Fibroblast growth factor receptor expression in aural polyps: predictor of cholesteatoma?

2004 ◽  
Vol 118 (5) ◽  
pp. 338-342 ◽  
Author(s):  
Salil Nair ◽  
Simon Watts ◽  
Liam Flood
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Wound Repair ◽  
Cellular Proliferation ◽  
Nuclear Translocation ◽  
Growth Factor Receptor ◽  
Staining Intensity ◽  
Receptor Expression ◽  
Fibroblast Growth ◽  
Middle Ear Mucosa

The cytokine, fibroblast growth factor (FGF) and its receptors (FGFR) have a pivotal role in wound repair and have been demonstrated in the perimatrix of active cholesteatoma. Aural polyps are a recognized inflammatory reaction of middle-ear mucosa to cholesteatoma, but may arise in its absence. This study examines 28 archival aural polyp specimens, seeking an increased expression for FGFR1 and FGFR3 in polyps associated with cholesteatoma, when compared with those arising in non-cholesteatomatous, mucosal disease, but produced a null result. There was no difference demonstrated in staining intensity between those polyps associated with cholesteatoma and those without. There was a strong correlation between staining patterns of FGFR1 and FGFR3 (r = 0.4, p <0.03). The expression pattern, of nuclear and perinuclear localization, may support the view that nuclear translocation of growth factors, and their receptors, could be related to the cellular proliferation that is associated with cholesteatoma.

scholarly journals Tyrosine Kinase Receptor Expression in Canine Liposarcoma

2016 ◽  
Vol 54 (2) ◽  
pp. 212-217 ◽  
Author(s):  
G. Avallone ◽  
V. Pellegrino ◽  
P. Roccabianca ◽  
E. Lepri ◽  
L. Crippa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tyrosine Kinase ◽  
Fibroblast Growth Factor ◽  
Growth Factor Receptor ◽  
Mitotic Count ◽  
Receptor Expression ◽  
Platelet Derived Growth Factor ◽  
Proliferation Index ◽  
Tyrosine Kinase Receptor ◽  
Fibroblast Growth

The expression of tyrosine kinase receptors is attracting major interest in human and veterinary oncological pathology because of their role as targets for adjuvant therapies. Little is known about tyrosine kinase receptor (TKR) expression in canine liposarcoma (LP), a soft tissue sarcoma. The aim of this study was to evaluate the immunohistochemical expression of the TKRs fibroblast growth factor receptor 1 (FGFR1) and platelet-derived growth factor receptor–β (PDGFRβ); their ligands, fibroblast growth factor 2 (FGF2) and platelet-derived growth factor B (PDGFB); and c-kit in canine LP. Immunohistochemical labeling was categorized as high or low expression and compared with the mitotic count and MIB-1–based proliferation index. Fifty canine LPs were examined, classified, and graded. Fourteen cases were classified as well differentiated, 7 as myxoid, 25 as pleomorphic, and 4 as dedifferentiated. Seventeen cases were grade 1, 26 were grade 2, and 7 were grade 3. A high expression of FGF2, FGFR1, PDGFB, and PDGFRβ was identified in 62% (31/50), 68% (34/50), 81.6% (40/49), and 70.8% (34/48) of the cases, respectively. c-kit was expressed in 12.5% (6/48) of the cases. Mitotic count negatively correlated with FGF2 ( R = –0.41; P < .01), being lower in cases with high FGF2 expression, and positively correlated with PDGFRβ ( R = 0.33; P < .01), being higher in cases with high PDGFRβ expression. No other statistically significant correlations were identified. These results suggest that the PDGFRβ-mediated pathway may have a role in the progression of canine LP and may thus represent a promising target for adjuvant cancer therapies.

Fibroblast growth factor receptor expression investibular schwannoma

2000 ◽  
Vol 25 (6) ◽  
pp. 570-576 ◽  
Author(s):  
S.B. Nair ◽  
H.Y. Leung ◽  
P. Ince ◽  
R.T. Ramsden ◽  
J.A. Wilson
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Receptor Expression ◽  
Fibroblast Growth

scholarly journals Regulation of Endocytosis, Nuclear Translocation, and Signaling of Fibroblast Growth Factor Receptor 1 by E-Cadherin

2005 ◽  
Vol 16 (1) ◽  
pp. 14-23 ◽  
Author(s):  
David M. Bryant ◽  
Fiona G. Wylie ◽  
Jennifer L. Stow
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Nuclear Translocation ◽  
Growth Factor Receptor ◽  
Initial Step ◽  
Mitogen Activated Protein Kinase ◽  
Endocytic Trafficking ◽  
Fibroblast Growth ◽  
Early Endosomes ◽  
E Cadherin

Fibroblast growth factor (FGF) receptors (FGFRs) signal to modulate diverse cellular functions, including epithelial cell morphogenesis. In epithelial cells, E-cadherin plays a key role in cell-cell adhesion, and its function can be regulated through endocytic trafficking. In this study, we investigated the location, trafficking, and function of FGFR1 and E-cadherin and report a novel mechanism, based on endocytic trafficking, for the coregulation of E-cadherin and signaling from FGFR1. FGF induces the internalization of surface FGFR1 and surface E-cadherin, followed by nuclear translocation of FGFR1. The internalization of both proteins is regulated by common endocytic machinery, resulting in cointernalization of FGFR1 and E-cadherin into early endosomes. By blocking endocytosis, we show that this is a requisite, initial step for the nuclear translocation of FGFR1. Overexpression of E-cadherin blocks both the coendocytosis of E-cadherin and FGFR1, the nuclear translocation of FGFR1 and FGF-induced signaling to the mitogen-activated protein kinase pathway. Furthermore, stabilization of surface adhesive E-cadherin, by overexpressing p120ctn, also blocks internalization and nuclear translocation of FGFR1. These data reveal that conjoint endocytosis and trafficking is a novel mechanism for the coregulation of E-cadherin and FGFR1 during cell signaling and morphogenesis.

scholarly journals Importin β–Mediated Nuclear Import of Fibroblast Growth Factor Receptor

2001 ◽  
Vol 152 (6) ◽  
pp. 1307-1312 ◽  
Author(s):  
John F. Reilly ◽  
Pamela A. Maher
Keyword(s):  
Signal Transduction ◽  
Growth Factor ◽  
Cell Surface ◽  
Fibroblast Growth Factor ◽  
Nuclear Import ◽  
Fibroblast Growth Factor Receptor ◽  
Nuclear Translocation ◽  
Growth Factor Receptor ◽  
Growth Factor Receptors ◽  
Fibroblast Growth

Although growth factor receptors are generally thought to carry out their role in signal transduction at the cell surface, many of these transmembrane proteins translocate to the nucleus after ligand stimulation. Here, we show that the nuclear translocation of fibroblast growth factor receptor (FGFR)1 occurs via a mechanism distinct from classical nuclear import but dependent on importin β, a component of multiple nuclear import pathways. Furthermore, we show that nuclear FGFR1 induces c-Jun and is involved in the regulation of cell proliferation. These data are the first description of a nuclear import pathway for transmembrane growth factor receptors and elucidate a novel signal transduction pathway from the cell surface to the nucleus.

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