Efficacy of Glucose Starvation of Cancer Cells in the Progress of Oral Squamous Cell Carcinoma Induced in Hamster.

BACKGROUND AND AIM OF THE STUDY: Oral squamous cell carcinoma (OSCC) is the most common form of oral cancer, showing poor prognosis and high mortality. Meanwhile, cancer metabolism is an essential contributor to its progression and response to treatment. This research aims to investigating the effect of a glucose-rich and glucose-free diet on the progress of oral squamous cell carcinoma induced in hamsters. MATERIALS AND METHODS: forty Syrian Hamsters were incubated in two groups. The first one consisted of twenty hamsters, in which the carcinogenic material (DMBA) was applied in the buccal pouch of the hamster three days per week with a glucose-rich diet). The second one was composed of twenty hamsters, in which the carcinogenic material (DMBA) was applied in the buccal pouch three days per week with a glucose-free diet). Hamsters in both groups were sacrificed in groups of five hamsters at a time and at intervals (two weeks, six weeks, ten weeks, and Fourteen weeks). A histological study was performed after conventional staining with hematoxylin and eosin was done. RESULTS: After two weeks of the experiment hyperplasia, mild dysplasia, and moderate dysplasia were recorded in hamster buccal pockets with a glucose-rich diet, and after six weeks moderate dysplasia, severe dysplasia, and carcinomas in situ were recorded, after ten weeks severe dysplasia, carcinomas in situ, and OSCC, after fourteen weeks OSCC were recorded. While with a glucose-free diet Hyperkeratosis, hyperplasia, and mild dysplasia were observed after a two-week the experiment,  after six weeks, mild dysplasia, moderate dysplasia, and severe dysplasia were recorded, after ten weeks, moderate dysplasia, severe dysplasia, and carcinoma in situ, after fourteen weeks Severe dysplasia, carcinoma in situ, and OSCC were reported. CONCLUSION: our results showed that a glucose-free diet slightly prevents oral squamous cell carcinoma, It may be a supportive treatment in addition to conventional cancer treatment.

The Apoptotic and Antiproliferative Effects of Capsaicin in the Developmental Stages of Oral Squamous Cell Carcinoma Induced in Hamsters.

Background and aim Several epidemiological and experimental studies have approve that the vegetarian diet has an anticancer effect. Capsaicin is the active botanical ingredient found in red chili peppers. While the data strongly argue for the significant anticancer benefits of capsaicin, nevertheless, much information is required to shed light on the anticancer molecular mechanisms to improve knowledge and suggest potential therapeutic mechanisms for the use of capsaicin against cancer. This study aimed to investigate the effect of capsaicin on the rate of cell division and apoptosis in the development of oral squamous cell carcinoma induced in the buccal pouch of hamsters. Materials and methods The sample consisted of two groups; the first group consisted of 20 hamsters with the application of carcinogenic 7,12-dimethylbenz(a)anthracene (DMBA) in the buccal pouch (the control group) and the second group (the study group) also consisted of 20 hamsters with the application of DMBA in alternatively with capsaicin. Tissue biopsies were taken from experimental animals after sacrificing. The samples were immunostained for the detection of Ki-67 and Bcl-2 proteins. Results Immunohistochemical staining by monoclonal antibody to Ki-67 and Bcl-2 in the study group showed lower expression at all stages of oral cancer development compared with their expression in the control group. After performing the one-way (ANOVA) test, we found statistically significant differences by comparing the expression degree of Ki-67 and Bcl-2 proteins in both study groups, where the p-value was less than 0.05. Conclusion We conclude from the data of our study that capsaicin has an anti-cancer role in oral squamous cell carcinoma if applied in the digestive tract of experimental animals by inhibiting the proliferation of cancer cells and activating apoptosis in them.

Ki-67 Prognostic Value in Different Histological Grades of Oral Epithelial Dysplasia and Oral Squamous Cell Carcinoma

Introduction: Abnormal cell proliferation appears to be a possible predictor of tumorigenesis, Ki-67 protein expression is closely related to the cell proliferation and could be used as a biomarker for the growth in the most of human tumors. The aim of the study: Investigating of Ki-67 expression in the pathological grades of oral epithelial dysplasia and oral squamous cell carcinomas. Materials and Methods: The sample consisted of 30 formalin-fixed, paraffin-embedded specimens of oral epithelial dysplasia (OED), 30 other of oral squamous cell carcinomas (OSCC), and 10 normal oral epithelium (NOE) were conventionally stained with hematoxylin and eosin and immunohistochemically stained with Ki-67 monoclonal antibody. Results: Expression of Ki-67 was restricted to the basal layers in the normal oral epithelium whereas Ki-67 positive cells in oral epithelial dysplasia (OED) were located in the basal, suprabasal and spinous layers, Ki-67 expression was increased in high-risk cases. Ki-67 positive cells in well-differentiated (OSCC) were located mainly in the periphery of the tumor nests, in moderately-differentiated (OSCC) were located in both peripheral and part of a center of the tumor nests whereas it was diffused in most of the Poorly-differentiated (OSCC). Statistical analysis indicated a significant difference between the expression in (OED) and (NOE), (OSCC) and (NOE), and no differences between (OED) and (OSCC). Conclusion: This study has concluded that Ki-67 antigen could be used as a marker for the histological grading of OED and OSCC, Expression of Ki 67 increased according to the severity of oral epithelial dysplasia.

Amelogenin is a Potential Biomarker for the Aggressiveness in Odontogenic Tumors

Amelogenin (AMEL), the major structural protein of the enamel organic matrix, constitutes more than 90% of the enamel's protein content, Aberrations of amelogenin are thought to be involved in the oncogenesis of odontogenic epithelium. The expression of amelogenin is possibly an indicator of differentiation of epithelial cells in the odontogenic tumors. Aim of the study: Investigating the expression of amelogenin in some odontogenic tumors, using an anti-amelogenin polyclonal antibody, and then compare it with AMEL expression in tooth buds as control. Materials and Methods: study sample consisted of 10 formalin-fixed, paraffin- embedded specimens of ameloblastoma, 10 Keratocystic odontogenic tumors, and 10 tooth buds were conventionally stained with hematoxylin-eosin and immunohistochemically with AMEL polyclonal antibody. Results: All of the odontogenic tumors expressed AMEL in the epithelial component, Intensity of expression in ameloblastoma and Keratocystic odontogenic tumor was lower, compared with tooth buds, Statistical analysis indicated a significant differences between the tumors and tooth buds. Conclusion: Amelogenin can be used as a marker for odontogenic epithelium, and the expression of amelogenin is possibly an indicator of epithelial cells differentiation in the odontogenic tumors, and therefore in prediction of the histological behavior of odontogenic tumors.