Abstract:Odontogenic tumors comprised of complex heterogeneous lesions that diverse from harmatomas to malignant tumors with different behavior and histology. The etiology of odontogenic tumors is not exactly determined and pathologists deal with challenges in diagnosis of odontogenic tumors because they are rare and obtained experiences are difficult to evaluate. In this study, we describe immunohistochemical and molecular markers in diagnosis of odontogenic tumors besides advanced diagnostic technique. Immunohistoche… Show more
“…[ 6 ] A study published by Farshbaf et al . [ 18 ] indicated an overexpression of SOX2 and PITX2 (TF in Wnt pathway) and high levels of Ki-67 protein. Also, an increased POLR2J, CDKN2C, and decreased EIF3S5 expression was seen.…”
Ameloblastic carcinoma (AC) is a rare, primary epithelial odontogenic malignant neoplasm. It is the malignant counterpart of ameloblastoma. It comprises 1% of all cysts and tumours occurring in the jaws, arising from tissues associated with odontogenic epithelium. The objective of the present study was to describe a clinical case of a 63-year-old male with an enlargement in the mandible on the left side. Panoramic radiography revealed a radiolucent area with poorly defined borders, and an incisional biopsy was performed for the histopathological study using immunomarkers such as SOX2 and Ki-67. Ki-67 is considered a marker of cell proliferation, and SOX2 reportedly participates in the development of the ameloblastic epithelium lineage and is associated with a more aggressive clinical course. A final histopathological diagnosis of AC was given. Unfortunately, the patient died one week before surgical resection (the surgical treatment of choice for AC).
“…[ 6 ] A study published by Farshbaf et al . [ 18 ] indicated an overexpression of SOX2 and PITX2 (TF in Wnt pathway) and high levels of Ki-67 protein. Also, an increased POLR2J, CDKN2C, and decreased EIF3S5 expression was seen.…”
Ameloblastic carcinoma (AC) is a rare, primary epithelial odontogenic malignant neoplasm. It is the malignant counterpart of ameloblastoma. It comprises 1% of all cysts and tumours occurring in the jaws, arising from tissues associated with odontogenic epithelium. The objective of the present study was to describe a clinical case of a 63-year-old male with an enlargement in the mandible on the left side. Panoramic radiography revealed a radiolucent area with poorly defined borders, and an incisional biopsy was performed for the histopathological study using immunomarkers such as SOX2 and Ki-67. Ki-67 is considered a marker of cell proliferation, and SOX2 reportedly participates in the development of the ameloblastic epithelium lineage and is associated with a more aggressive clinical course. A final histopathological diagnosis of AC was given. Unfortunately, the patient died one week before surgical resection (the surgical treatment of choice for AC).
“…In recent years, “‐omics” technology, such as genomics, epigenomics, transcriptomics, proteomics, and metabolomics, has helped identify specific molecular alterations associated with aetiology. These results show superiority compared with traditional immunohistochemistry (IHC) staining 16 . The present study aimed to explore the outstanding differentially expressed proteins in ameloblastoma and screen potential therapeutic targets.…”
Section: Introductionmentioning
confidence: 98%
“…These results show superiority compared with traditional immunohistochemistry (IHC) staining. 16 The present study aimed to explore the outstanding differentially expressed proteins in ameloblastoma and screen potential therapeutic targets. The protein-level differences between ameloblastoma, odontogenic keratocyst, dentigerous cyst, and normal gingival tissue were analysed using bioinformatics techniques.…”
Background
Reports on the proteomic studies of ameloblastoma and other common odontogenic lesions are limited. We thus explored the differential proteins among ameloblastoma, odontogenic keratocyst, dentigerous cyst, and normal gingival tissue using proteomics and identified hub proteins involved in the local aggressiveness and recurrence of ameloblastoma.
Methods
Samples were obtained from 14 patients with ameloblastoma, 6 with odontogenic keratocyst, 9 with a dentigerous cyst, and 5 with normal gingival tissue. Proteins were then extracted, purified, quantified, and analysed using Easy‐nLC chromatography and mass spectrometry. Further functional annotation and enrichment analyses were performed using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes on the target protein collection. Protein clustering and protein–protein interaction network analyses were used to screen the hub proteins. Proteins with significant interactions were screened according to their degree index. These results were verified by immunohistochemical staining. Proteins meeting the screening criteria of expression difference ploidy >1.2‐fold (upregulation and downregulation) and p < 0.05 were considered differential proteins.
Results
In ameloblastoma, 808 differential proteins were upregulated and 505 were downregulated compared with those in odontogenic keratocyst; 309 were upregulated and 453 were downregulated compared with those in dentigerous cyst; and 2210 were upregulated and 829 were downregulated compared with those in normal gingival tissue. The three groups of differential proteins were associated with cellular exosomes, antigen binding, complement activation, human papillomavirus infection, focal adhesion, cell adhesion molecules, and metabolic pathways.
Conclusion
CDH3 is associated with the local aggressiveness and recurrence of ameloblastoma and is a potential therapeutic target.
“…e recurrence rate of ameloblastoma is high if the lesions are not cut o perfectly during surgery [5]. Although several types of research have been executed to elucidate molecular changes in odontogenic tumors such as ameloblastoma, their exact underlying mechanisms, including cellular di erentiation and tumorigenesis, are unclear and need more studies in this eld [6]. Inside human cells, thousands of genes, transcriptomes, and proteins function in various complicated biological networks, including protein-protein interaction (PPI), gene regulatory, metabolic, and signaling networks [7].…”
Objective. Ameloblastoma is a benign odontogenic tumor that may lead to ameloblastic carcinoma. is study aimed to determine potential signaling pathways and biological processes, critical genes and their regulating transcription factors (TFs), and miRNAs, as well as protein kinases involved in the etiology of primary ameloblastoma. Methods. e dataset GSE132472 was obtained from the GEO database, and multivariate statistical analyses were applied to identify di erentially expressed genes (DEGs) in primary ameloblastoma tissues compared to the corresponding normal gingiva samples. A protein-protein interaction (PPI) map was built using the STRING database. e Cytoscape software identi ed signi cant modules and the hub genes within the PPI network. Gene Ontology annotation and signaling pathway analyses were executed by employing the DAVID and Reactome databases, respectively. Signi cant TFs and miRNAs acting on the hub genes were identi ed using the iRegulon plugin and MiRWalk 2.0 database, respectively. A protein kinase enrichment analysis was conducted using the online Kinase Enrichment Analysis 2 (KEA2) web server. e approved drugs acting on the hub genes were also found. Results. A total of 1,629 genes were di erentially expressed in primary ameloblastoma (P value <0.01 and |Log2FC| > 1). HRAS, CDK1, MAPK3, ERBB2, COL1A1, CYCS, and BRCA1 demonstrated high degree and betweenness centralities in the PPI network. E2F4 was the most signi cant TF acting on the hub genes. BTK was the protein kinase signi cantly enriched by the TFs. Cholesterol biosynthesis was considerably involved in primary ameloblastoma. Conclusions. is study provides an intuition into the potential mechanisms involved in the etiology of ameloblastoma.
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