Characteristics of tumor cell bioactivity in oncogenic osteomalacia

被引：46

作者：

Nelson, AE

Namkung, HJ

Patava, J

Wilkinson, MR

Chang, ACM

Reddel, RR

Robinson, BG

Mason, RS

机构：

[1] UNIV SYDNEY, DEPT PHYSIOL, SYDNEY, NSW 2006, AUSTRALIA

[2] ROYAL N SHORE HOSP, KOLLING INST MED RES, DEPT MOL GENET, SYDNEY, NSW 2065, AUSTRALIA

[3] ROYAL N SHORE HOSP, DEPT ENDOCRINOL, SYDNEY, NSW 2065, AUSTRALIA

[4] CHILDRENS MED RES INST, SYDNEY, NSW 2145, AUSTRALIA

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 1996年 / 124卷 / 1-2期

关键词：

hypophosphatemia; oncogenic osteomalacia; parathyroid hormone-like; sodium-dependent phosphate uptake;

D O I：

10.1016/S0303-7207(96)03928-7

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Oncogenic osteomalacia is a condition where renal phosphate wasting occurs causing defective mineralisation, in the presence of a tumor. Cultures of cells were established from a hemangiopericytoma resected from a patient with oncogenic osteomalacia. Conditioned media from the cells inhibited phosphate uptake in opossum kidney cells and stimulated production of cAMP in rat osteosarcoma cells, a standard parathyroid hormone (PTH)-like assay. This cAMP stimulation was suppressed by the PTH analogue, 3-34 bPTH and also by heat and trypsin treatment of the media. Tests of conditioned media for PTH and parathyroid hormone related protein (PTHrP) immunoreactivity were negative, however, and no hybridisation to probes for PTH, PTHrP or human stanniocalcin was detected in tumor cell RNA on Northern blot. These data support the hypothesis that tumors responsible for oncogenic osteomalacia produce a humoral substance that reduces renal phosphate reabsorption and provide evidence that the factor may act via PTH/PTHrP receptors. Copyright (C) 1996 Elsevier Science Ireland Ltd.

引用

页码：17 / 23

页数：7

共 27 条

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