Oral Pathology
Hamideh Kadeh; Mohammad Eini; Maliheh Parsasefat; Ebrahim Miri-Moghaddam
Abstract
Background & Objective: CCL4 (C-C chemokine ligand4) is a chemoattractant involved in tumors' development, progression, and metastasis. The relationship between the ccl4 gene polymorphisms and the risk of OSCC has not been studied in Iran. This study aimed to identify the effect of ccl4 gene polymorphism ...
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Background & Objective: CCL4 (C-C chemokine ligand4) is a chemoattractant involved in tumors' development, progression, and metastasis. The relationship between the ccl4 gene polymorphisms and the risk of OSCC has not been studied in Iran. This study aimed to identify the effect of ccl4 gene polymorphism on OSCC susceptibility in the population of Southeastern Iran.Methods: In this case-control study, a total of 100 participants, 50 patients with OSCC who were referred to the Department of Oral Pathology, Faculty of Dentistry, Zahedan University of Medical Sciences, Iran, and 50 healthy people were included. The DNA was extracted from the tissue blocks of OSCC patients. The rs10491121 and rs1634507 in the ccl4 gene were evaluated by the tetra-ARMS (Amplification Refractory Mutation System)- PCR technique. Data were analyzed in SPSS (version 21) using the Chi-square and logistic regression test.Results: CCL4 genotyping showed that AA+AG genotype in rs10491121 and AA+CA genotype in rs1634507 were slightly higher in control than in the case. Still, the risk of OSCC in both polymorphisms was not significantly different. The minor allele (A) in the rs10491121 and rs1634507 polymorphisms were more common in OSCC compared to the control group (OR = 1.2, 95% CI: 0.66 – 2.22, P=0.54) (OR = 1.6, 95% CI: 0.85-3.07, P=0.15). There was no association between OSCC histopathological grades and CCL4 genotypes at these two sites.Conclusion: Our results showed no association between ccl4 gene polymorphism and the risk of oral cancer in the population of Southeastern Iran.
Head and Neck Pathology
Hamideh Kadeh; Shirin Saravani; Ebrahim Miri-Moghadam
Abstract
Background & Objective: Epithelial-Mesenchymal transition (EMT) is known to be a possible mechanism in tumor progression; however, there is insufficient evidence to support the contribution of this process in human cancers. The present study aimed to evaluate the expression of EMT markers in normal ...
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Background & Objective: Epithelial-Mesenchymal transition (EMT) is known to be a possible mechanism in tumor progression; however, there is insufficient evidence to support the contribution of this process in human cancers. The present study aimed to evaluate the expression of EMT markers in normal oral epithelium and oral squamous cell carcinoma and also correlates with some clinicopathological parameters.Methods: This study was conducted on 70 samples, including 20 cases of normal epithelium and 50 cases of Oral Squamous cell Carcinoma (OSCC). To examine the expression level of these proteins, immunohistochemical staining was performed for samples using E-cadherin and N-cadherin monoclonal antibodies.Results: Reduced expression of E-cadherin was observed in 74% of OSCC and 15% of normal epithelium samples; this difference was statistically significant (P˂0.000). With the progression of SCC from well towards poor differentiation, the E-cadherin expression decreased; however, this difference was not statistically significant (P=0.642). Normal epithelial specimens were negative for N-cadherin expression in 75% of cases, whereas OSCC specimens showed high expression of N-cadherin in 46% of cases, this difference was statistically significant (P=0.01). Although 62.5% of poorly differentiated OSCC showed high expression of N-cadherin, the difference between the histopathological grades was not significant (P=0.586). No significant relationship was found between markers expression and patient’s age, gender, and tumor location.Conclusion: This study showed that OSCC tissues showed high EMT phenotype (reduced E-cadherin expression and high expression of N-cadherin) compared to normal oral mucosa which may indicate the possible key role of EMT mechanism during oral carcinogenesis.