Aberrant expression of Smad4, a TGF-beta signaling molecule, in oral squamous cell carcinoma.

Although carcinogenesis of oral squamous cell carcinoma (OSCC) has been studied by many investigators in the past decade, the available evidence about its molecular mechanism is inconclusive. The objective of the present study was to compare expression of Smad4, a signaling molecule of the transforming growth factor beta (TGF-beta) pathway, between OSCC and normal oral mucosa. We assayed expression of Smad4 in OSCC and normal oral mucosa by performing immunohistochemistry using paraffin-embedded tissue samples.

Scoring system for monitoring oral lichenoid lesions: a preliminary study.

Background: Currently, there is no universal system for scoring the severity of lichenoid lesions of the oral cavity that is easy to use, reproducible and that is representative of the different clinical forms of the disease.

Objectives: In this study, a scoring system was developed to monitor the severity of oral lichen planus (OLP) and chronic oral graft-versus-host disease (cGVHD).

Methods: Six patients with OLP and three with cGVHD were studied.

Cyclin-dependent kinase inhibitor indirubin-3'-oxime selectively inhibits human papillomavirus type 16 E7-induced numerical centrosome anomalies.

Dysregulation of the centrosome duplication cycle has been implicated in tumorigenesis. Our previous work has shown that the human papillomavirus type 16 (HPV-16) E7 oncoprotein rapidly induces aberrant centrosome and centriole duplication in normal human cells. We report here that HPV E7-induced abnormal centriole duplication is specifically abrogated by a small molecule CDK inhibitor, indirubin-3'-oxime (IO), but not a kinase-inactive derivative.