Expression of transforming growth factor beta type II receptors in head and neck squamous cell carcinoma

Citation
Ca. Muro-cacho et al., Expression of transforming growth factor beta type II receptors in head and neck squamous cell carcinoma, CLIN CANC R, 5(6), 1999, pp. 1243-1248
Citations number
20
Categorie Soggetti
Oncology
Journal title
CLINICAL CANCER RESEARCH
ISSN journal
10780432 → ACNP
Volume
5
Issue
6
Year of publication
1999
Pages
1243 - 1248
Database
ISI
SICI code
1078-0432(199906)5:6<1243:EOTGFB>2.0.ZU;2-1
Abstract
Transforming growth factor (TGF)-beta is a potent regulator of growth and d ifferentiation in normal squamous epithelium, TGF-beta exerts its antiproli ferative effect via the TGF-beta type II receptor (T beta R-II). A decrease in T beta R-II expression is believed to be responsible, in part, for the resistance of squamous cell carcinoma (SqCC) to the antiproliferative effec ts of TGF-beta. In the present study, we used immunohistochemistry and in s itu hybridization to analyze the expression of T beta R-II along the succes sive oncogenic stages of head and neck squamous neoplasia, from normal epit helium to dysplasia to carcinoma. Quantitation of T beta R-II expression in 38 SqCCs was assessed on a visual scale ranging from negative (absence of staining) to 3+ (strong staining), Normal squamous epithelium and squamous epithelium in the vicinity of the tumors showed homogenous receptor express ion with moderate intensity. Dysplastic epithelium and carcinoma in situ sh owed a mild decrease in receptor expression intensity. Well-differentiated to moderately differentiated carcinomas showed heterogeneous expression of variable intensity and poorly differentiated carcinomas were completely dev oid of T beta R-II, In every tumor, the superficial component showed more i ntense receptor expression than the invasive component. These results indic ate that T beta R-II expression inversely correlates with disease aggressiv eness and suggest that aberrant T beta R-II expression is a contributing fa ctor to the pathogenesis of SqCC.