Analyzing Pooled Microarray Gene Expression Data to Uncover Common Pathways in Periodontitis and Oral Squamous Cell Carcinoma from the Gene Expression Omnibus.

Periodontitis and oral squamous cell carcinoma (OSCC) are prevalent oral diseases with distinct etiologies, yet they share certain molecular and biological characteristics. Gene expression datasets from the gene expression omnibus (GEO) repository (GSE30784 for OSCC and GSE10334 for periodontitis) were analyzed. Data preprocessing and differential gene expression analysis using GEO2R identified common differentially expressed genes (DEGs), and FunRich software facilitated the construction of a protein-protein interaction (PPI) network on the STRING database. Cytoscape, coupled with the CytoHubba plugin, identified Cluster of Differentiation 19 (CD19) and Von Willebrand Factor (VWF) as the top hub genes, with Complement C3 (C3) also highly ranked. Functional enrichment analysis highlighted pathways such as the B-cell receptor signaling pathway, complement and coagulation cascades, and hematopoietic cell lineage. Additionally, miRNet analysis identified key miRNAs, including hsa-mir-26a-5p, hsa-mir-129-2-3p, and hsa-mir-27a-3p, associated with these pathways. These findings suggested an association of molecular mechanisms between periodontitis and OSCC, with identified hub genes and miRNAs potentially serving as therapeutic targets.

Immunohistochemical evaluation of Glut1 in dentigerous cysts, odontogenic keratocysts, and ameloblastoma.

Context: Glucose uptake may be considered the rate-limiting step for the growth and metabolism of the cancer cell. Studies on GLUT1 have shown that GLUT1 is involved in cell survival and proliferation in both healthy and pathological circumstances. GLUT1 expression is regarded as one of the crucial elements in the development of local aggressiveness, tumour invasiveness, and metastasis, particularly in malignant tumours. The role of glut1 in odontogenic cysts and tumours has remained uncertain. Aim: The aim of the study is to assess the expression of Glut1 in dentigerous cysts, odontogenic keratocysts, and ameloblastoma. Settings and Design: The study was conducted in GSL Dental College. The study design was a resprospective immunohistochemical study. Methods and Material: Formalin-fixed, paraffin-embedded blocks of histologically confirmed cases (n = 50), 10 cases of odontogenic keratocysts, dentigerous cysts, ameloblastomas solid, ameloblastomas unicystic, and dental follicles each. Brown colour staining was considered as positive staining for GLUT1. Quantitative analysis was performed by counting the number of labelled cells, and semi-quantitative analysis was conducted by assigning immunostaining intensity scores. Statistical Analysis: Chi-square test was used to compare differences between the groups. A P value of ≤0.05 was considered as statistically significant. Results: Odontogenic keratocysts and unicystic ameloblastoma showed ≥50% of label cells with strong intensity of staining. Odontogenic keratocysts and solid ameloblastoma showed sub-cellular localisation of staining in the cytoplasm and membrane. Dentigerous cysts exhibited combined nucleus, cytoplasm, and membrane sub-cellular localisation of staining. Conclusions: The development of ameloblastomas, odontogenic keratocysts, and dentigerous cysts appears to be influenced by GLUT-1. Variation in its expression may aid in explanation of some of the differences in biological activity of these lesions.

Expression of heat shock protein 70 in oral epithelial dysplasia and squamous cell carcinoma.

BACKGROUND: Heat shock proteins (HSPs) are overexpressed in a variety of human malignancies. They are involved in tumor cell proliferation, differentiation, invasion, metastasis, death, and immune system detection. HSP 70 has been shown to resist cytotoxicity in cancer cells and even enhance tumor development through an immune escape mechanism, suggesting that HSP70 may play a role in carcinogenesis. The aim of our study was to evaluate the role of HSP70 as a predictive marker for malignant transformation in oral epithelial dysplasia. MATERIALS AND METHODS: Thirty samples of epithelial dysplasia (10 mild dysplasia, 10 moderate dysplasia, and 10 severe dysplasia/carcinoma-in-situ cases), 10 samples of well-differentiated oral squamous cell carcinoma (OSCC), and 10 samples of normal oral mucosa were routinely processed, formalin-fixed, paraffin-embedded, and immunohistochemically examined for HSP70 expressions. To determine the statistical difference between two groups, a one-way analysis of variance (ANOVA) and the Mann-Whitney test were used. RESULTS: HSP70 expression was high but not homogenous in normal mucosa. Dysplasia showed an initial drop, and the expression increased with increasing degrees of dysplasia. There was no statistically significant difference across various types of epithelial dysplasia. From dysplasias to well-differentiated carcinoma, HSP70 exhibited a considerable rise. CONCLUSION: Overexpression of HSP70 in clinically suspicious and histologically established epithelial dysplasia may suggest a likelihood of transformation to well-differentiated OSCC and may have a prognostic value. However, more studies with a bigger sample size are needed to prove HSP70's role as a predictor.

Differential Expression of Heat Shock Protein 27 in Oral Epithelial Dysplasias and Squamous Cell Carcinoma.

BACKGROUND: Oral squamous cell carcinoma (OSCC) is the most devastating neoplasm with dramatic increase in morbidity and mortality. The detection and prognostic evaluation of precancerous lesions could aid in early control of cancer. Heat shock protein (HSP) 27 has found to be a biomarker and therapeutic target in different types of cancer. AIM: This study aims to investigate the role of HSP 27 as prognostic molecular indicator of malignant transformation in oral epithelial dysplasias. MATERIALS AND METHODS: Thirty samples of epithelial dysplasia (10 mild dysplasia, 10 moderate dysplasia, and 10 severe dysplasia/carcinoma in situ cases), 10 samples each of well-differentiated OSCC and normal oral mucosa were routinely processed, formalin-fixed, paraffin-embedded, and analyzed for HSP27 expression by immunohistochemistry. Statistical analysis was done by one way-ANOVA and Mann-Whitney test to assess the differences between two individual groups. RESULTS: Normal mucosa showed intense, but nonuniform, expression of HSP27. An initial decline was noted in dysplasias. A significant correlation of HSP27 expression was observed with the severity of dysplasia and well-differentiated OSCC (P < 0.05). CONCLUSION: Low HSP 27 expression can be considered as early molecular indicator of initial dysplastic change in normal mucosa. An overexpression of HSP 27 in clinically and histologically confirmed dysplasia could indicate likely transformation to well-differentiated OSCC and could be of prognostic value. However, further studies with a larger sample size are required to confirm the role of HSP 27 as predictive indicator.