IMR Press / FBS / Volume 4 / Issue 2 / DOI: 10.2741/s280

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


The contrasting oncogenic and tumor suppressor roles of FES

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1 Department of Pathology and Molecular Medicine, Queen’s University, Division of Cancer Biology and Genetics, Queen’s Cancer Research Institute, Kingston, Ontario, K7L 3N6, Canada
2 Department of Experimental and Clinical Laboratory Medicine, National Hospital Organization, Nagasaki Hospital, 41-6 Sakuragi-machi, Nagasaki 850-8523, Japan
3 Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA

*Author to whom correspondence should be addressed.

Front. Biosci. (Schol Ed) 2012, 4(2), 489–501;
Published: 1 January 2012

The fes gene was first discovered as a proteintyrosine kinase-encoding retroviral oncogene. The ability of v-fes to transform cells in vitro and initiate cancer in vivo has been established by cell culture, engraftment and transgenic mouse studies. The corresponding cellular c-fes proto-oncogene encodes a cytoplasmic FES proteintyrosine kinase with restrained catalytic activity relative to its retrovirally encoded homologs. These observations have stimulated a search for mutations or inappropriate expression of c-fes in human cancers and research aimed at understanding the functions of the FES kinase and its potential involvement in cancer and other diseases. Paradoxically, although first identified as an oncogene, genetic evidence has also implicated c-fes as a potential tumor suppressor. This review will describe observations from basic and translational research which shapes our current understanding of the physiological, cellular and molecular functions of the FES protein-tyrosine kinase and its potential roles in tumorigenesis. We also propose a model to reconcile the conflicting oncogenic and tumor suppressor roles of c-fes in tumorigenesis.

Tyrosine Kinase
Tumor Suppressor
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