Study on clinical and biological characteristics of ameloblastic carcinoma

Niu, Zhixing; Li, Ye; Chen, Wantao; Zhao, Junfang; Zheng, Hongyu; Deng, Qing; Zha, Zhian; Zhu, Haijing; Sun, Qiang; Su, Lei

doi:10.1186/s13023-020-01603-5

Cited by 32 publications

(45 citation statements)

References 24 publications

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“…Additionally, oncogene-induced senescence may limit the proliferation status of nevi in the tumorigenic process [ 79 ]. However, BRAF p.V600E mutation has been recently reported in 5/5 ameloblastic carcinoma cases submitted to molecular screening [ 76 ]. These results could encourage targeted therapy as a new direction in the future.…”

Section: Mapk/erk Mutations In Odontogenic Tumorsmentioning

confidence: 99%

The Molecular Pathology of Odontogenic Tumors: Expanding the Spectrum of MAPK Pathway Driven Tumors

Guimarães

Coura

Gomez

et al. 2021

Front. Oral. Health

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Odontogenic tumors comprise a heterogeneous group of lesions that arise from the odontogenic apparatus and their remnants. Although the etiopathogenesis of most odontogenic tumors remains unclear, there have been some advances, recently, in the understanding of the genetic basis of specific odontogenic tumors. The mitogen-activated protein kinases/extracellular signal-regulated kinases (MAPK/ERK) pathway is intimately involved in the regulation of important cellular functions, and it is commonly deregulated in several human neoplasms. Molecular analysis performed by different techniques, including direct sequencing, next-generation sequencing, and allele-specific qPCR, have uncovered mutations in genes related to the oncogenic MAPK/ERK signaling pathway in odontogenic tumors. Genetic mutations in this pathway genes have been reported in epithelial and mixed odontogenic tumors, in addition to odontogenic carcinomas and sarcomas. Notably, B-Raf proto-oncogene serine/threonine kinase (BRAF) and KRAS proto-oncogene GTPase (KRAS) pathogenic mutations have been reported in a high proportion of ameloblastomas and adenomatoid odontogenic tumors, respectively. In line with the reports about other neoplasms that harbor a malignant counterpart, the frequency of BRAF p.V600E mutation is higher in ameloblastoma (64% in conventional, 81% in unicystic, and 63% in peripheral) than in ameloblastic carcinoma (35%). The objective of this study was to review MAPK/ERK genetic mutations in benign and malignant odontogenic tumors. Additionally, such genetic alterations were discussed in the context of tumorigenesis, clinical behavior, classification, and future perspectives regarding therapeutic approaches.

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Section: Mapk/erk Mutations In Odontogenic Tumorsmentioning

confidence: 99%

The Molecular Pathology of Odontogenic Tumors: Expanding the Spectrum of MAPK Pathway Driven Tumors

Guimarães

Coura

Gomez

et al. 2021

Front. Oral. Health

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“…However, whether odontogenic or not, lesions presenting ghost cells appear to share similar developmental pathways involving β-catenin protein and mutations on its coding gene CTNNB1 [3p22.1], causing deregulation in the Wnt/β-catenin/TCF signaling pathway, related to various human tumorigenesis [12][13][14][15][16][17]. Recent studies have shown potential applications of target therapies in odontogenic tumors due to specific molecular alterations [18][19][20][21]. An updated review of the current knowledge about the genomic features of the GCONs can not only collaborate to clarify its etiology but also guide and foster future molecular studies that investigate new therapeutic proposals and the role of modulators of the Wnt/β-catenin/TCF pathway in human neoplasms [17].…”

Section: Introductionmentioning

confidence: 99%

Comparative Analysis Between Dentinogenic Ghost Cell Tumor and Ghost Cell Odontogenic Carcinoma: A Systematic Review

Vieira

Montovani

Rozza-De-Menezes

et al. 2021

Head and Neck Pathol

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Dentinogenic ghost cell tumor (DGCT) and ghost cell odontogenic carcinoma (GCOC) form a spectrum of rare benign and malignant odontogenic neoplasms, respectively. The aim of this study was to perform a comparative systematic review of the clinicopathological, genetic, therapeutic, and prognostic features of DGCT and GCOC. The electronic search was performed until December 2020 on seven electronic databases. Case reports, series, and research studies with enough histopathological criteria for diagnosis and all genomic studies were included. Both DGCT and GCOC showed a male prevalence (p = 0.043), with mandibular and maxillary predilections, respectively (p = 0.008). Peripheral DGCT (DGCTp) affected most elderly people (p < 0.001), and central DGCT (DGCTc) and GCOC occurred mainly in younger individuals. Unilateral enlargement of maxilla or mandible was the most common clinical sign associated with a radiolucent or mixed image. Ameloblastomatous epithelium was often present in both neoplasms. Basaloid and large cells with vesicular nuclei were also frequently seen in GCOC. β-catenin expression and mutations (CTNNB1 gene) were found in DGCT and GCOC. Conservative surgery was mostly used for DGCTp, while radical resection was chosen for DGCTc and GCOC. High recurrence rates were found in DGCTc and GCOC. Metastasis occurred in 16.7% of GCOC cases and the 5-year survival rate was 72.6%. DGCT and GCOC share numerous clinicopathological features and demand a careful histopathological evaluation, considering the overlap features with other odontogenic tumors and the possibility of malignant transformation of DGCT. A strict regular post-operative follow-up is mandatory due to high recurrence rates and metastatic capacity in GCOC.

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“…The WHO 2005 classification made significant changes to the classification of malignant odontogenic tumours which were mainly centred on the histogenesis of the lesion [ 40 ]. This version included within the odontogenic carcinomas group metastasizing ameloblastoma (a histologically benign ameloblastoma that metastasizes) and defined three subtypes of ameloblastic carcinoma, the first referred to the primary type as corresponded to an ameloblastic carcinoma that arises de novo and, two secondary subtypes that arise in a pre-existing ameloblastoma (intra or extraosseous).…”

Section: Discussionmentioning

confidence: 99%

“…At present, there is limited genetic research into the components of this family of MOTs, although some data is appearing from ameloblastic carcinomas [ 40 , 42 ]. Further insight into each of the main subgroups as described will help elucidate key biological events that identify tumours at risk of malignant transformation and risk of metastasis and further improvements in prognostication and standardisation in treatment algorithms.…”

Section: Discussionmentioning

confidence: 99%

Malignant Odontogenic Tumours: A Systematic Review of Cases Reported in Literature

Marín

Dave

Hunter

2021

Front. Oral. Health

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Background: Malignant odontogenic tumours (MOTs) arise either de novo from the tooth forming tissues, their developmental residues or from existing odontogenic epithelial or mesenchymal neoplasms in the jaws. Their management requires extensive surgery due to their infiltrative nature and risk of metastasis. There is a need to understand the clinical and pathological features of MOTs to inform both treatment algorithms and prognostication. This is an area of diagnostic pathology which presents substantial difficulties in diagnosis, compounded by inconsistent use of terminology. Thus, this systematic review aimed to describe the clinical and pathological features of MOTs with a view to consolidating the literature and defining problematic areas in diagnosis and classification.Methods: An electronic database search was conducted in Web of Science, PubMed/Medline, and Embase. Additionally, the grey literature and reference lists of selected papers searched for completeness. Nine hundred and sixty articles were initially identified. Following removal of duplicates and application of inclusion/exclusion criteria, 312 articles were included for qualitative analysis.Results: The 312 articles encompassed a total of 507 patients with most lesions located within the mandible (74.3%). The most common first histological diagnosis was ameloblastic carcinoma (25.7% of all diagnoses), but there is considerable variation in how and when various diagnostic terms are used, and several misdiagnoses were reported. An initial benign diagnosis was made in 24.7% of patients, followed by a later malignant diagnosis and in this sub-group, the most common benign first diagnosis was ameloblastoma (42.4%). Cervical lymph nodes were the most common site of metastasis (9.3% of patients). With respect to distant metastasis (DM), the lungs were the most common organ affected (11.2% of DM patients) with metastasising ameloblastoma the most commonly reported tumour which metastasised to the lungs. Overall, 26.8% of patients developed recurrence.Conclusion: Overall, the quality of the literature on MOTs is poor. This review of the literature has highlighted variations in diagnostic terms and criteria which has resulted in areas of confusion with potential for misdiagnosis. This consolidation of primary data has identified key areas for targeted research including further discussion on the malignant potential of ameloblastoma.

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Study on clinical and biological characteristics of ameloblastic carcinoma

Cited by 32 publications

References 24 publications

The Molecular Pathology of Odontogenic Tumors: Expanding the Spectrum of MAPK Pathway Driven Tumors

The Molecular Pathology of Odontogenic Tumors: Expanding the Spectrum of MAPK Pathway Driven Tumors

Comparative Analysis Between Dentinogenic Ghost Cell Tumor and Ghost Cell Odontogenic Carcinoma: A Systematic Review

Malignant Odontogenic Tumours: A Systematic Review of Cases Reported in Literature

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