Heparanase gene and protein expression in ameloblastoma: possible role in local invasion of tumor cells

被引:17
|
作者
Nagatsuka, H
Han, PP
Tsujigiwa, H
Siar, CH
Gunduz, M
Sugahara, T
Sasaki, A
Nakajima, M
Naomoto, Y
Nagai, N
机构
[1] Okayama Univ, Grad Sch Med & Dent, Dept Oral Med & Pathol, Okayama 7008525, Japan
[2] Univ Malaya, Fac Dent, Dept Oral Pathol Oral Med & Periodontol, Kuala Lumpur 50603, Malaysia
[3] Okayama Univ, Grad Sch Med & Dent, Dept Oral & Maxillofacial Reconstruct Surg, Okayama 7008525, Japan
[4] Okayama Univ, Grad Sch Med & Dent, Dept Oral & Maxillofacial Surg, Okayama 7008525, Japan
[5] Novartis Pharma KK, Tsukuba Res Inst, Tsukuba, Ibaraki, Japan
[6] Okayama Univ, Grad Sch Med & Dent, Dept Gastroenterol Surg Transplant & Surg Oncol, Okayama 70085558, Japan
关键词
ameloblastoma; heparanase; heparan sulfate; local invasion;
D O I
10.1016/j.oraloncology.2005.01.004
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Ametoblastoma is the most common odontogenic neoplasm, particularized by its local invasiveness. Heparanase is the endo-glucuronidase enzyme that specifically cleaves heparan sulfate, the important modulator of extracellular matrix, and related to invasion of tumor cells. In this study, we addressed to show the gene expression and localization of heparanase in ametoblastoma. Immunohistochemistry and in situ hybridization of heparanase were carried out in 23 ameloblastomas. Strong expression of heparanase at both mRNA and protein levels was detected in all ameloblastomas studied. Small tumor nests and budding epithelial. branches showed stronger staining pattern and the stromal tissues at the immediate vicinity of the tumor nests with strong heparanase expression were loose and edematous. Cystic areas and squamous metaplastic areas of the tumor showed intense staining with heparanase antibody proposing the implication of heparanase in these processes. These results suggest the possible contribution of heparanase in the local invasiveness and secondary morphologic changes of ameloblastoma. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:542 / 548
页数:7
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