Mitra Askari
1, Masoud Darabi
2, Esa Jahanzad
3, Zahra Mostakhdemian Hosseini
4, Marjan Musavi Chavoshi
5, Maryam Darabi
6*1 Assistant Professor, Department of Oral & Maxillofacial Pathology, Faculty of Dentistry, Tehran University of Medical Sciences, International Campus, Tehran, Iran
2 Assistant Professor, Department of Biochemistry and Clinical Laboratories, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
3 Associate Professor, Department of Pathology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
4 Assistant Professor, Iran Tumor Bank, Cancer Institute, Imam Hospital, Tehran University of Medical Sciences, Tehran, Iran
5 Student of Dentistry, Faculty of Dentistry, Tehran University of Medical Sciences, International Campus, Tehran, Iran
6 Assistant Professor, Dental and Periodontal Research Center, Faculty of Dentistry, Tabriz University of Medical Sciences, Tabriz, Iran
Abstract
Background and aims. Various morphologies are seen in different salivary gland tumorsor within an individual tumor, and the lesions show divers biological behaviors. Experimental results support the hypothesis that increased CrkII proto-oncogene is associated with cytokine-induced tumor initiation and progression by altering cell motility signaling pathway. The aim of this study was to assess the CrkII expression in common malignant salivary gland tumors and pleomorphic ade-noma. Materials and methods. Immunohistochemical analysis of CrkII expression was performed on paraffin blocks of 64 car-cinomas of salivary glands, 10 pleomorphic adenomas, and 10 normal salivary glands. Biopsies were subjected to immu-nostaining with EnVision detection system using monoclonal anti-CrkII. Evaluation of immunoreactivity of CrkII was based on the immunoreaction intensity and percentage of stained tumor cells which were scored semi-quantitatively on a scale with four grades 0 to 3. Kruskal-wallis test and additional Mann-Whitney statistical test were used for analysis of CrkII expression levels. Results. Increased expression of CrkII was seen (P=0.005) in malignant tumors including: mucoepidermoid carcinoma, adenoid cystic carcinoma, and carcinoma ex pleomorphic adenoma, but CrkII expression in acinic cell carcinoma was weak. CrkII expression in pleomorphic adenoma was weak or negative. A weak staining was sparsely seen in normal acinar serous cell. Conclusion. Increased expression of CrkII and its higher intensity of staining in tumors with more aggressive biologic behavior in carcinomas of salivary gland is consistent with a role for this proto-oncogene in salivary gland tumorigenesis and cancer progression.