scholarly journals New oncogenic signalling pathway: EWS‐Oct4 mediates bone and soft tissue tumourigenesis by activating fibroblast growth factor‐4

FEBS Journal ◽  
2019 ◽  
Vol 286 (22) ◽  
pp. 4418-4421
Author(s):  
Dongmei Chen ◽  
Tae Ho Lee
Keyword(s):  
Growth Factor ◽  
Soft Tissue ◽  
Fibroblast Growth Factor ◽  
Signalling Pathway ◽  
Fibroblast Growth ◽  
Oncogenic Signalling

scholarly journals Cells retrovirally transfected with fibroblast growth factor-2 isoforms exhibit altered adenylate cyclase activity and G-protein functionality

1996 ◽  
Vol 315 (2) ◽  
pp. 619-624 ◽  
Author(s):  
Agnes ESTIVAL ◽  
Patrick ROBBERECHT ◽  
Marjorie FANJUL ◽  
Bruno ROUOT ◽  
Etienne HOLLANDE ◽  
...  
Keyword(s):  
Growth Factor ◽  
Adenylate Cyclase ◽  
Molecular Mass ◽  
Fibroblast Growth Factor ◽  
G Proteins ◽  
Signalling Pathway ◽  
Peptide Sequence ◽  
Fibroblast Growth ◽  
Intact Cells

Basic fibroblast growth factor (FGF-2) is synthesized as different molecular mass isoforms all lacking the signal-peptide sequence. The high molecular-mass isoforms (21–24 kDa) possess a signal sequence directing their nuclear translocation. The role of each isoform is still poorly understood, however, modifications in intracellular signalling pathways could explain some effects of these peptides. In order to evaluate the role of FGF-2 isoforms on the adenylate cyclase (AC) signalling pathway, we retrovirally infected a rat pancreatic cell line (AR4-2J) with point-mutated FGF-2 cDNAs, allowing the expression of the 18 (A5 cells) or 22.5 kDa isoform (A3 cells) at a low level. In membrane preparations of A3 cells, unscheduled expression of the 22.5 kDa FGF-2 isoform induced a 2-fold decrease in both basal and forskolin-stimulated AC activity. Studies carried out on intact cells also showed decreased accumulation of cAMP in A3 cells in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. Both FGF-2 peptides also induced functional modifications of G-proteins without affecting their levels. The 22.5 kDa peptide led to enhanced ADP-ribosylation of both αs-subunits in vitro, whereas the expression of the low molecular-mass 18 kDa peptide resulted in a 2-fold increase in αi2 and α0 ADP-ribosylations. Furthermore, control CAT cells (AR4-2J cells transfected with the retrovirus containing the chloramphenicol acetyltransferase gene) and A5 cells were growth-inhibited by 8-Br-cAMP, in contrast to A3 cells. These data provide evidence that the expression of FGF-2 peptides could play a role in cell functions by modifying the AC signalling pathway. FGF-2 peptides are able to modulate both AC activity and the regulatory G-proteins. Finally FGF-2 expression may interfere with cAMP-regulated cell proliferation.

scholarly journals Targeting Fibroblast Growth Factor Receptor 1 for Treatment of Soft-Tissue Sarcoma

2016 ◽  
Vol 23 (4) ◽  
pp. 962-973 ◽  
Author(s):  
Priya Chudasama ◽  
Marcus Renner ◽  
Melanie Straub ◽  
Sadaf S. Mughal ◽  
Barbara Hutter ◽  
...  
Keyword(s):  
Growth Factor ◽  
Soft Tissue ◽  
Soft Tissue Sarcoma ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Fibroblast Growth

Phosphaturic Mesenchymal Tumor; A Diagnostically Elusive Cause Of Oncogenic Osteomalacia; Case Study

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S114-S114
Author(s):  
M Chand ◽  
J Edens ◽  
R Danforth
Keyword(s):  
Growth Factor ◽  
Soft Tissue ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Benign Neoplasm ◽  
Mesenchymal Tumor ◽  
Fibroblast Growth ◽  
Phosphaturic Mesenchymal Tumor ◽  
Oncogenic Osteomalacia ◽  
Pathologic Fractures

Abstract Casestudy: Phosphaturic mesenchymal tumor (PMT) is a rare, benign neoplasm. It is associated with oncogenic osteomalacia, a paraneoplastic condition caused by secretion of a peptide hormone-like substance, fibroblast growth factor 23, which increases renal clearance of phosphate and increased mobilization of calcium and phosphate from bone. PMT is difficult to diagnose as a primary etiology because patients usually experience non- specific symptoms associated with hypophosphatemia like bone pain, muscular weakness, and pathologic fractures. Because PMT is a benign neoplasm, surgical excision is curative and rapid resolution of symptoms typically ensues. Discussed here is a case of PMT arising in the soft tissue of the medial thigh of a 65 year old man with a five year history of osteomalacia with pathologic fractures and complicated healing. Lab studies revealed hypophosphatemia, hyperphosphaturia, hypercalcemia, and elevated serum fibroblast growth factor 23 during workup for fracture. A small superficial soft tissue mass was discovered in the proximal thigh via octreotide scan which was subsequently excised. On histologic examination it was composed of an encapsulated proliferation of spindle cells in a chondromyxoid background with distinctive areas of flocculent calcification and osteoclast-like giant cells. A diagnosis of PMT was rendered. The patient’s symptoms resolved rapidly after surgery. Despite the benign characteristics and behavior of this rare neoplasm; delayed or mis-diagnosis can have severe implications for patient’s health. Interdisciplinary communication, shrewd clinical index of suspicion, and awareness of the causes of, and the tests available to diagnose oncogenic osteomalacia can speed accurate diagnosis leading to better outcomes for patients.

Fibroblast growth factor receptor‐1 interacts with the T‐cell receptor signalling pathway

2003 ◽  
Vol 81 (6) ◽  
pp. 440-450 ◽  
Author(s):  
Victor M Byrd ◽  
Dawn M Kilkenny ◽  
Michael M Dikov ◽  
Martha B Reich ◽  
Jonathan V Rocheleau ◽  
...  
Keyword(s):  
T Cell ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
T Cell Receptor ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Cell Receptor ◽  
Signalling Pathway ◽  
Fibroblast Growth ◽  
Receptor Signalling
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