Cloning and characterization of FGF23 as a causative factor of tumor-induced osteomalacia

By T. Shimada, S. Mizutani, T. Muto, T. Yoneya, Rieko Hino, S. Takeda, Y. Takeuchi, T. Fujita, S. Fukumoto, T. Yamashita. Proceedings of the National Academy of Sciences of the United States of America, 2001

1,382 citations recorded by the source corpus.

Subfields: Nephrology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/6cbd322be9ca8ae07c9f4c54fcd2ef4ea9b63148

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In Nephrology

1. M. Mohammadi
2. D. Bikle
3. A. Beenken

In Oncology

1. J. Y. Chiang

Citations in the corpus

• Fibroblast growth factors: from molecular evolution to roles in development, metabolism and disease. (2011, background): “characterized by hypophosphataemia caused by renal phosphate wasting (100).”
• Regulation of Phosphate Homeostasis by PTH, Vitamin D, and FGF23 (2010, background): “Furthermore, clones encoding FGF23 were isolated from cDNA libraries of tumors causing oncogenic osteomalacia (OOM) and recombinant FGF23 was shown to induce renal phosphate-wasting leading to hypophosphatemia and osteomalacia (57).”
• Structural basis for fibroblast growth factor receptor activation. (2005, background): “In the adult, FGFs continue to regulate tissue homeostasis but also play important roles in wound healing, tissue repair, cholesterol metabolism [47,48] and serum phosphate regulation [49–54].”
• Resurrection of vitamin D deficiency and rickets. (2006, neutral): “Patients with autosomal dominant hypo-phosphatemic rickets (ADHR) have a mutation in the FGF23 gene that prevents or reduces FGF23 metabolic breakdown, leading to elevated FGF23 levels (70, 75).”
• FGF‐23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis (2003, background): “uous administration of recombinant FGF-23 reproduced hypophosphatemia, inappropriately low 1,25(OH)2D, and rickets/osteomalacia in animals.((5,11)) However, it remains unclear how FGF-23 causes hypophosphatemia and an abnormal vitamin D metabolism.”
• Definition of a novel growth factor-dependent signal cascade for the suppression of bile acid biosynthesis. (2003, background): “For many years, it has been understood that the FGFs regulate cell growth, differentiation, and morphogenesis, however, it is now apparent that some of these proteins are also important components of specific homeostatic pathways (Yu et al. 2000; Shimada et al. 2001; Tomlinson et al. 2002).”
• Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D. (2006, background): “Increased production of FGF23 is the cause of phosphaturia and disordered vitamin D metabolism in tumor-induced osteomalacia (6,7), X-linked hypophosphatemic rickets (XLH) (7,8), and McCune-Albright syndrome (9).”
• FGF/FGFR signaling in health and disease (2020, background): “the cause of tumor-induced osteomalacia and fibrous dysplasia because of its overexpression in tumors and osteogenic cells in fibrous dysplastic lesions.(575) Furthermore, multiple FGF23 gene mutations lead to reduced FGF23 level in patients, which is responsible for hyperphosphatemic familial tumor”
• Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. (2005, background): “Indeed, intravenous or intraperitoneal infusion of recombinant FGF-23 in mice induces phosphaturia and hypophosphatemia (30,31), and transgenic mice expressing FGF-23 under the control of different promoters develop hypophosphatemia and rickets (32–34).”
• Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. (2003, background): “transgenic expression of this growth factor leads to hypophosphatemia, while ablation of the FGF-23 gene in mice results in significant hyperphosphatemia [6–8].”