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FGF-9 Protein |
A Biomarker for Lung Cancers |
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Fibroblast growth factor (FGF) 9 is essential for lung development and is highly expressed in a subset of human lung adenocarcinomas. We recently described a mouse model in which FGF9 expression in the lung epithelium caused proliferation of the airway epithelium at the terminal bronchioles and led to rapid development of adenocarcinoma. Here, we used this model to characterize the effects of prolonged FGF9 induction on the proximal and distal lung epithelia, and examined the propagation potential of FGF9-induced lung tumors. We show that prolonged FGF9 overexpression in the lung resulted in the development of adenocarcinomas arising from both alveolar type II and airway secretory cells in the lung parenchyma and airways, respectively. We found that tumor cells harbored tumor-propagating cells that were able to form secondary tumors in recipient mice regardless of FGF9 expression. However, the highest degree of tumor propagation was observed when unfractionated tumor cells were coadministered with autologous, tumor-associated mesenchymal cells. Although the initiation of lung adenocarcinomas was dependent on activation of the FGF9/FGF receptor (FGFR) 3 signaling axis, maintenance and propagation of the tumor was independent of this signaling. Activation of an alternative FGF/FGFR and the interaction with tumor stromal cells is likely to be responsible for the development of this independence. This study demonstrates the complex role of FGF/FGFR signaling in the initiation, growth, and propagation of lung cancer. Our findings suggest that analyzing the expressions of FGFs/FGFRs in human lung cancer will be a useful tool for guiding customized therapy. |
Arai D., et al. J Pathol. 2014 Nov 21. doi: 10.1002/path.4486 |
OBJECTIVES: Fibroblast growth factor (FGF) 9 is a member of the FGF family, which modulates cell proliferation, differentiation, and motility. Recent studies show that the activation of FGF signals including FGF9 is associated with the pathogenesis of several cancers; however, its clinicopathological and biological significance in non-small cell lung cancer (NSCLC) is unclear. The purpose of this study was to clarify the characteristics of NSCLC with FGF9 expression.
MATERIALS AND METHODS:
We evaluated the expression of FGF9 in resected NSCLC specimens and corresponding non-tumorous lung tissue samples using cDNA microarray and evaluated its clinicopathological characteristics.
RESULTS: Nine out of 90 NSCLC specimens (10%) had "high" FGF9 expression compared with corresponding non-cancerous lung tissues. Histologically, of the 9 NSCLC specimens with high FGF9 expression, 5 were adenocarcinoma, whereas none were squamous cell carcinoma. FGF9 expression was not associated with sex, smoking history, or clinical stage. However, in patients with high and low FGF9 expression, the postoperative recurrence rates were 78% and 24% (p=0.033), respectively. Overall survival was significantly shorter in patients with high FGF9 expression than in those with low FGF9 expression (p<0.001).
CONCLUSION: Our data indicate that FGF9 may be a novel unfavorable prognostic indicator and a candidate therapeutic target of NSCLC.
Ohgino K., et al. Lung Cancer. 2014 Jan;83(1):90-6. doi: 10.1016/j.lungcan.2013.10.016. Epub 2013 Oct 30. |
PURPOSE:Fibroblast growth factor 2 (FGF2; basic fibroblast growth factor, b-FGF) and its main receptor FGFR-1 are important in both hemangiogenesis and lymphangiogenesis. Murine studies have indicated a close interplay between both FGF2 and platelet-derived growth factor-B (PDGF-B) as well as FGF2 and vascular endothelial growth factor-3 (VEGFR-3). This study investigates the prognostic impact of FGF2 and FGFR-1 in tumor cells and tumor stroma of resected non-small cell lung carcinomas (NSCLC) and explores the importance of their coexpression with VEGFR-3 or PDGF-B.
METHODS:Tumor tissue samples from 335 resected patients with stage I to IIIA NSCLC were obtained and tissue microarrays were constructed from duplicate cores of tumor cells and tumor-related stroma from each specimen. Immunohistochemistry was used to evaluate the expression of the molecular markers FGF2, FGFR-1, VEGFR-3, and PDGF-B.
RESULTS:
In univariate analyses, high tumor cell FGF2 expression (p = 0.015) was a negative prognostic indicator for disease-specific survival. In tumor stroma, high FGF2 (p = 0.024) expression correlated with good prognosis. In multivariate analyses, high expression of FGF2 in tumor cells (p = 0.038) was an independent negative prognostic factor whereas increased FGF2 in stroma (p = 0.015) was a positive prognosticator. Tumor cell coexpressions of FGF2/VEGFR-3 (p < 0.001) and FGFR-1/PDGF-B (p = 0.002) were significant indicators of poor prognosis.
CONCLUSIONS:Expression of FGF2 in tumor cells is an independent negative prognostic factor, and the coexpressions of FGF2/VEGFR-3 and FGFR-1/PDGF-B are strongly associated with poor survival in NSCLC patients.
Donnem T., et al. J Thorac Oncol. 2009 May;4(5):578-85 |
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Human
FGF9 Recombinant
Code No.: 00655-01-100
Size: 100 ug
Price: $360.00 USD
Protein ID:NP_001614
Gene ID: NM_ 001623
Sequence:Mature form
Tag: His Tag on N-Terminus
Expression: E. Coli
Purity:> 95% in SDS-PAGE gel
MW: 22 KDa
Data Sheet: PDF
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Name |
Code No. |
Size |
Price ($) |
FGF9 Human) ELISA Kit |
SK00655-01 |
96 T |
360.00 |
FGF9 Human) Recombinant |
00655-01-50 |
50 ug |
250.00 |
FGF9 Human) Recombinant |
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100 ug |
360.00 |
FGF9 Human) Recombinant |
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10 x 100 ug |
1600.00 |
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