Clonal nature of odontogenic tumours

This study was focused on the immunohistochemical profile of the adenomatoid odontogenic tumor. A Pub/Medline search revealed a number of immunohistochemical studies including cytokeratin profiles, extracellular matrix proteins, Integrins, ameloblast-associated proteins resorption regulators (RANK, RANKL), p53, PCNA, MDM2 protein, cyclin D1, Ki-67, Bcl-2 metallothionein, metalloproteinases, D56 hepatocyte growth factor, c-met, DNA methyltransferase, podoplanin, TGF-βI, Smad-2/3, Smad-I-5/-8, Smad 4, beta- catenin, calretinin, and clonality. Careful interpretation of the findings indicates that the adenomatoid odontogenic tumor may be more of a hamartomatous than neoplastic nature.

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“…Gomes et al () investigated the clonal origin of OTs including various OTs and AOTs. The HUMARA gene polymorphism assay was used in their study.…”

Section: Resultsmentioning

confidence: 99%

Immunoprofile of the adenomatoid odontogenic tumor

Reichart

Philipsen²,

Khongkhunthian

et al. 2016

Oral Diseases

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“…An essential step in the study of the pathogenesis of tumours is the determination of its clonal pattern. Recently, our group has demonstrated monoclonality of the solid/multicystic ameloblastoma (2). This finding gives strength to the idea that an initial mutation/molecular alteration is the first event in the development of the tumour.…”

Section: Clonalitymentioning

confidence: 99%

REVIEW ARTICLE: Current concepts of ameloblastoma pathogenesis

Gomes

Duarte

Diniz

et al. 2010

Journal of Oral Pathology &Amp; Medicine

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Ameloblastoma is a locally destructive and invasive tumour that can recur despite adequate surgical removal. Molecular studies have offered interesting findings regarding ameloblastoma pathogenesis. In the present review, the following topics are discussed regarding its molecular nature: clonality, cell cycle proliferation, apoptosis, tumour suppressor genes, ameloblastin and other enamel matrix proteins, osteoclastic mechanism and matrix metalloproteinases and other signalling molecules. It is clear from the literature reviewed that translational studies are necessary to identify prognostic markers of ameloblastoma behaviour and to establish new diagnostic tools to the differential diagnosis of unicystic from multicystic ameloblastoma. Finally, molecular biology studies are also important to develop more effective alternative approaches to the treatment of this aggressive odontogenic tumour.

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“…The study of rare tumor types contributes to the understanding of the more common ones, and it is now evident that genetic alterations in genes such as BRAF , RAS , TP53 , CDKN2A , among several others, previously considered hallmark drivers of specific malignant neoplasm can also occur in benign tumors, at frequencies even higher than in the malignant ones . The molecular pathogenesis of OM is still poorly understood, and its clonal nature is still controversial . Protein kinase cAMP‐dependent type I regulatory subunit alpha ( PRKAR1A ) mutations have been described in sporadic, and Carney Syndrome cardiac myxomas and such genetic alteration have been reported in a low proportion of OMs .…”

Section: Introductionmentioning

confidence: 99%

“…2 The molecular pathogenesis of OM is still poorly understood, and its clonal nature is still controversial. 3,4 Protein kinase cAMP-dependent type I regulatory subunit alpha (PRKAR1A) mutations have been described in sporadic, and Carney Syndrome cardiac myxomas and such genetic alteration have been reported in a low proportion of OMs. [5][6] GNAS1 mutations were previously reported in intramuscular myxomas but could not be detected in odontogenic myxomas.…”

Section: Introductionmentioning

confidence: 99%