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A cultured cell line was derived from a hemangiopericytoma obtained at surgery from a 9 year-old boy with hypophosphatemic rickets. Hypophosphatemia and metabolic bone disease were cured in the patient after tumor removal. Cells from passage 5 were transplanted into 8 week-old athymic female mice. Additional animals received innocula of cells thawed from the stored original tumor tissue, as well as MRC-5 fibroblasts. Serum phosphate levels 3-7 months post-transplantation were lowest in mice which received the cultured cell line (n = 5) 6.1 +/- 0.6 mg/dl (p &lt; 0.05 compared to the other groups), thawed tumor cells (n = 8) 7.2 +/- 0.7 mg/dl, MRC fibroblasts (n = 4) 8.1 +/- 1.0 mg/dl, no transplant (n = 10) 8.7 +/- 1.9 mg/dl. Repeat of the experiment with cultured tumor cells from passage 12 no longer altered phosphate levels. A substance produced and release by the tumor in situ and by tumor-derived cultured cells is capable of producing hypophosphatemia. Experimental manipulation of functional tumor-derived cell lines may help elucidate the factor(s) causing hypophosphatemia in oncogenic osteomalacia/rickets.

Hypophosphatemia Induced in Mice by Transplantation of a Tumor-Derived Cell Line from a Patient with Oncogenic Rickets