Search

The aim of this study was to identify tumor suppressor genes (TSGs) in oral squamous cell carcinoma (OSCC) using whole-genome analysis of microarray technology and real-time quantitative polymerase chain reaction (QPCR). We applied whole-genome analysis of TSGs in the specimens from 3 patients of OSCC by microarray technology. A total of 11 genes, CRISP3, SCGB3A1, AGR2, PIP, C20orf114, TFF1, STATH, AZGP1, MUC7, DMBT1 and LOC389429, were found to be down-regulated, and 2, matrix metallopeptidase (MMP) 1 and MMP3, were found to be up-regulated in the 3 OSCC patients using microarray technology. In this study, we selected the CRISP3 gene. CRISP3 belongs to the cystein-rich secretary protein gene family in chromosome 6p12.3. CRISP3 has been found in the salivary gland, spleen and prostate gland and is a prominent biomarker in the gene expression of prostate cancer. Down-regulation of this gene was previously observed in OSCC. No studies examining the DNA copy number of CRISP3 in detail exist. We analyzed the DNA copy number of CRISP3 in 5 OSCC-derived cell lines (SAS, Ca9-22, KON, HSC2 and HSC4) and 60 OSCC tissues by real-time QPCR. The DNA copy number loss of CRISP3 was observed in 2 of the 5 OSCC-derived cell lines (SAS, HSC2) and in 24 of 60 patients (40.0%) using real-time QPCR. A significant statistical correlation between the copy number loss and gender and T classification was observed. These results indicate that the inactivation of CRISP3 is an early event in OSCC, since the T1/T2 classification is correlated with DNA copy number loss of CRISP3, whereas T3/T4 classification is not. We conclude that CRISP3 may be involved in the carcinogenesis of OSCC.

Oral squamous cell carcinoma (OSCC) is one of the most common cancers in geographic regions where betel quid (BQ) chewing is prevalent; OSCC is an extremely malignant neoplasm whose prognostic factors are multiple and complex. The purpose of this study was to assess clinicopathological prognostic factors and treatment outcomes in 698 consecutive OSCC patients who had undergone surgery as the primary treatment in an area with a high prevalence of both betel quid chewing and tobacco smoking. The prognostic factors were predicted using Cox's proportional-hazards regression model, and the survival rate was calculated using Kaplan-Meier analysis. The median followup for all patients was 44 months. The 5-year cumulative overall, disease-specific, and locoregional control survival rates were 61%, 62%, and 46%, respectively. Multivariate analysis showed that the lower level of nodal metastasis, advanced stage, tumor thickness >7 mm, and treatment failures were independent risk factors of overall survival. Furthermore, history of alcohol drinking, lower level of nodal metastasis, advanced stage, poor cell differentiation, and treatment failures were independent predictors of poor disease-specific survival. However, we did not find any significant factor that affected locoregional recurrence. Due to the high frequencies of locoregional recurrence and second primary cancer, our findings emphasize that aggressive surgical excision, adjuvant treatments according to clinicopathological prognostic factors and close surveillance are important to the survival of OSCC patients in an area with a high prevalence of betel quid chewing and tobacco smoking., (Copyright 2010 Elsevier Ltd. All rights reserved.)

Background/purpose: Supraomohyoid neck dissection (SOHND) is commonly used to treat oral squamous cell carcinoma (OSCC) patients with clinical N0 or selected N1 status. The purpose of this study was to evaluate the clinical outcome of OSCC patients treated with SOHND., Methods: This retrospective study reviewed the clinical outcome of 257 patients (247 men, 10 women) with N0, N1 and N2a OSCC treated with wide excision of the main tumor and SOHND between 1992 and 1999. All patients were followed up for at least 5 years. Survival distributions were analyzed using Kaplan-Meier curves. N status was compared using chi2 and log rank tests., Results: The neck failure rate was 20% for clinically false negative cases, 6.1% for clinically true negative cases, 21.8% for clinically false positive cases, and 40% for clinically true positive cases. The 3- and 5-year overall neck disease-free survival rates were 79.8% and 77.6%, respectively. The 3- and 5-year neck disease-free survival rates were 86.7% and 84.2% for pathologic N0 cases, 56.9% and 56.9% for pathologic N1 cases, and 27.5% and 27.5% for pathologic N2 cases, respectively. Log rank test showed that the p value for difference in survival at 3-5 years was 0.064 for pathologic N0 vs. N1 cases, < 0.0001 for pathologic N0 vs. N2 cases, and 0.008 for pathologic N1 vs. N2 cases., Conclusion: This study showed that SOHND is effective for pathologic N0 OSCC, relatively effective for pathologic N1, and less effective for pathologic N2a. These findings also support that when SOHND is used to treat N2a OSCC, postoperative radiotherapy or radical neck dissection may be needed to improve the neck disease-free survival rate.

The Pim-1 proto-oncogene, encoding a serine-threonine kinase, has been found to play an important role in regulating apoptosis, differentiation, proliferation and tumourigenesis. The present study was conducted to assess the importance of Pim-1 in oral tumourigenesis in vivo. Reverse transcriptase-polymerase chain reaction and immunohistochemistry were used to study the expression of Pim-1 in oral squamous cell carcinoma (OSCC) and non-cancerous match tissue (NCMT) sampled from the periphery of the tumours. Pim-1 mRNA expression in OSCC was significantly higher than that in NCMT in 36 tissue pairs (1.33+/-0.41 versus 0.97+/-0.29, P=0.03). The percentage of OSCCs exhibiting strong cytoplasmic Pim-1 immunoreactivity was significantly higher than that of NCMT (60% versus 19%, P=0.007). Pim-1 immunoreactivity is higher in the more differentiated components of a tumour. In around 10% of OSCC cases, Pim-1 immunoreactivity was found in the nucleus as well. These results show novel findings of the up-regulation of Pim-1 expression from NCMT to OSCC. The pathogenetic role of Pim-1 expression in oral tumourigenesis deserves further investigation.