FGFR3-TACC3 fusion in solid tumors: mini review
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Ricardo Costa1,2, Benedito A. Carneiro1,2, Timothy Taxter1,3, Fabio A. Tavora4, Aparna Kalyan1,2, Sachin A. Pai1,2, Young Kwang Chae1,2 and Francis J. Giles1,2
1 Developmental Therapeutics Program, Division of Hematology and Oncology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
2 Robert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, Illinois, USA
3 Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
4 Department of Pathology, Messejana Heart and Lung Hospital, Fortaleza, Brazil
Ricardo Costa, email:
Keywords: FGFR3-TACC3 fusion, non-small cell lung cancer, phosphatidylinositol 3-Kinase (PI3K), aneuploidy, glioblastoma multiforme
Received: April 30, 2016 Accepted: June 09, 2016 Published: July 07, 2016
Fibroblast growth factor receptors (FGFR) are transmembrane kinase proteins with growing importance in cancer biology given the frequency of molecular alterations and vast interface with multiple other signaling pathways. Furthermore, numerous FGFR inhibitors in clinical development demonstrate the expanding therapeutic relevance of this pathway. Indeed, results from early phase clinical trials already indicate that a subset of patients with advanced tumors derive benefit from FGFR targeted therapies. FGFR gene aberrations and FGFR gene rearrangements are relatively rare in solid malignancies. The recently described FGFR3-TACC3 fusion protein has a constitutively active tyrosine kinase domain and promotes aneuploidy. We summarize the prevalence data on FGFR3-TACC3 fusions among different histological tumor types and the preliminary evidence that this rearrangement represents a targetable molecular aberration in some patients with solid tumors.
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