Review • Journal • IO biomarker
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    MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    MET mutation
    18d
    LUNG-MAP SUB-STUDY: Targeted Treatment for Advanced Non-Small Cell Lung Cancer That Has Increased Copies of the MET Gene (An Expanded Lung-MAP Treatment Trial) (clinicaltrials.gov)
    P2, N=88, Recruiting, SWOG Cancer Research Network | Not yet recruiting --> Recruiting
    Enrollment open • Metastases
    |
    EGFR (Epidermal growth factor receptor) • HER-2 (Human epidermal growth factor receptor 2) • KRAS (KRAS proto-oncogene GTPase) • BRAF (B-raf proto-oncogene) • ALK (Anaplastic lymphoma kinase) • MET (MET proto-oncogene, receptor tyrosine kinase) • RET (Ret Proto-Oncogene) • ROS1 (Proto-Oncogene Tyrosine-Protein Kinase ROS) • NTRK (Neurotrophic receptor tyrosine kinase)
    |
    BRAF V600E • KRAS mutation • EGFR mutation • BRAF V600 • HER-2 mutation • MET amplification • EGFR T790M • MET exon 14 mutation • ALK fusion • ROS1 fusion • MET mutation • RET rearrangement
    |
    Rybrevant (amivantamab-vmjw)
    20d
    Xanthohumol overcomes osimertinib resistance via governing ubiquitination-modulated Ets-1 turnover. (PubMed, Cell Death Discov)
    Overall, the research highlights the critical role of targeting c-Met to address osimertinib resistance in NSCLC. By demonstrating the efficacy of xanthohumol in overcoming resistance and enhancing therapeutic outcomes, this study provides valuable insights and potential new strategies for improving the clinical management of NSCLC.
    Journal
    |
    EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase) • ETS1 (ETS Proto-Oncogene 1) • USP9X (Ubiquitin Specific Peptidase 9 X-Linked)
    |
    EGFR mutation • MET overexpression • MET expression
    |
    Tagrisso (osimertinib)
    25d
    CHRYSALIS-2: A Study of Lazertinib as Monotherapy or in Combination With Amivantamab in Participants With Advanced Non-small Cell Lung Cancer (clinicaltrials.gov)
    P1, N=701, Active, not recruiting, Janssen Research & Development, LLC | Recruiting --> Active, not recruiting | N=460 --> 701
    Enrollment closed • Enrollment change
    |
    EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    EGFR mutation • EGFR L858R • EGFR exon 19 deletion • EGFR exon 20 insertion • EGFR expression • MET expression • EGFR exon 20 mutation • EGFR expression + MET expression
    |
    Tagrisso (osimertinib) • carboplatin • pemetrexed • Rybrevant (amivantamab-vmjw) • Lazcluze (lazertinib)
    25d
    Concordance of ctDNA and tissue genomic profiling in advanced biliary tract cancer. (PubMed, J Hepatol)
    Among patients with advanced BTC, ctDNA-based genotyping showed acceptable concordance with tissue genomic profiling. Liquid biopsy using ctDNA could be a valuable complement to tissue-based genomic analysis in BTC.
    Journal • BRCA Biomarker • Circulating tumor DNA • Metastases • Discordant
    |
    HER-2 (Human epidermal growth factor receptor 2) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • MET (MET proto-oncogene, receptor tyrosine kinase) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • MSI (Microsatellite instability) • FGFR2 (Fibroblast growth factor receptor 2) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1)
    |
    BRCA2 mutation • BRCA1 mutation • HER-2 amplification • PIK3CA mutation • IDH1 mutation • MET amplification • FGFR2 mutation • FGFR2 fusion • MET mutation • PIK3CA amplification
    |
    AlphaLiquid® 100
    |
    cisplatin • gemcitabine
    26d
    A Study of TAVO412 in Patients with Cancer (clinicaltrials.gov)
    P1, N=50, Active, not recruiting, Tavotek Biotherapeutics | Recruiting --> Active, not recruiting | Trial completion date: Dec 2025 --> Jun 2026 | Trial primary completion date: Jun 2024 --> Dec 2025
    Enrollment closed • Trial completion date • Trial primary completion date • Metastases
    |
    EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    EGFR mutation • EGFR expression • EGFR overexpression • MET overexpression • MET mutation
    |
    TAVO412
    27d
    Investigating the interplay between the mir-183/182/96 cluster and the adherens junction pathway in early-stage breast cancer. (PubMed, Sci Rep)
    This suggests that regulatory effects of microRNAs are less pronounced in cancer, as has been shown by other studies. Furthermore, WASF3, EGFR, and MET are oncogenes that tend to be upregulated in later BC stages, implying that the role of some AJ genes changes with different BC stages.
    Journal
    |
    EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase) • MIR182 (MicroRNA 182) • MIR183 (MicroRNA 183) • WASF3 (WASP Family Member 3)
    28d
    ALK-tyrosine kinase inhibitor intrinsic resistance due to de novo MET-amplification in metastatic ALK-rearranged non-small cell lung cancer effectively treated by alectinib-crizotinib combination-case report. (PubMed, Transl Lung Cancer Res)
    A 43-year-old, female diagnosed with T4N3M1c NSCLC harboring the echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusion variant 1 (EML4-ALK v.1) and TP53 co-mutation, displayed only mixed response after three months and highly symptomatic progression after 6 months of first-line brigatinib treatment. The latter may represent a mechanism of intrinsic ALK-TKI resistance and its recognition by FISH, in NGS-negative cases, may be considered before initiating first-line treatment. This recognition is clinically important as combined therapy with ALK-TKI and MET-inhibitor should be the preferred first-line treatment.
    Journal • Metastases
    |
    ALK (Anaplastic lymphoma kinase) • TP53 (Tumor protein P53) • MET (MET proto-oncogene, receptor tyrosine kinase) • EML4 (EMAP Like 4)
    |
    TP53 mutation • MET amplification • ALK rearrangement • MET overexpression • ALK fusion • MET expression
    |
    Xalkori (crizotinib) • Alecensa (alectinib) • Alunbrig (brigatinib)
    28d
    Exploring the Impact of the β-Catenin Mutations in Hepatocellular Carcinoma: An In-Depth Review. (PubMed, Cancer Control)
    Relevant clinical trials will be essential for advancing personalized therapies and enhancing patient outcomes. This review provides a comprehensive analysis of β-Catenin signaling in HCC, highlighting its role in pathogenesis, diagnosis, and therapeutic targeting, and identifies key research directions to improve understanding and clinical outcomes.
    Review • Journal
    |
    MET (MET proto-oncogene, receptor tyrosine kinase) • STK11 (Serine/threonine kinase 11)
    |
    MET mutation
    28d
    Exploration of efficacy of the first-line treatment for advanced non-small cell lung cancer with primary MET-amplification: Retrospective evaluation of 36 cases. (PubMed, Int Immunopharmacol)
    Immuno-chemotherapy is a first-line optional treatment strategy in addition to targeted therapy for NSCLC patients with primary METamp. Foxp3-negative expression better predicts the near-term efficacy of immunotherapy.
    Retrospective data • Journal • PD(L)-1 Biomarker • IO biomarker • Metastases
    |
    PD-L1 (Programmed death ligand 1) • MET (MET proto-oncogene, receptor tyrosine kinase) • PD-1 (Programmed cell death 1) • FOXP3 (Forkhead Box P3)
    |
    PD-L1 expression • MET amplification • PD-L1 negative • FOXP3 expression
    1m
    Therapeutic Potential of Momordicine I from Momordica charantia: Cardiovascular Benefits and Mechanisms. (PubMed, Int J Mol Sci)
    To date, no review article has been published on the role of bitter-melon bioactive metabolites in cardiovascular prevention and therapy. The present work constitutes a comprehensive, up-to-date review of the literature, which highlights the promising therapeutic potential of momordicine I on the cardiovascular system and discusses future research recommendations.
    Review • Journal
    |
    MET (MET proto-oncogene, receptor tyrosine kinase)
    1m
    NRG-LU003: Targeted Treatment for ALK Positive Patients Who Have Previously Been Treated for Non-squamous Non-small Cell Lung Cancer (clinicaltrials.gov)
    P2, N=10, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2024 --> Sep 2025
    Trial completion date
    |
    MET (MET proto-oncogene, receptor tyrosine kinase)
    |
    ALK positive • MET amplification • ALK rearrangement
    |
    cisplatin • Xalkori (crizotinib) • carboplatin • Alecensa (alectinib) • Lorbrena (lorlatinib) • Zykadia (ceritinib) • pemetrexed • Alunbrig (brigatinib) • Ensacove (ensartinib)