Oral squamous cell carcinoma (OSCC) has been a focus of cancer prevention studies due to the fact that it occurs by a multistep process and that a precancerous lesion in the oral mucosa is easily accessible. The present study was aimed at developing an optical detection system using autofluorescence spectrum measurements for the early detection of oral cancer. The optical detection system was designed to use an excitation wavelength of 337 nm emanating from a Xenon lamp. Precancerous and cancerous lesions were created in the hamster buccal pouch by treatment with 7,12-dimethylbenz[a]anthracene (DMBA). Four groups of five hamsters each were used in this experiment. The right buccal pouch was treated with 0.5% DMBA to induce carcinogenesis while the left buccal pouch was treated with mineral oil as a control. The autofluorescence of both buccal pouches was measured weekly. A difference in the excitation pattern between the normal and the carcinogen-treated tissue was noticed after three weeks. Specifically, the intensity of the autofluorescence spectrum in the DMBA-treated buccal pouch was increased at wavelengths between 400 and 450 nm. The results of the autofluorescence measurements were compared to histological findings and show that the intensity of the autofluorescence increased along with the stage of epithelial dysplasia. Based on the fact that one of the autofluorophores in this tissue is NADH, we measured the fluorescence at the 450-nm NADH wavelength to conclude that the increased autofluorescence in the dysplastic areas may be caused by NADH. Based on these data, we suggest that autofluorescence optical methods are a useful tool for the early detection of oral cancer.

It is well known that the imbalance between epithelial cell growth and inhibitor factors may cause human epithelial cancer. Over-expression of the epidermal growth factor receptor(EGFR) has been implicated in the development of oral squamous cell carcinoma. ZD1839 inhibits selectively the EGFR tyrosine kinase activity and is clinically used for cancer patients. However the mechanisms by which it exerts its anti-tumor activity remains unclear. This study attempted to determine the mechanisms underlying the effects of ZD1839 on the cellular level and to characterize the effects of ZD1839 with regard to human oral squamous cell carcinoma(OSCC) cell growth. The YD-10B and YD-38 cell lines established from OSCC in the department of Oral Pathology, Yonsei University College of Dentistry and ZD1839(Iressa) were used for this study. The inhibition of cell proliferation induced by ZD1839 was reversible and the lowest dose of ZD1839 that produced statistically significant growth inhibition in YD cell lines were 0.1 μM. The delay in cell cycle progression was induced by 0.1 μM of ZD1839 treatment after 24 hr. This reduction in cell proliferation and cell cycle delay were associated with up-regulation of the cyclin dependent kinase inhibitor(CDKI), P21CIP1/WAF1 and P27KIP1. Reduced expression of cyclin D1 was also observed after treatment with ZD 1839 to YD-38 cells but not to YD-38. The present results suggest that the antiproliferative effects of ZD1839, in vitro was associated with degradation of cyclin D1, which may be used as a possible indicator of a high cell sensitivity to ZD1839.