scholarly journals Fibroblast growth factor family as a potential target in the treatment of hepatocellular carcinoma

2014 ◽  
pp. 43
Author(s):  
Richard Grose ◽  
Stacey Coleman ◽  
Hemant Kocher
1990 ◽  
Vol 1990 (Supplement 13) ◽  
pp. 87-96 ◽  
Author(s):  
C. DICKSON ◽  
P. ACLAND ◽  
R. SMITH ◽  
M. DIXON ◽  
R. DEED ◽  
...  

Hepatology ◽  
2008 ◽  
Vol 47 (4) ◽  
pp. 1211-1222 ◽  
Author(s):  
Jin-Ping Lai ◽  
Dalbir S. Sandhu ◽  
Chunrong Yu ◽  
Tao Han ◽  
Catherine D. Moser ◽  
...  

Hepatology ◽  
2011 ◽  
Vol 53 (3) ◽  
pp. 854-864 ◽  
Author(s):  
Christine Gauglhofer ◽  
Sandra Sagmeister ◽  
Waltraud Schrottmaier ◽  
Carina Fischer ◽  
Chantal Rodgarkia-Dara ◽  
...  

Author(s):  
A. Akshaya ◽  
J. Vijayashree Priyadharsini ◽  
A. S. Smiline Girija ◽  
P. Sankar Ganesh ◽  
Nidhi Poddar

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.


Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 536 ◽  
Author(s):  
Aroosha Raja ◽  
Inkeun Park ◽  
Farhan Haq ◽  
Sung-Min Ahn

Hepatocellular carcinoma (HCC) is the sixth most common type of cancer, with an increasing mortality rate. Aberrant expression of fibroblast growth factor 19–fibroblast growth factor receptor 4 (FGF19–FGFR4) is reported to be an oncogenic-driver pathway for HCC patients. Thus, the FGF19–FGFR4 signaling pathway is a promising target for the treatment of HCC. Several pan-FGFR (1–4) and FGFR4-specific inhibitors are in different phases of clinical trials. In this review, we summarize the information, recent developments, binding modes, selectivity, and clinical trial phases of different available FGFR4/pan-FGF inhibitors. We also discuss future perspectives and highlight the points that should be addressed to improve the efficacy of these inhibitors.


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