Upregulation of fibroblast growth factor-receptor messenger RNA expression in rat brain following transient forebrain ischemia

1993 ◽  
Vol 97 (2) ◽  
Author(s):  
K. Takami ◽  
Y. Kiyota ◽  
M. Iwane ◽  
M. Miyamoto ◽  
R. Tsukuda ◽  
...  
Keyword(s):  
Growth Factor ◽  
Rat Brain ◽  
Fibroblast Growth Factor ◽  
Messenger Rna ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Rna Expression ◽  
Fibroblast Growth ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia

Characterization of Fibroblast Growth Factor Receptor 1 RNA Expression in the Embryonic Mouse Heart

1995 ◽  
Vol 752 (1 Cardiac Growt) ◽  
pp. 406-416 ◽  
Author(s):  
KISHORE B. S. PASUMARTHI ◽  
YAN JIN ◽  
MARGARET E. BOCK ◽  
ARISTIDES LYTRAS ◽  
ELISSAVET KARDAMI ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Mouse Heart ◽  
Rna Expression ◽  
Fibroblast Growth ◽  
Embryonic Mouse

Ectopic expression of fibroblast growth factor receptor 3 promotes myeloma cell proliferation and prevents apoptosis

Blood ◽  
2000 ◽  
Vol 95 (3) ◽  
pp. 992-998 ◽  
Author(s):  
Elizabeth E. Plowright ◽  
Zhihua Li ◽  
P. Leif Bergsagel ◽  
Marta Chesi ◽  
Dwayne L. Barber ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Messenger Rna ◽  
Fibroblast Growth Factor Receptor ◽  
Ectopic Expression ◽  
Tumor Development ◽  
Growth Factor Receptor ◽  
Myeloma Cell ◽  
Fibroblast Growth ◽  
Wild Type

The t(4;14) translocation occurs in 25% of multiple myeloma (MM) and results in both the ectopic expression of fibroblast growth factor receptor 3 (FGFR3) from der4 and immunoglobulin heavy chain-MMSET hybrid messenger RNA transcripts from der14. The subsequent selection of activating mutations of the translocated FGFR3 by MM cells indicates an important role for this signaling pathway in tumor development and progression. To investigate the mechanism by which FGFR3 overexpression promotes MM development, interleukin-6 (IL-6)-dependent murine B9 cells were transduced with retroviruses expressing functional wild-type or constitutively activated mutant FGFR3. Overexpression of mutant FGFR3 resulted in IL-6 independence, decreased apoptosis, and an enhanced proliferative response to IL-6. In the presence of ligand, wild-type FGFR3-expressing cells also exhibited enhanced proliferation and survival in comparison to controls. B9 clones expressing either wild-type FGFR3 at high levels or mutant FGFR3 displayed increased phosphorylation of STAT3 and higher levels of bcl-xL expression than did parental B9 cells after cytokine withdrawal. The mechanism of the enhanced cell responsiveness to IL-6 is unknown at this time, but does not appear to be mediated by the mitogen-activated protein kinases SAPK, p38, or ERK. These findings provide a rational explanation for the mechanism by which FGFR3 contributes to both the viability and propagation of the myeloma clone and provide a basis for the development of therapies targeting this pathway.

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