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Molecular Basis of Odontogenic Tumors and Odontogenic Cysts
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Molecular Basis of Odontogenic Tumors and Odontogenic Cysts

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 2960

Special Issue Editor

Dr. Paolo Boffano

E-Mail Website
Guest Editor
Division of Maxillofacial Surgery, University Hospital “Maggiore della Carità”, University of Eastern Piedmont, 28100 Novara, Italy
Interests: oral surgery; odontogenic tumors; pathogenesis; ameloblastoma; odontogenic keratocyst

Special Issue Information

Dear Colleagues,

The management of aggressive odontogenic tumors and cysts, such as ameloblastomas and odontogenic keratocysts, is a major worldwide medical challenge in the 21st century. Odontogenic tumors may be benign, locally aggressive neoplasms that need extensive surgical resection.

One roadblock to effectively treating odontogenic tumors and cysts is understanding the complexity of the cellular and molecular mechanisms underlying the pathogenesis of such lesions to enhance the precision of their management.

This Special Issue will contain a selection of papers highlighting the current advances in molecular aspects of odontogenic tumors and cysts to offer a new perspective on the molecular mechanisms and targeted therapies on these lesions. We welcome the submission of original research, short communications and review manuscripts focusing on the pathogenesis, diagnosis and targeted molecular therapy of odontogenic cysts and tumors.

Topics include, but are not limited to:

  1. Ameloblastomas;
  2. Odontogenic tumors;
  3. Molecular pathways of pathogenesis of odontogenic cysts and tumors.

Dr. Paolo Boffano
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • odontogenic cysts
  • ameloblastoma
  • odontoma
  • odontogenic keratocysts
  • odontogenic tumor
  • pathogenesis
  • diagnosis
  • targeted therapy

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Published Papers (2 papers)

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Research

10 pages, 518 KiB  
Article
In Silico Analysis of Genes Associated with the Pathogenesis of Odontogenic Keratocyst
by Carla Monserrat Ramírez-Martínez, Itzel Legorreta-Villegas, Claudia Patricia Mejía-Velázquez, Javier Portilla-Robertson, Luis Alberto Gaitán-Cepeda, Jessica Tamara Paramo-Sánchez, Osmar Alejandro Chanes-Cuevas, Alejandro Alonso-Moctezuma and Luis Fernando Jacinto-Alemán
Int. J. Mol. Sci. 2024, 25(4), 2379; https://doi.org/10.3390/ijms25042379 - 17 Feb 2024
Viewed by 1212
Abstract
Odontogenic keratocyst (OK) is a benign intraosseous cystic lesion characterized by a parakeratinized stratified squamous epithelial lining with palisade basal cells. It represents 10–12% of odontogenic cysts. The changes in its classification as a tumor or cyst have increased interest in its pathogenesis. [...] Read more.
Odontogenic keratocyst (OK) is a benign intraosseous cystic lesion characterized by a parakeratinized stratified squamous epithelial lining with palisade basal cells. It represents 10–12% of odontogenic cysts. The changes in its classification as a tumor or cyst have increased interest in its pathogenesis. Objective: Identify key genes in the pathogenesis of sporadic OK through in silico analysis. Materials and methods: The GSE38494 technical sheet on OK was analyzed using GEOR2. Their functional and canonical signaling pathways were enriched in the NIH-DAVID bioinformatic platform. The protein–protein interaction network was constructed by STRING and analyzed with Cytoscape-MCODE software v 3.8.2 (score > 4). Post-enrichment analysis was performed by Cytoscape-ClueGO. Results: A total of 768 differentially expressed genes (DEG) with a fold change (FC) greater than 2 and 469 DEG with an FC less than 2 were identified. In the post-enrichment analysis of upregulated genes, significance was observed in criteria related to the organization of the extracellular matrix, collagen fibers, and endodermal differentiation, while the downregulated genes were related to defensive response mechanisms against viruses and interferon-gamma activation. Conclusions. Our in silico analysis showed a significant relationship with mechanisms of extracellular matrix organization, interferon-gamma activation, and response to viral infections, which must be validated through molecular assays. Full article
(This article belongs to the Special Issue Molecular Basis of Odontogenic Tumors and Odontogenic Cysts)
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14 pages, 10734 KiB  
Article
Association of MDM2 Overexpression in Ameloblastomas with MDM2 Amplification and BRAFV600E Expression
by Konstantinos I. Tosios, Eleni-Marina Kalogirou and Ioannis G. Koutlas
Int. J. Mol. Sci. 2024, 25(4), 2238; https://doi.org/10.3390/ijms25042238 - 13 Feb 2024
Cited by 2 | Viewed by 1228
Abstract
Ameloblastoma is a rare tumor but represents the most common odontogenic neoplasm. It is localized in the jaws and, although it is a benign, slow-growing tumor, it has an aggressive local behavior and high recurrence rate. Therefore, alternative treatment options or complementary to [...] Read more.
Ameloblastoma is a rare tumor but represents the most common odontogenic neoplasm. It is localized in the jaws and, although it is a benign, slow-growing tumor, it has an aggressive local behavior and high recurrence rate. Therefore, alternative treatment options or complementary to surgery have been evaluated, with the most promising one among them being a targeted therapy with the v-Raf murine sarcoma viral oncogene homologue B (BRAF), as in ameloblastoma the activating mutation V600E in BRAF is common. Studies in other tumors have shown that the synchronous inhibition of BRAF and human murine double minute 2 homologue (MDM2 or HDM2) protein is more effective than BRAF monotherapy, particularly in the presence of wild type p53 (WTp53). To investigate the MDM2 protein expression and gene amplification in ameloblastoma, in association with BRAFV600E and p53 expression. Forty-four cases of ameloblastoma fixed in 10% buffered formalin and embedded in paraffin were examined for MDM2 overexpression and BRAFV600E and p53 expression by immunohistochemistry, and for MDM2 ploidy with fluorescence in situ hybridization. Sixteen of forty-four (36.36%) cases of ameloblastoma showed MDM2 overexpression. Seven of sixteen MDM2-positive ameloblastomas (43.75%) were BRAFV600E positive and fifteen of sixteen MDM2-positive ameloblastomas (93.75%) were p53 negative. All MDM2 overexpressing tumors did not show copy number alterations for MDM2. Overexpression of MDM2 in ameloblastomas is not associated with MDM2 amplification, but most probably with MAPK activation and WTp53 expression. Further verification of those findings could form the basis for the use of MDM2 expression as a marker of MAPK activation in ameloblastomas and the trial of dual BRAF/MDM2 inhibition in the management of MDM2-overexpressing/BRAFV600E-positive/WTp53 ameloblastomas. Full article
(This article belongs to the Special Issue Molecular Basis of Odontogenic Tumors and Odontogenic Cysts)
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