Scientists reveal a deadly weakness of anti-MET drugs

MET, also known as hepatocyte growth factor receptor (HGFR), is a popular anti-tumor target, just like other growth factor receptors (EGFR, HER2, VEGFR, PDGFR, FGFR, etc.). However, failures of onartuzumab, tivantinib, and foretinib have shaken many investors’ confidence. A new paper in the journal Nature reveals a deadly weakness of anti-MET drugs[1].

MET is expressed not only by cancer cells but also by immune cells. The authors showed that neutrophils need MET to migrate through the vessel wall of inflamed tissues, where neutrophils exert anti-tumor functions. Met deletion in mouse neutrophils enhances tumor growth and metastasis.

These findings indicate that anti-MET drugs may have both positive and negative effects on tumors. On the one hand, anti-MET drugs can kill cancer cells that depend on MET hyperactivation; on the other hand, anti-MET drugs blunt the anti-tumor immune responses of the neutrophils.

Selecting the right patients is key to MET inhibitor development. The study suggests that patients that have high MET expression in neutrophils should be excluded in clinical trials.

[1] Nature. 2015, doi: 10.1038/nature14407.

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