BRAF p.V600E mutations are not unique to ameloblastoma and are shared by other odontogenic tumors with ameloblastic morphology

Brunner, Philippe; Bihl, Michel; Jundt, Gernot; Baumhoer, Daniel; Hoeller, Sylvia

doi:10.1016/j.oraloncology.2015.07.010

Cited by 61 publications

(82 citation statements)

References 6 publications

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“…and our results failed to identify this association between BRAF mutation and tumour location. Although BRAF‐V600E mutation was believed originally to be specific for ameloblastoma, it was found later to be present in other odontogenic tumours and malignancies such as ameloblastic fibroma, ameloblastic fibro‐odontoma, ameloblastic carcinoma and clear cell odontogenic carcinoma, all of which had ameloblastic features …”

Section: Discussionmentioning

confidence: 99%

BRAF‐V600E expression correlates with ameloblastoma aggressiveness

et al. 2016

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Section: Discussionmentioning

confidence: 99%

BRAF‐V600E expression correlates with ameloblastoma aggressiveness

et al. 2016

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“…Of note, BRAF V600E was detected in unicystic and multicystic ameloblastomas (83% and 78%, respectively) [40]. This mutation was also detected in desmoplastic ameloblastomas, ameloblastic fibro-odontomas, ameloblastic fibromas, and ameloblastic carcinomas [40, 41]. Sweeney et al (2014) reported that ameloblastoma tumors with BRAF V600E mutations were commonly those from mandibular tumors; in constrast, maxillary tumors predominantly had SMO mutations [22].…”

Section: Braf/ras/mapkmentioning

confidence: 99%

“…BRAF V600E was also found in a case of clear cell odontogenic carcinoma. KCOT (n=20), ghost cell odontogenic carcinomas (n=1), adenomatoid odontogenic tumors (n=2), calcifying cystic odontogenic tumors (n=2) and odontogenic fibromas (n=5) were all found to be negative for the BRAF V600E mutation [21, 40, 41]. Brunner et al (2015) concluded that the BRAF mutation was present only in the epithelial tumor tissue, but was absent from the surrounding stromal tissue [41].…”

Section: Braf/ras/mapkmentioning

confidence: 99%

“…KCOT (n=20), ghost cell odontogenic carcinomas (n=1), adenomatoid odontogenic tumors (n=2), calcifying cystic odontogenic tumors (n=2) and odontogenic fibromas (n=5) were all found to be negative for the BRAF V600E mutation [21, 40, 41]. Brunner et al (2015) concluded that the BRAF mutation was present only in the epithelial tumor tissue, but was absent from the surrounding stromal tissue [41]. These data show that the activation of the Ras pathway by oncogenic mutation may be an important factor that drives the development and/or progression of odontogenic tumors with an ameloblastic component.…”

Section: Braf/ras/mapkmentioning

confidence: 99%

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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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“…In the ameloblastoma, SMO and BRAF mutations were frequently seen . Interestingly, BRAF mutation was also reported in AC . Nobusawa et al reported a case of AC which developed in preexisting AB with a mutation of p53 gene .…”

Section: Discussionmentioning

confidence: 99%

Hypoxia‐induced HIF‐1α and ZEB1 are critical for the malignant transformation of ameloblastoma via TGF‐β‐dependent EMT

et al. 2019

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Ameloblastic carcinoma (AC) is defined as a rare primary epithelial odontogenic malignant neoplasm and the malignant counterpart of benign epithelial odontogenic tumor of ameloblastoma (AB) by the WHO classification. AC develops pulmonary metastasis in about one third of the patients and reveals a poor prognosis. However, the mechanisms of AC oncogenesis remain unclear. In this report, we aimed to clarify the mechanisms of malignant transformation of AB or AC carcinogenesis. The relatively important genes in the malignant transformation of AB were screened by DNA microarray analysis, and the expression and localization of related proteins were examined by immunohistochemistry using samples of AB and secondary AC. Two genes of hypoxia‐inducible factor 1 alpha subunit (HIF1A) and zinc finger E‐box‐binding homeobox 1 (ZEB1) were significantly and relatively upregulated in AC than in AB. Both genes were closely related in hypoxia and epithelial‐mesenchymal transition (EMT). In addition, expressions of HIF‐1α and ZEB1 proteins were significantly stronger in AC than in AB. In the cell assays using ameloblastoma cell line, AM‐1, hypoxia condition upregulated the expression of transforming growth factor‐β (TGF‐β) and induced EMT. Furthermore, the hypoxia‐induced morphological change and cell migration ability were inhibited by an antiallergic medicine tranilast. Finally, we concluded that hypoxia‐induced HIF‐1α and ZEB1 were critical for the malignant transformation of AB via TGF‐β‐dependent EMT. Then, both HIF‐1α and ZEB1 could be potential biomarkers to predict the malignant transformation of AB.

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BRAF p.V600E mutations are not unique to ameloblastoma and are shared by other odontogenic tumors with ameloblastic morphology

Cited by 61 publications

References 6 publications

BRAF‐V600E expression correlates with ameloblastoma aggressiveness

BRAF‐V600E expression correlates with ameloblastoma aggressiveness

Molecular Signaling in Benign Odontogenic Neoplasia Pathogenesis

Hypoxia‐induced HIF‐1α and ZEB1 are critical for the malignant transformation of ameloblastoma via TGF‐β‐dependent EMT

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