Urokinase-type plasminogen activator (uPA) and its receptor (uPAR) act in the proteolysis of basement membrane and extracellular matrix structures, facilitating tumor invasion. The purpose of this study was to evaluate the relationship between these proteins and clinicopathological parameters in squamous cell carcinoma of the oral tongue (SCCOT). Sixty cases of SCCOT were submitted to immunohistochemistry and analyzed semiquantitatively at the invasion front and in the tumor core. The results were associated with lymph node metastasis, clinical stage, locoregional recurrence, clinical outcome and histological grade of malignancy. A higher expression of uPA was observed in cases of tumors of high-grade versus low-grade malignancy (p = 0.010). Moreover, the cases with the worst pattern of invasion presented an overexpression of uPA (p = 0.011). The presence of locoregional recurrence was associated with uPAR (p = 0.039), and the expression of both biomarkers was much higher at the invasion front than in the tumor core (p < 0.001). The results suggest uPA and uPAR are involved in the progression and aggressiveness of SCCOT, mainly at the tumor-host interface.
Introduction: Oral squamous cell carcinoma (OSCC), which represents more than 90% of head and neck malignant neoplasms, has a poor prognosis due to its high frequency of lymph node metastasis and local invasion. Previous studies have investigated parameters related to the biological behavior of OSCC and its correlation with disease outcome (DO). Objective: To evaluate clinical and morphological data in cases of tongue squamous cell carcinoma (TSCC), correlating these findings with prognosis. Material and methods: Fifty-seven specimens of TSCC were obtained from patients undergoing surgical excision at a referral hospital in Natal, Brazil. Clinical data, such as tumor-node-metastasis (TNM) stage and DO, were collected from medical records. Hematoxylin and eosin-stained sections were analyzed regarding histological grade of malignancy (HGM), based on the system proposed by Bryne (1998). Results: The majority of patients (38.6%) were diagnosed as TNM stage III, and 57.9% developed metastases. Remission of the tumor occurred in 77.2% of the cases. The parameter "metastasis" exhibited a significant association with DO (p = 0) and TNM stage (p = 0.001), thus constituting a good indicator of tumor progression. Correlation of HGM and TNM stage with DO was not evidenced. Nevertheless, statistical analysis showed a significant association between HGM and TNM stage (p = 0.006). Conclusion: TNM clinical staging and HGM, evaluated in association, may be useful to estimate the prognosis of TSCC.
Background: Oral potentially malignant disorders (OPMDs) comprise a range of clinical-pathological alterations that are frequently characterized as architectural and cytological derangements upon histological analysis. Epithelial-mesenchymal transition (EMT) has been proposed as a critical mechanism for the acquisition of the malignant phenotype in neoplastic epithelial processes. This study aims to systematically review the current findings on the immunohistochemical expression of epithelial-mesenchymal transition markers in oral potentially malignant disorders and to evaluate their possible application as biomarkers associated with the progression of oral epithelial dysplasias. Material and Methods: A systematic search was performed in the following databases: PubMed, EMBASE, Chinese BioMedical Literature Database, and Cochrane Library. Articles that evaluated the relationship between the expression of EMT markers and the degree of oral epithelial dysplasia were selected for the systematic review. The quality of each eligible study was evaluated by independent reviewers that used operationalized prognostic biomarker reporting guidelines (REMARK). Results: Seventeen articles met all inclusion criteria and were selected. The EMT markers analyzed exhibited an important association with the prognosis of the cases evaluated. The results showed a progressive increase in the expression of nuclear transcription factors and markers of mesenchymal differentiation, as well as negative regulation of epithelial and cell adhesion markers, according to the stage of oral epithelial dysplasia.
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