Published online Mar 24, 2019. doi: 10.5306/wjco.v10.i3.136
Peer-review started: December 6, 2018
First decision: December 30, 2018
Revised: January 16, 2019
Accepted: January 30, 2019
Article in press: January 30, 2019
Published online: March 24, 2019
Processing time: 106 Days and 14.1 Hours
Head and neck squamous cell carcinoma (HNSCC) is considered to be a progressive disease resulting from alterations in multiple genes regulating cell proliferation and differentiation like Receptor Tyrosine Kinases (RTKs) especially members of the Fibroblast Growth Receptor (FGFR)-family. Single-nucleotide polymorphism (SNP) Arg388 allele of the Fibroblast Growth Factor Receptor 4 (FGFR4) is associated with a reduced overall survival in patients with cancers of various types. We speculate that FGFR4 expression and Gly388Arg polymorphism are associated with worse survival in patients with HSNCC. To investigate the potential clinical significance of the FGFR4 Arg388 allele in the context of tumors arising in HNSCC, a comprehensive analysis of FGFR4 receptor expression and genotype in tumor tissues and correlated results with patients’ clinical data in a large cohort of patients with HNSCC was conducted.
We undertook the study to investigate the impact of FGFR4 expression in tumor tissue of HNSCC and the FGFR4 SNP Glycine to Arginine at position388 with regards to clinical pathological characteristics in a large patient cohort. Our previous study revealed significant results in a smaller group of patients with HNSCC, where this SNP was associated with reduced survival and tumor progression whilst strong evidence for implication of this SNP was demonstrated in other tumor entities. In the context of exploring future tumor therapeutic interventions we aimed at providing strong evidence a possibly relevant useful target.
The aim of this study was to evaluate the relevant impact of FGFR4 expression and FGFR4 SNP Gly/Arg388 in tumor progression of patients with HNSCC utilizing a large cohort analysis for the respective aspects and correlate it with the patients’ clinical data with special emphasis on patients’ overall survival and disease progression.
We analyzed tumor specimens of 284 patients with HNSCC and used Immunhistochemistry to assess FGFR4 expression in tumor tissues and PCR-RLFP to identify FGFR4 genotype in the same tumor samples. Obtained data was correlated in a comprehensive statistical analysis, including multivariant analysis and logistic regression models.
We have shown that FGFR4 expression was almost evenly distributed among 3 groups with strong, mediate and low expression levels. FGFR4 polymorphism Arg388 was prevalent in 33.8% of patient. Strong FGFR4 expression in tumor cells was significantly associated with worse overall survival. Furthermore, FGFR4 Arg388 genotype was strongly associated with tumor progression, lymph node metastasis and reduced disease-free survival.
Our results show the relevant impact of FGFR4 signaling for tumor progression and worse survival in patients with HNSCC. These results confirm previous small-scale studies with similar outcomes, now providing statistically robust results in order to underline the potential to develop new target therapies in HNSCC.
Facing the complexity of tumor biology with implications of multiple alterated pathways in tumor development while therapy success in cancer therapy is still limited and therapies are mostly limited to surgery and radiochemotherapy, there is still a strong need for new targets in order to improve therapies in a multimodal setting. Obviously, further investigations are mandatory to better understand the mechanisms how altered signaling pathways in cancer affect tumor biology for future development of new target therapies.