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Background This study elucidated the association between histopathological factors and the prognosis of oral carcinoma. As the histopathological factors were determined from the surgical specimen and this can only be used for the choices of postoperative regimens, this study also investigated the linkage between prognostic factors and the expression of key molecules to examine the feasibility of markers as predictors. Methods Clinicopathological factors of 101 oral carcinomas were cross-analyzed with disease-free survival. The expression of nerve growth factor ( NGF) and its receptor, tyrosine kinase A receptor, was assayed with immunohistochemistry. Results Nodal metastasis was the most crucial clinical predictor for disease-free survival. Perineural invasion ( PNI) was an independent histopathological predictor for both nodal metastasis ( P = 0.004) and disease-free survival ( P = 0.019). Patients with advanced tumor and PNI exhibited the high hazard for tumor progression and poor disease-free survival. NGF immunoreactivity in tumors was correlated with PNI ( P = 0.005) and neck lymph node metastasis ( P = 0.036). Conclusion Perineural invasion is the indicator of worst prognosis. As NGF immunoreactivity was found to be associated with PNI and nodal metastasis, the NGF immunoreactivity of oral carcinoma revealed by diagnostic biopsy suggests that alternative therapeutic approaches might be appropriate. [ABSTRACT FROM AUTHOR]

Background: The main cause of treatment failure in resectable oral squamous cell carcinoma (OSCC) is metastasis. E-cadherin (E-cad) plays a principal role in cell adhesion and motility, and is associated with OSCC progression. The aim of this study was to investigate the clinical significance of E-cad expression in OSCC with lymph node metastasis which had radical neck dissection done. Method: Immunohistochemistry was used to detect E-cad expression in normal oral mucosa (NOM) ( n = 10), oral precancerous lesions (OPLs) ( n = 20), primary OSCC ( n = 45), and their paired metastatic lesions ( n = 45). E-cad immunoreactivity correlated with the clinicopathologic features. Results: E-cadherin immunoreactivity was progressively reduced in the NOM followed by OPLs and primary OSCC (58%). It decreased significantly in the advanced stages of OSCC. However, the increase in E-cad immunoreactivity was observed in the majority (60%) of metastatic lesions in relation to primary OSCC. Patients with such increased or positive immunoreactivity of E-cad in metastatic lesions exhibited worse prognosis. Conclusion: The findings suggested a dynamic change in E-cad immunoreactivity during tumorigenesis and metastasis of OSCC. In a multivariate analysis, E-cad immunoreactivity in metastasis lesions (odds ratio 3.74, 95% CI 1.15–14.67; P = 0.040) implied the potential role of mortality predictors for OSCC cases with nodal involvement. [ABSTRACT FROM AUTHOR]

Background: Insertion/deletion (−1171 5A→6A) polymorphisms in the promoter region of matrix metalloproteinase 3 ( MMP3) gene result in different transcriptional activities. MMP3 is able to degrade collagens types II, V, IX, and X, and other extracellular matrix. The functional promoter polymorphism of MMP3 has been related to the susceptibility in some inflammatory diseases and metastasis of cancers. Methods: Oral submucous fibrosis (OSF) and oral squamous cell carcinoma (OSCC) are prevalent among Asian areca users. In this study, genomic DNA obtained from the blood of OSCC ( n = 150), OSF ( n = 71), and control non-diseased areca user ( n = 98) in male were subjected to polymerase chain reaction (PCR)-based genotyping of MMP3. Results: The 5A genotype in MMP3 promoter was observed more frequently in OSF group than in control group ( P = 0.01). No significant difference was noted between OSCC and control groups on the 5A genotype frequency ( P = 0.18). No association was found between 5A genotype in MMP3 promoter and site or lymph node metastasis and stage of OSCC. Conclusion: The results indicated that the 5A genotype of MMP3 promoter was associated with the risk of OSF but not OSCC. [ABSTRACT FROM AUTHOR]