mRNA expression and phenotype of odontogenic tumours in the v-Ha-ras transgenic mouse

Dodds, Anne; Cannon, Ronald E.; Suggs, C.; Wright, J. Timothy

doi:10.1016/s0003-9969(03)00178-x

Cited by 14 publications

(15 citation statements)

References 32 publications

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“…Investigations focusing on Ras activation in odontogenic tumors were initiated with the observation that mice expressing a Ras oncogene often developed ameloblastomas, odontomas, or other odontogenic tumors [37, 38]. In 2014, three studies identified a BRAF mutation ( BRAF V600E) in human ameloblastomas and an ameloblastoma cell line (AM-1) [21, 22, 39].…”

Section: Braf/ras/mapkmentioning

confidence: 99%

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

Amm

MacDougall

2016

Curr Oral Health Rep

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Several molecular pathways have been shown to play critical roles in the pathogenesis of odontogenic tumors. These neoplasms arise from the epithelial or mesenchymal cells of the dental apparatus in the jaw or oral mucosa. Next generation genomic sequencing has identified gene mutations or single nucleotide polymorphisms associated with many of these tumors. In this review, we focus on two of the most common odontogenic tumor subtypes: ameloblastoma and keratocystic odontogenic tumors. We highlight gene expression and protein immunohistological findings and known genetic alterations in the hedgehog, BRAF/Ras/MAPK, epidermal growth factor receptor, Wnt and Akt signaling pathways relevant to these tumors. These various pathways are explored to potentially target odontogenic tumors cells and prevent growth and recurrence of disease. Through an understanding of these signaling pathways and their crosstalk, molecular diagnostics may emerge as well as the ability to exploit identified molecular differences to develop novel molecular therapeutics for the treatment of odontogenic tumors.

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Section: Braf/ras/mapkmentioning

confidence: 99%

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

Amm

MacDougall

2016

Curr Oral Health Rep

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“…According to 2005 WHO classification, it has been divided into four groups namely solid / multicystic, desmoplastic, unicystic and extra-osseous ameloblastoma. [5] Though ameloblastoma is benign, it deserves special attention because of its particular biological behavior exhibiting greater infiltrative potential, high recurrence rate (55-90%) [6] and capacity to metastasize or undergo malignant transformation when compared to its other epithelial counterpartthe adenomatoid odontogenic tumor (AOT). Molecular studies have offered interesting findings regarding ameloblastoma pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of MDM2 protein in ameloblastomas as compared to adenomatoid odontogenic tumor

et al. 2012

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The MDM2 overexpression noticed in plexiform ameloblastoma, follicular ameloblastoma with granular cell changes and acanthomatous ameloblastoma when compared to simple unicystic and desmoplastic ameloblastoma suggest a relatively enhanced proliferative phenotype of these solid multicystic variants of ameloblastomas. On overall comparison, higher expression was noted in ameloblastomas when compared to AOT. This indicates differences in the aggressive nature between these two groups of odontogenic tumors favoring the perception of a greater aggressive nature of ameloblastomas.

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“…One type of odontogenic tumor appears to arise from cells in the periodontal ligament, which is located in the mid-root region of the incisor (Wright et al, 1995;Mahler et al, 1998). In a more recent investigation, it was found that genes displaying differential expression in the ameloblastoma-like tumors of Tg.AC mice were also the same genes thought to be important in the odontogenesis and odontogenic tumor formation in human ameloblatomas (Dodds et al, 2003). Other reported spontaneous tumors include squamous cell carcinomas (SCC) of the salivary gland, ovarian teratomas, a rare ovarian yolk sac carcinoma, squamous cell papillomas of the forestomach and lung alveolar/bronchiolar adenomas (Hansen et al, 1996;Mahler et al, 1998).…”

mentioning

confidence: 99%