To the Editor: The letter by Hoshino and coworkers (Jan. 30 issue)(1) hypothesizes an immune-mediated pathogenesis of tumor-induced osteomalacia in patients in whom the neoplasia was not localized. This suggestion may open the way to new therapeutic options in addition to conventional and burosumab treatments. However, we think there is a theoretical pathogenesis that has been overlooked. Previous studies have shown that a number of phosphatonins genes, in addition to fibroblast growth factor 23 (FGF23), are markedly overexpressed in tumors associated with tumor-induced osteomalacia. Among these are matrix extracellular phosphoglycoprotein, secreted frizzled-related protein 4, and fibroblast growth factor 7 (FGF7).(2) . . .
More on Acquired Osteomalacia and Autoantibodies against PHEX / Minisola, Salvatore; Pepe, Jessica; Cipriani, Cristiana. - In: THE NEW ENGLAND JOURNAL OF MEDICINE. - ISSN 0028-4793. - 392:18(2025), pp. 1871-1872. [10.1056/NEJMc2502747]
More on Acquired Osteomalacia and Autoantibodies against PHEX
Minisola, Salvatore;Pepe, Jessica;Cipriani, CristianaUltimo
2025
Abstract
To the Editor: The letter by Hoshino and coworkers (Jan. 30 issue)(1) hypothesizes an immune-mediated pathogenesis of tumor-induced osteomalacia in patients in whom the neoplasia was not localized. This suggestion may open the way to new therapeutic options in addition to conventional and burosumab treatments. However, we think there is a theoretical pathogenesis that has been overlooked. Previous studies have shown that a number of phosphatonins genes, in addition to fibroblast growth factor 23 (FGF23), are markedly overexpressed in tumors associated with tumor-induced osteomalacia. Among these are matrix extracellular phosphoglycoprotein, secreted frizzled-related protein 4, and fibroblast growth factor 7 (FGF7).(2) . . .I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


