Premium
Fibroblast growth factor family aberrations as a putative driver of head and neck squamous cell carcinoma in an epidemiologically low‐risk patient as defined by targeted sequencing
Author(s) -
Tillman Brittny N.,
Yanik Megan,
Birkeland Andrew C.,
Liu ChiaJen,
Hovelson Daniel H.,
Cani Andi K.,
Palanisamy Nallasivam,
Carskadon Shan,
Carey Thomas E.,
Bradford Carol R.,
Tomlins Scott A.,
McHugh Jonathan B.,
Spector Matthew E.,
Brenner J. Chad
Publication year - 2016
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.24292
Subject(s) - head and neck squamous cell carcinoma , fibroblast growth factor receptor 1 , fibroblast growth factor , cancer research , biology , targeted therapy , head and neck cancer , deep sequencing , fibroblast growth factor receptor , cancer , oncology , medicine , gene , genetics , genome , receptor
Background Targeted sequencing of patients with epidemiologically low‐risk (ELR) head and neck squamous cell carcinoma (HNSCC) could help identify novel drivers or lost suppressors leading to precision medicine protocols and improved survival rates. Methods A patient with ELR‐HNSCC was selected for targeted sequencing. We then assessed next generation sequencing cohorts from the Oncomine Powertool Database, which contains pan‐cancer data from The Cancer Genome Atlas (TCGA). Results Targeted sequencing revealed fibroblast growth factor receptor‐1 ( FGFR1 ) amplifications as a putative driver of the patient's tumor. Patients with HNSCC from TCGA data demonstrated fibroblast growth factor ( FGF ) family mutations, rearrangements, or amplifications in over 35% of HNSCC cases, with a statistically significant higher frequency in African American populations. FGF alterations were unique from activating phosphatidylinositol 3‐kinase ( PIK3CA ) mutations. Conclusion Together, these data suggest that FGF signaling may be critical for a subset of patients with HNSCC independent of other known pathways and provides rationale for leveraging patients with ELR‐HNSCC to define molecular subsets of high‐risk HNSCC. © 2016 Wiley Periodicals, Inc. Head Neck 38 : E1646–E1652, 2016