Format

Send to

Choose Destination
Eur Arch Otorhinolaryngol. 2004 Nov;261(10):526-30. Epub 2004 Jan 9.

Cyclin D1 expression does not effect cell proliferation in adenoid cystic carcinoma of the salivary gland.

Author information

1
Department of Otorhinolaryngology, Graduate School of Medical Sciences of Kyushu University, 3-1-1 Maidashi, Higashi-ku, 812-8582 Fukuoka, Japan. ryasuma@ybb.ne.jp

Abstract

Adenoid cystic carcinoma is a malignant tumor of salivary gland origin. It tends to grow slowly, but shows frequent recurrence and metastasis. Cyclin D1, a cell-cycle regulation protein, has been reported to be overexpressed in various types of cancer and to correlate with poor survival of the patients. However, the prognostic significance of cyclin D1 expression in ACC of the salivary glands has not yet been determined. To evaluate the role of cyclin D1 in the biological regulation of ACC, we constitutively expressed an antisense cyclin D1 complementary DNA (cDNA) in an established ACC cell line that exhibits high endogenous expression of cyclin D1. The effect of cyclin D1 expression on in vitro cell growth and cell cycle were examined. In addition, we also examined the immunohistochemical expression of cyclin D1 protein in 31 cases of ACC of the salivary gland and correlated its expression with proliferative activity or prognosis. There were no significant differences of the in vitro growth and in the percentage of the total cell population in the G1 phase and S phase between antisense cyclin D1 clones and control clones. Thirty-two percent of tumors derived from surgical specimens examined were immunohistochemically positive for cyclin D1 protein. No association was found between cyclin D1 expression and cell proliferation or the clinical outcome of the patients. It is concluded that cyclin D1 overexpression alone does not induce a marked increase in the proliferative activity of ACC cells and that expression of this protein is not linked to poor prognosis in adenoid cystic carcinoma of the salivary gland.

PMID:
14714130
DOI:
10.1007/s00405-003-0724-6
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center