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Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing
Published on: July 5, 2019
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FGFR3-TACC3 fusion in solid tumors: mini review
Ricardo Costa1,2, Benedito A Carneiro1,2, Timothy Taxter1,3
1Developmental Therapeutics Program, Division of Hematology and Oncology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Oncotarget
|July 14, 2016
Summary
Fibroblast growth factor receptor 3- Transforming Acidic Coiled-Coil 3 (FGFR3-TACC3) fusions are rare in solid tumors but represent a targetable aberration. Early clinical trials show FGFR inhibitors benefit some patients with advanced cancers.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Fibroblast growth factor receptors (FGFR) are key transmembrane kinase proteins implicated in cancer biology.
- Alterations in FGFR signaling pathways are frequent and interact with other oncogenic pathways.
- Numerous FGFR inhibitors are in clinical development, highlighting therapeutic relevance.
Purpose of the Study:
- To summarize the prevalence of FGFR3-TACC3 fusions across various tumor types.
- To review preliminary evidence supporting FGFR3-TACC3 as a targetable molecular aberration.
Main Methods:
- Literature review of prevalence data for FGFR3-TACC3 fusions.
- Analysis of preliminary clinical evidence for FGFR targeted therapies.
Main Results:
- FGFR gene aberrations and rearrangements are relatively rare in solid malignancies.
- The FGFR3-TACC3 fusion protein exhibits a constitutively active tyrosine kinase domain, promoting aneuploidy.
- Preliminary data suggest FGFR3-TACC3 fusions are targetable in a subset of patients.
Conclusions:
- FGFR3-TACC3 fusions, though rare, represent a distinct molecular aberration in solid tumors.
- Targeted therapies against FGFR may offer clinical benefit to patients with specific FGFR alterations.
- Further research is warranted to fully elucidate the clinical utility of targeting FGFR3-TACC3 fusions.

