| کلیدواژههای انگلیسی مقاله |
Mel-CAM, Mucoepidermoid carcinoma, Oral squamous cell carcinoma, Salivary glands, IntroductionMucoepidermoid carcinoma (MEC) is one of the most common salivary gland malignancies that mainly affect the parotid. The tumor occurs within the second to the seventh decades of life, and is the most common malignant salivary gland tumor in children [ 1,]. The biologic behaviors of MEC range from slow-growing mass to destructive rapidly growing mass [ 2,]. Prognosis of the MEC is usually related to the clinical stage and histological grade [ 3,]. Despite the advancements in diagnosis and treatment of high-grade MEC over the last two decades, the 5-year survival rate is still less than 50% [ 4,- 5,]. High-grade MEC can be misdiagnosed for oral squamous cell carcinoma (OSCC), which is the most common malignancy of the oral cavity and accounts for al-most 2% of the cancer burden worldwide. The overall 5-year survival rate has not significantly increased in the last few years despite the advanced treatment modality [ 6, ]. Mel-CAM (CD146, MUC18) is a 113-kD heterophilic cell-cell adhesion glycoprotein, which belongs to the immunoglobulin supergene family [ 7,]. It was initially identified as a marker of melanoma progression and metastasis [ 8,]. This marker is primarily expressed by vascular endothelium and smooth muscle but has also been detected in subpopulation of activated T lymphocytes, bone marrow,Schwann cells, ductal, and myoepithelial cells of the salivary glands [ 9,].Expression of Mel-CAM in tumor tissues is related to the tumor size, progression, metastatic potential, and aggressiveness [ 9,]. Indeed, the biologic functions and role of the Mel-CAM as a diagnostic marker in pathology are now being recognized. The present study aims to assess the expressionof Mel-CAM in salivary gland MEC and OSCC to find its possible correlation with the histological grade, tumor size, lymph node, and metastasis, besides its utility to differentiate the OSCC from high-grade MEC. Materials and Method Sample selection The samples of this cross-sectional study were 36 formalin-fixed, paraffin-embedded tissue blocks including 17 cases of OSCC and 19 cases of MEC, which were obtained from the archive of the Department of Pathology of Taleghani Hospital, affiliated to Shahid Beheshti University of Medical Sciences, Tehran, Iran. Anonymity of the patients&,rsquo records was strictly respected.Hematoxylin and eosin (H&,amp amp E) stained sections were used to confirm the diagnosis. Clinicopathologic information of each case including age, sex, tumor location, and histological grade were collected from the patients&apos, records and reviewing slides. For OSCC samples, mode of invasion was also identified. Cases with incomplete data, insufficient paraffin-embedded tumor material, inappropriate fixation, and incisional biopsy were excluded. Immunohistochemistry (IHC)Sections of 4-&,micro m thickness were cut from all samples and mounted on silane-coated slides. The sections were deparaffinized with 100% xylene and rehydrated in graded ethanol series. Sections were immersed in Tris-buffered saline (TBS) with a pH of 6.0, and heated in a microwave oven at 750 watts for antigen retrieval. After cooling into room temperature, the sections were incubated with primary antibody (Anti-CD146, monoclonal mouse Anti-Human clone, AA1, Ready to use, ABcam, USA) at 1,2000 for an hour. Having been washed in TBS, the sections were treated with Dako EnVision (Dako, Germany). The DAB chromogen was applied to visualize the antibody expression, and then, counterstained with Mayer&,rsquo s hematoxylin. Normal parotid salivary gland was used as positive control. Evaluation of IHCCD146 immunoreaction in the tumoral cells was determined in 10 randomly-selected fields by counting all the positive cells in each field according to the median index of positive cells obtained from 10 high-power fields (HPF) and scored as negative (0-5%), weak (6-25%), moderate (26-50%) and strong (51-100%) [ 10,]. The staining intensity was evaluated as 0=no positive cells, += mild, ++= moderate, +++= strong [ 11,]. Mode of inv-asion in OSCC samples was assessed on the H&,amp amp E slides according to Jacobson method (scored I to IV) [ 12,].According to WHO classification (2005), the histopathologic grade of OSCC samples was classified into well-, moderate- and poorly-differentiated. The histopathologic grade of the MEC was categorized as low, intermediate and high grade based on Auclair classification [ 10,]. All slides were evaluated by two pathologists.Statistical analysis The statistical analysis was carried out on the tabulated data by using SPSS software, version 18.0 (SPSS Inc., Chicago, IL, USA). Mann-Whitney test was used to assess the correlation between CD146 expression and the clinicopathologic variables including age, histological grade, nodal metastasis, and mode of invasion. Spearman&apos,s correlation coefficient and Kruskal-Wallis test were done to determine the correlation of CD146 expression with the tumor size and expression location, respectively. The significance level of all tests was set at 0.05. All the procedures performed in the current study were approved by the Ethics Committee of Shahid Beheshti University of Medical Sciences (#9204) in accordance with the Declaration of Helsinki (1964) and its later amendments. Formal written informed consent was not required with a waiver by the Ethics Committee of Shahid Beheshti University of Medical Sciences.Results The samples were 23 men and 13 women (Table 1,). CD146 was expressed in all MEC samples as cytoplasmic and membranous staining. VariablesMECOSCCSexMale 1013Female 94Age(Mean&,plusmn SD)45.58&,plusmn 14.3164.76&,plusmn 9.28Site of tumor Alveolar mucosa66Parotid5Sublingual1Tongue7Hard palate5Flour of the mouth2Other sites 22Histopathologic gradeHigh grade73Moderate grade103Low grade 211Size(Cm) Range (mean)2.68-3.56 (2.86) 3.5-6.12 (5.08)Lymph node metastasis Yes2 (10.5%)5 (29.5%)No17(89.5%)12(70.5%)Mode of invasion*,I9II-0III4IV4*Mode of invasion was classified only for OSCC |
| نویسندگان مقاله |
Nafise Shamloo |
Dept. of Oral and Maxillofacial Pathology, School of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Nasim Taghavi |
Dept. of Oral and Maxillofacial Pathology, School of Dentistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Samira Behrad |
Dept. of Oral and Maxillofacial Pathology, School of Dentistry, Semnan University of Medical Sciences, Semnan, Iran
Ali Dehghani Nazhvani |
Dept. of Oral and Maxillofacial Pathology, Biomaterials Research Center, School of Dentistry, Shiraz University of Medical Sciences, Shiraz, Iran.
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