Nature Reviews Cancer 12, 89-103 (February 2012) | doi:10.1038/nrc3205
Corrected online: 17 August 2012

There is a Corrigendum (1 September 2012) associated with this article.

Targeting MET in cancer: rationale and progress

Ermanno Gherardi1,2,5, Walter Birchmeier3,5, Carmen Birchmeier3 & George Vande Woude4  About the authors


Uncontrolled cell survival, growth, angiogenesis and metastasis are essential hallmarks of cancer. Genetic and biochemical data have demonstrated that the growth and motility factor hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, the tyrosine kinase MET, have a causal role in all of these processes, thus providing a strong rationale for targeting these molecules in cancer. Parallel progress in understanding the structure and function of HGF/SF, MET and associated signalling components has led to the successful development of blocking antibodies and a large number of small-molecule MET kinase inhibitors. In this Review, we discuss these advances, as well as results from recent clinical studies that demonstrate that inhibiting MET signalling in several types of solid human tumours has major therapeutic value.

Author affiliations

  1. Medical Research Council (MRC) Centre, Hills Road, Cambridge CB2 2QH, UK.
  2. Division of Immunology and General Pathology, Department of Molecular Medicine, University of Pavia, 1 via A Ferrata, 27100 Pavia, Italy.
  3. Max-Delbrück Center for Molecular Medicine (MDC), Berlin 13125, Germany.
  4. Van Andel Research Institute, Grand Rapids, Michigan MI 49503, USA.
  5. These authors contributed equally to this work.

Correspondence to: Ermanno Gherardi1,2,5 Email:

Correspondence to: Walter Birchmeier3,5 Email:

Correspondence to: Carmen Birchmeier3 Email:

Correspondence to: George Vande Woude4 Email:

Published online 24 January 2012

* In the legend to Figure 6c, the distribution according to therapeutic strategy (monotherapy versus combined therapy) involving HGF/SF–MET monotherapies should have read 44%.