BES2003 Poster Presentations Cytokines and Growth Factors (9 abstracts)
1Endocrinology Department. Oxford Centre for Diabetes, Endocrinology and Metabolism. Radcliffe Infirmary, Oxford, UK; 2Histology Department. John Radcliffe Hospital, Oxford, UK; 3Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK.
Background: Growth of solid tumours is angiogenesis dependent. Vascular endothelial growth factor (VEGF-A) and fibroblast growth factor-2 (FGF-2) are potent endothelial cell mitogens that play a central role in angiogenesis. Very recently intratumoral lymphangiogenesis has been reported. There are currently no data on the presence of angiogenesis or lymphangiogenesis in parathyroid proliferative lesions compared to normal glands.
Objectives: (1) To analyse microvascular density (MVD) and lymphatic vascular density (LVD) in normal parathyroid glands (PTG), parathyroid adenomas (PTA) and primary parathyroid hyperplasias (PPH). (2) To study the expression of pro-angiogenic growth factors in parathyroid tissue.
Methods: Immunohistochemistry for CD34 (to assess MVD), LYVE-1 (to assess LVD), VEGF-A, and FGF-2 was performed in 13 PTG, 77 PTA and 17 PPH.
Results: MVD was higher in PPH (16.50 ± 2.25) compared to PTA (14.53 ± 2.56) and in PTA compared to PTG (12.84 ± 2.19), (P<0.001). LVD was not significantly different between the three groups. There was no difference in VEGF-A expression, however FGF-2 expression was higher in PPH (3.91 ± 0.21) compared to PTA (2.74 ± 1.10) and in PTA compared to PTG (2.11 ± 0.86), (P<0.0001). In addition FGF-2 scores and MVD were significantly correlated (r=0.43, P<0.001).
Conclusions: (1) This study shows for the first time increased angiogenesis in parathyroid proliferative lesions compared to normal glands, and in hyperplasias compared to adenomas. (2) The correlation of MVD with FGF-2 expression suggests that FGF-2 is pro-angiogenic in parathyroid tissue. (3) This is the first demonstration of lymphatic vessels in parathyroid glands.
The higher angiogenesis of primary hyperplasias associated with increased FGF-2 expression suggests a possible genotype-phenotype interaction.