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. 1999 Feb 15;85(4):960-9.
doi: 10.1002/(sici)1097-0142(19990215)85:4<960::aid-cncr26>3.0.co;2-p.

Expression of thymidine phosphorylase and vascular endothelial cell growth factor in human head and neck squamous cell carcinoma and their different characteristics

T Fukuiwa  1 , Y Takebayashi, S Akiba, T Matsuzaki, Y Hanamure, K Miyadera, Y Yamada, S Akiyama
Affiliations

Expression of thymidine phosphorylase and vascular endothelial cell growth factor in human head and neck squamous cell carcinoma and their different characteristics

T Fukuiwa et al. Cancer. .

Abstract

Background: Thymidine phosphorylase (dThdPase) is identical to platelet-derived endothelial cell growth factor (PD-ECGF). dThdPase is known to promote the development of new blood vessels, which are fundamental to tumor growth and metastasis. Vascular endothelial growth factor (VEGF) is a 34-42 kilodalton (kD) protein that induces both angiogenesis and vascular permeability. Proliferating cell nuclear antigen (PCNA) is a 36 kD nuclear protein, and its expression is associated with DNA synthesis and cell proliferation.

Methods: The authors investigated the correlations of dThdPase and VEGF with the growth of head and neck squamous cell carcinoma (HNSCC) in 95 patients by examining PCNA expression as a marker of tumor proliferation. They also retrospectively examined the expression of dThdPase in primary HNSCC and its association with angiogenesis and clinicopathologic findings.

Results: Microvessel count was significantly correlated with the expression of VEGF (P = 0.046) but not with dThdPase expression. The expression of PCNA was significantly correlated with dThdPase (P < 0.001) but not VEGF expression. A significant correlation was found between VEGF and dThdPase expression (P = 0.003). Neither dThdPase nor VEGF correlated with clinicopathologic findings, except for the correlation between tumor location and VEGF expression (P 0.020).

Conclusions: These findings suggest that VEGF is involved in angiogenesis in HNSCC. dThdPase may have effects on tumor growth other than angiogenic activity in HNSCC.

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