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Indian Journal of Pathology and Microbiology
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ORIGINAL ARTICLE
Year : 2013  |  Volume : 56  |  Issue : 2  |  Page : 151-154

Immunohistochemical expression of endothelin protein in oral squamous cell carcinoma


1 Department of Oral Pathology, Faculty of Oral and Dental Medicine, Cairo University, Giza, Egypt; Department of Oral Pathology, Faculty of Oral and Dental Medicine, Sana'a University, Yemen
2 Department of Oral Pathology, Faculty of Oral and Dental Medicine, Cairo University, Giza, Egypt

Correspondence Address:
Nermine Raouf Amin
Faculty of Oral and Dental Medicine, Cairo University, Giza, Egypt

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.118677

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Context: Endothelin-1 (ET-1) plays a significant role in cancer biology and is considered as a potential target for molecular therapy. Alteration of ET-1 was detected in oral squamous cell carcinoma (OSCC). Aim: To evaluate the immunohistochemical expression and distribution of ET-1 in OSCC and to correlate its expression with the degree of histopathologic differentiation as well as the regional metastatic status of OSCC. Materials and Methods: The immunohistochemical expression and distribution of ET-1 was evaluated in total number of 30 cases of OSCC. The specimens were retrieved as formalin-fixed, paraffin-embedded blocks from the archival files. Detection of ET-1 expression in different grades of metastatic and non-metastatic OSCC was quantified using an image analyzer computer system. Statistical Analysis Used: Statistical software package SPSS v. 19. Results: ET-1 immunoreactivity was observed in all studied specimens. On comparing optical density values for ET-1 expression in different grades of OSCC, poorly differentiated OSCC showed a significantly greater expression than moderately differentiated OSCC, which was also significantly greater than well-differentiated OSCC ( P = 0.001). Moreover, ET-1 expression was higher in metastatic OSCC than that in non-metastatic OSCC ( P = 0.018). Conclusions: Increased ET-1 expression could enhance the aggressive behavior of poorly differentiated OSCC, especially metastasis. Accordingly, ET-1 could be a therapeutic target in OSCC.


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