ABSTRACT
OBJECTIVE: Lymphomas are the third most common cancer after squamous cell carcinoma and salivary gland tumors. Extranodal diffuse B cell lymphoma (DBCL) represents 30 to 58% of non-Hodgkin's lymphoma. One of the major problems of DBCL is the high likelihood of disease relapse following treatment. A recent trend in the treatment of diffuse large B cell lymphoma (DLBCL) is blockage of an immune checkpoint inhibitor that targets the programmed death of cell ligand 1 receptors (PD-L1). PD-L1 activation results in negative regulatory signals that induce apoptosis and inhibit tumor antigen-specific T cells allowing immune evasion of the tumor.The aim of this aim is to measure the expression level of PD-L1 on oral tissue samples from DLBCL patients using immunohistochemistry. MATERIALS AND METHODS: This current study was performed at the Faculty of Dentistry, Tanta University, Egypt. Ethical approval was conducted from Faculty of Dentistry, Tanta University. Tissue samples were collected from 13 patients diagnosed with oral extranodal DLBCL) nongerminal center B cell like subtype. Both hematoxylin and eosin and immunohistochemical staining (The avidin-biotin-complex procedure) was performed with anti-PD-L1 antibody (clone number: 28-8, Abcam, Cambridge, Massachusetts, United States).Cytoplasmic and/or membranous positive intensity was graded as follows: very mild staining, mild staining, moderate staining, and intense staining using Image J, 1.41a (National Institutes of Health, United States) image analysis software. The mean area fraction of the stained cells was calculated by counting immunostained cells in three fields of each case by two pathologists. Data was entered in SPSS program for analysis. RESULTS: PD-L1 was overexpressed on tumor cells of oral extranodal DLBCL than control cells from lesion free areas of oral tissues of the same patient.
ABSTRACT
INTRODUCTION: The major transcription factor, which modulates the epithelial-mesenchymal transition in different types of cancers, is known as TWIST oncogene. It binds to the promoter of E-cadherin and suppresses its transcription. The current study aims to assess the expression of TWIST protein in oral squamous cell carcinoma (OSCC), epithelial dysplasia (ED), and normal oral mucosa to verify whether such protein is useful as a marker in oral epithelium malignant transformation. METHODS: Thirty-five paraffin-embedded tissue samples of oral lesions with ED and OSCC and five samples of normal oral mucosa were immuostained with anti-TWIST antibody using the streptavidin peroxidase method. RESULTS: TWIST expression was negative in all cases of normal oral mucosa, whereas all cases of ED and OSCC showed positive immunoreactivity to TWIST varied from weak to strong expression. In ED, there was a significant difference between severe dysplasia and the other two types (P = 0.03). TWIST expression had no significant relationship with the clinical parameters of OSSC clinical stage and grade (degree of differentiation). Only two cases of OSCC with lymph node metastasis showed strong nuclear TWIST expression. Intergroups assessment indicated a significant increase of TWIST expression in OSCC compared to ED (P = 0.000). CONCLUSION: A significant increase of TWIST expression in OSCC compared to ED may suggest its role in carcinogenesis, it may be a useful marker in malignant transformation of oral epithelium. Therefore, TWIST might be an important target for therapeutic approaches in patients with OSCC, which requires further investigations.
ABSTRACT
OBJECTIVE: The present work evaluated histologically and immunohistochemically the expression of leptin during healing of the incisional oral mucosal wound in diabetic rats as compared to healthy rats. METHODS: Twenty-four adult male Sprague-Dawley rats weighing on average 150-200 g were allocated equally into two groups: Group I (control) and Group II (diabetic). Diabetes was induced by a single intraperitoneal injection of streptozotocin dissolved in distilled water. Each animal received experimental incision in buccal mucosa and sutured, and the specimens were collected from the buccal mucosa of each animal at intervals of 7, 14, and 21 days and routinely processed for H and E and immunohistochemical staining for leptin. All measurement data were calculated as a mean ± standard deviation. RESULTS: Leptin expression was observed in the epithelium and the vascular endothelial cells in both groups. In both the control and diabetic groups, the expression of leptin was significantly increased with time, and there was an extreme highly significant increase in the control group than in diabetic group after 7, 14, and 21 days (P = 0.000). CONCLUSION: The results of the present study suggested that leptin may promote wound healing in rat's normal oral mucosa more than in diabetic. Further studies are needed to clarify the exact molecular mechanisms of leptin's effects on wound healing and to determine the usefulness of leptin as a treatment to promote wound healing in the oral mucosa in diabetic and non-diabetic patients.
