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Updated: Jul 2, 2026

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

Expression and mutational analysis of MET in human solid cancers.

Patrick C Ma¹, Maria S Tretiakova, Alexander C MacKinnon

¹Division of Hematology/Oncology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.

Genes, Chromosomes & Cancer

|August 19, 2008

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The MET receptor tyrosine kinase and hepatocyte growth factor (HGF) pathway are frequently dysregulated in human cancers. MET overexpression, mutation, and autocrine signaling contribute to tumor growth and metastasis, highlighting MET as a therapeutic target.

Area of Science:

Oncology
Molecular Biology
Cancer Research

Background:

The MET receptor tyrosine kinase and its ligand, hepatocyte growth factor (HGF), play crucial roles in normal cellular functions.
Dysregulation of MET signaling is implicated in the development and progression of various human cancers, promoting processes like invasion and metastasis.

Purpose of the Study:

To systematically analyze the expression of the MET receptor and HGF in human solid tumors.
To investigate the presence and types of MET mutations in cancer tissues.
To evaluate the potential of the MET-HGF pathway as a diagnostic and therapeutic target.

Main Methods:

Utilized tumor tissue microarrays (TMA) for systematic analysis.
Employed standard immunohistochemistry (IHC) with automated scoring for protein expression analysis.

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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

Multiomics Analysis of TMEM200A as a Pan-Cancer Biomarker

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Performed DNA sequencing to identify mutations in MET's kinase and nonkinase domains.

Main Results:

MET was found to be differentially overexpressed across a wide range of human solid cancers.
HGF was widely expressed in both tumor and nonmalignant tissues, suggesting potential autocrine activation of MET.
Novel MET mutations were identified, particularly in the extracellular semaphorin and juxtamembrane domains, indicating altered receptor function.

Conclusions:

The MET-HGF pathway is frequently overexpressed and potentially activated in human solid cancers.
MET activation via overexpression, mutation, or autocrine signaling is common in malignancy.
MET represents a significant therapeutic target, and in lung cancer, it may serve as an early progenitor cell marker.