Send to

Choose Destination
World J Surg. 1998 Jun;22(6):520-5.

Fibroblast growth factors and their receptors in parathyroid disease.

Author information

Department of Surgical Sciences, Northern General Hospital, Sheffield, UK.


Fibroblast growth factors (FGFs) comprise a family of polypeptide growth factors implicated in the control of proliferation of glandular tissues. The aim of this study was to determine whether FGFs are produced in normal and abnormal parathyroid glands and if these tissues have the potential to respond to this growth factor family. We have examined the expression of FGF receptor (FGF-R) types 1 and 2 and of FGFs 1, 2, 3, and 7 in a series of human parathyroid tissues using the reverse transcription polymerase chain reaction (RT-PCR). Samples of 10 parathyroid adenomas and 10 hyperplastic glands from patients with renal hyperparathyroidism (HPT) were compared with samples from normal parathyroid glands from patients with primary HPT in the study. FGF-R1 was expressed in all samples and FGF-R2 in most. FGF1 and FGF2 were expressed in all samples at variable levels, with no correlation between disease type and amplified RT-PCR product levels. FGF7 was expressed in normal parathyroid tissue and in all adenomas but was absent in all but one of the hyperplastic parathyroid glands from renal failure patients. FGF3 was expressed at low levels in normal tissue and variably expressed in diseased tissue, in some instances at high levels. These findings suggest that parathyroid tissue is potentially responsive to FGFs. The absence of FGF7 expression in all but one of the renal parathyroid samples compared with normal and adenomatous tissue requires further investigation. The presence of elevated levels of FGF3 expression in abnormal parathyroid tissue may be significant, as the FGF3 gene (int-2 proto-oncogene) is located on chromosome 11q13.3, a region already identified as being susceptible to rearrangement/mutation in parathyroid disease.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center