Decoding the Genetic Alterations in Genes of Fibroblast Growth Factor Family and Their Possible Association with HNSCC

Introduction: HNSCC is a type of cancer in the oral and pharynx region. Several mutations/variations are observed in these cancer phenotypes. Fibroblast growth factor belongs to the family of heparin binding growth factors. FGFs are multifunctional proteins with a wide variety of effects; they are most commonly mitogens. Their expression pattern correlates with invasion of HNSCC. Aim: To assess the genetic alterations in genes of the fibroblast growth factor family and their association with HNSCC. Materials and Methods: The demographic data and samples of 528 HNSCC patients was collected from the cBioportal database. Oncoprint analysis was done to assess the amplification and genetic alterations of the members of the FGF gene family. String analysis was performed to evaluate the protein-protein interaction. The information about previous reported mutation and correlation with novel and reported mutation was obtained using GnomAD analysis. Results and Discussion: FGF3,4 and 19 genes showed maximum variation (25%). FGF4 and FGF19 genes showed maximum amplification in addition to deletion mutation. Excitingly FGF3, FGF4 and FGF19 genes showed similar amplification patterns in most of the HNSCC patients. Statistical significant difference in the gene expression of FGF3 9.578 x 10-3 observed between normal and primary tumour. S. Findings showed many novel mutations and also 4 reported mutations ie:FGF1, FGF12, FGF20, FGF21 Conclusion: Our present study concludes that more evidence is required to confirm their association with HNSCC.

Fibroblast Growth Factor Family in the Progression of Prostate Cancer

Fibroblast growth factors (FGFs) and FGF receptors (FGFRs) play an important role in the maintenance of tissue homeostasis and the development and differentiation of prostate tissue through epithelial-stromal interactions. Aberrations of this signaling are linked to the development and progression of prostate cancer (PCa). The FGF family includes two subfamilies, paracrine FGFs and endocrine FGFs. Paracrine FGFs directly bind the extracellular domain of FGFRs and act as a growth factor through the activation of tyrosine kinase signaling. Endocrine FGFs have a low affinity of heparin/heparan sulfate and are easy to circulate in serum. Their biological function is exerted as both a growth factor binding FGFRs with co-receptors and as an endocrine molecule. Many studies have demonstrated the significance of these FGFs and FGFRs in the development and progression of PCa. Herein, we discuss the current knowledge regarding the role of FGFs and FGFRs—including paracrine FGFs, endocrine FGFs, and FGFRs—in the development and progression of PCa, focusing on the representative molecules in each subfamily.