Davis Ian J, Fisher David E
Division of Hematology/Oncology, Department of Pediatrics, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7295, USA.
Cell Cycle. 2007 Jul 15;6(14):1724-9. doi: 10.4161/cc.6.14.4484. Epub 2007 May 24.
The discovery of recurrent genetic abnormalities in cancer cells has often led to the identification of novel oncogenic genes and gene families. The nature of these alterations may also offer insights into the mechanisms by which these genes mediate their oncogenic role. Amplification, translocation, deletion and point mutation are common mechanisms that result in gain- or loss-of-function of cancer associated genes. Several studies have recently demonstrated multiple genetic strategies that ultimately converge to dysregulate members of the MiT transcription factor family in cancer. The shared dependence on aberrant MiT activity thus defines an expanding family of human solid tumors.
