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QJM : Monthly Journal of the... Aug 2019
Topics: Adult; Ameloblastoma; Cone-Beam Computed Tomography; Hemangioma; Humans; Male; Mandibular Neoplasms
PubMed: 31120127
DOI: 10.1093/qjmed/hcz117 -
Archives of Oral Biology Aug 2022This article aims to systematically and comprehensively discuss molecular biology-related progress and targeted therapeutic strategies for ameloblastoma, which are... (Review)
Review
OBJECTIVE
This article aims to systematically and comprehensively discuss molecular biology-related progress and targeted therapeutic strategies for ameloblastoma, which are expected to be helpful for the diagnosis and treatment of ameloblastoma.
DESIGN
A comprehensive review of scientific literature relevant to ameloblastoma, including the latest classification, global epidemiology, molecular biology advances, and targeted therapy.
RESULTS
Among the 156 articles cited, a total of 20 non-coding RNAs, 13 genes, 27 proteins, and 8 pathways were involved, which play a variety of roles in ameloblastoma. These roles include participation in the biological behaviours of ameloblastoma migration, differentiation, and apoptosis; detection of ameloblastoma proliferative properties; detection of ameloblastoma angiogenesis; and identification of ameloblastoma carcinogenesis.
CONCLUSIONS
At present, some progress has been made in molecular biology and targeted therapy for ameloblastoma involving BRAF and SMO genes. The related non-coding RNAs, genes, proteins, and pathways involved in this review provide new ideas and directions for the occurrence and development of ameloblastoma and have the potential to become new gene therapy targets.
Topics: Ameloblastoma; Humans; Molecular Biology; Mutation; Proto-Oncogene Proteins B-raf
PubMed: 35597128
DOI: 10.1016/j.archoralbio.2022.105454 -
Indian Journal of Dental Research :... 2022Ameloblastoma is a benign, locally aggressive neoplasm that needs extensive surgical resection. The goal of this article is to obtain an in-depth review of benign... (Review)
Review
Ameloblastoma is a benign, locally aggressive neoplasm that needs extensive surgical resection. The goal of this article is to obtain an in-depth review of benign ameloblastomas to determine the available level of evidence and the possible benefit of targeted therapeutics for the treatment of ameloblastoma and BRAF V600E mutation in ameloblastoma. An electronic literature search was conducted according to PRISMA guidelines in PubMed/MEDLINE, EBSCO, and Web of Science for eligible studies published between 1975 and 2021. The systematic review is registered with INPLASY (INPLASY202260018). The review included 2 case series and 17 case reports. The histopathological type, anatomic location, expression of BRAF mutation, additional mutations, and molecular-targeted therapies of the 19 reviewed articles were summarized and tabulated. Interestingly, the majority of the primary site of ameloblastoma was located in the mandible (80.9%) compared to the maxilla (17%). The tumour size was reported in nine of the included studies. Most of the included studies in the review exhibited ameloblastoma with BRAF V600E mutations and responded to molecular-targeted therapies. Molecular therapies employing BRAF and/or MEK inhibitors in ameloblastoma with BRAF V600E mutations proved to be an appropriate treatment based on the limited available evidence. It is essential further to deepen our understanding at the clinical and molecular level to enhance the precision of management of ameloblastoma.
Topics: Humans; Ameloblastoma; Molecular Targeted Therapy; Mutation; Proto-Oncogene Proteins B-raf
PubMed: 36656197
DOI: 10.4103/ijdr.ijdr_456_22 -
Acta Odontologica Scandinavica Nov 2016Ameloblastoma is an aggressive odontogenic tumour, which is locally invasive and highly recurrent. Studies show that ameloblastoma is a benign odontogenic neoplasia,... (Review)
Review
Ameloblastoma is an aggressive odontogenic tumour, which is locally invasive and highly recurrent. Studies show that ameloblastoma is a benign odontogenic neoplasia, being relatively rare and occasionally presenting behaviour of malignant lesions. In addition to these particularities, the histological diagnosis of ameloblastoma can be challenging when the tumour shows high rates of mitosis, absence of nuclear pleomorphism, basilar hyperplasia and neural invasion. In order to help in the diagnosis, prognosis and treatment of this neoplasia, some immunohistochemical markers were shown to be associated with tumoural epithelium. The identification of these markers as well as of their association with clinical signs can be useful to elaborate more efficient treatment strategies and to control this pathology, including improvement of the quality of life of patients affected by this neoplasia. This article aims to review some markers associated with specific molecular pathways, bone remodelling, cell proliferation, apoptosis, cell signalling and tumour suppression.
Topics: Adult; Ameloblastoma; Apoptosis; Biomarkers, Tumor; Cell Proliferation; Gene Expression; Humans; Jaw Neoplasms; Proto-Oncogene Proteins c-mdm2
PubMed: 27571891
DOI: 10.1080/00016357.2016.1224918 -
Modern Pathology : An Official Journal... Nov 2022Adenoid ameloblastoma is a very rare benign epithelial odontogenic tumor characterized microscopically by epithelium resembling conventional ameloblastoma, with...
Adenoid ameloblastoma is a very rare benign epithelial odontogenic tumor characterized microscopically by epithelium resembling conventional ameloblastoma, with additional duct-like structures, epithelial whorls, and cribriform architecture. Dentinoid deposits, clusters of clear cells, and ghost-cell keratinization may also be present. These tumors do not harbor BRAF or KRAS mutations and their molecular basis appears distinct from conventional ameloblastoma but remains unknown. We assessed CTNNB1 (beta-catenin) exon 3 mutations in a cohort of 11 samples of adenoid ameloblastomas from 9 patients. Two of the 9 patients were female and 7 male and in 7/9 patients the tumors occurred in the maxilla. Tumors of 4 of these 9 patients harbored CTNNB1 mutations, specifically p.Ser33Cys, p.Gly34Arg, and p.Ser37Phe. Notably, for one patient 3 samples were analyzed including the primary tumour and two consecutive recurrences, and results were positive for the mutation in all three tumors. Therefore, 6/11 samples tested positive for the mutation. In the 6 mutation-positive samples, ghost cells were present in only 2/6, indicating beta-catenin mutations are not always revealed by ghost cell formation. Dentinoid matrix deposition was observed in 5/6 mutation-positive samples and clear cells in all 6 cases. None of the cases harbored either BRAF or KRAS mutations. Beta-catenin immunoexpression was assessed in the samples of 8 patients. Except for one wild-type case, all cases showed focal nuclear expression irrespective of the mutational status. Together with the absence of BRAF mutation, the detection of beta-catenin mutation in adenoid ameloblastomas supports its classification as a separate entity, and not as a subtype of ameloblastoma. The presence of this mutation may help in the diagnosis of challenging cases.
Topics: Humans; Male; Female; Ameloblastoma; beta Catenin; Proto-Oncogene Proteins B-raf; Adenoids; Proto-Oncogene Proteins p21(ras); Odontogenic Tumors; Mutation
PubMed: 35840721
DOI: 10.1038/s41379-022-01125-4 -
Current Opinion in Otolaryngology &... Apr 2016This review focuses on issues in managing ameloblastomas of the mandible and maxilla. We will refer to current practice in the treatment of ameloblastomas based on the... (Review)
Review
PURPOSE OF REVIEW
This review focuses on issues in managing ameloblastomas of the mandible and maxilla. We will refer to current practice in the treatment of ameloblastomas based on the available evidence.
RECENT FINDINGS
Recent reviews have been trying to establish natural history, growth patterns and malignant potential. This provides the clinicians and the patients with useful prognostic information. Controversies in management of ameloblastomas in relation to the type, age and site exist. This paper aims to categorize these issues. More recently, the authors have adopted the staged treatment approach as an additional step to ensure margin clearance.
SUMMARY
Current evidence favours radical resection to provide better control rates. This applies to maxillary lesions of all ages, and solid mandibular lesions in adults (>18 years) where growth has ceased and the patient has matured enough to withstand the impact of resection and reconstruction. Conservative management is advocated for unicystic lesions with good control rates. In children and adolescents, a conservative approach is recommended. This approach aids to minimize both psychological and the impact on growth. Furthermore, most of the lesions are unicystic and the recurrent lesions have been shown to be much smaller and can be managed promptly within a good healthcare system.
Topics: Ameloblastoma; Disease Management; Humans; Mandibular Neoplasms; Maxillary Neoplasms; Prognosis
PubMed: 26886591
DOI: 10.1097/MOO.0000000000000238 -
La Revue Du Praticien May 2024
Topics: Humans; Ameloblastoma; Jaw Neoplasms
PubMed: 38833232
DOI: No ID Found -
Oral Oncology Sep 2020Ameloblastoma is a rare human disease of benign neoplasm odontogenic tumor with a lower prevalence but higher recurrence rate. Etiology of ameloblastoma is not fully... (Review)
Review
Ameloblastoma is a rare human disease of benign neoplasm odontogenic tumor with a lower prevalence but higher recurrence rate. Etiology of ameloblastoma is not fully understood thus lacks implementation of curative treatments. One of the proposed models of evolution of ameloblastoma is related to alteration in DNA damage and repair effects. Growing body of literature has associated defect in DNA damage and repair mechanisms with cancer risk and various adverse health outcomes in humans. Persistent defect of repair and escape of these genomic unstable cells from cell death mechanisms can contribute towards accumulation of oncogene driver or tumor suppressor mutations selective for malignant transformations. In addition, growth, progression and survival of tumor depends upon its DNA repair mechanisms too, thus identifying a DNA repair biomarker can be of advantageous to eliminate the tumor. Understanding the interconnection of oral lesion and role of various DNA repair mechanisms in context to ameloblastoma will assist to build up a platform for translational based research. This study is a literature review of research work published up to date in the field of ameloblastoma in regard to DNA damage and repair effects.
Topics: Ameloblastoma; DNA Damage; Humans
PubMed: 32474390
DOI: 10.1016/j.oraloncology.2020.104804 -
Journal of Oral Pathology & Medicine :... Apr 2023The advances in molecular technologies have allowed a better understanding of the molecular basis of odontogenic cysts and tumours. PTCH1 mutations have been reported in... (Review)
Review
The advances in molecular technologies have allowed a better understanding of the molecular basis of odontogenic cysts and tumours. PTCH1 mutations have been reported in a high proportion of odontogenic keratocyst. BRAF p.V600E are recurrent in ameloblastoma and KRAS p.G12V/R in adenomatoid odontogenic tumour, dysregulating the MAPK/ERK pathway. Notably, BRAF p.V600E is also detected in ameloblastic carcinoma, but at a lower frequency than in its benign counterpart ameloblastoma. Recently, adenoid ameloblastoma has been shown to be BRAF wild-type and to harbour CTNNB1 (β-catenin gene) mutations, further suggesting that it is not an ameloblastoma subtype. CTNNB1 mutations also occur in other ghost-cell-containing tumours, including calcifying odontogenic cysts, dentinogenic ghost cell tumours and odontogenic carcinoma with dentinoid, but the link between CTNNB1 mutations and ghost cell formation in these lesions remains unclear. Regarding mixed tumours, BRAF p.V600E has been reported in a subset of ameloblastic fibromas, ameloblastic-fibrodentinomas and fibro-odontomas, in addition to ameloblastic fibrosarcoma. Such mutation-positivity in a subset of samples can be helpful in differentiating some of these lesions from odontoma, which is BRAF-wild-type. Recently, FOS rearrangements have been reported in cementoblastoma, supporting its relationship with osteoblastoma. Collectively, the identification of recurrent mutations in these aforementioned lesions has helped to clarify their molecular basis and to better understand the interrelationships between some tumours, but none of these genetic abnormalities is diagnostic. Since the functional effect of pathogenic mutations is context and tissue-dependent, a clear role for the reported mutations in odontogenic cysts and tumours in their pathogenesis remains to be elucidated.
Topics: Humans; Ameloblastoma; Proto-Oncogene Proteins B-raf; Odontogenic Tumors; Odontogenic Cysts; Odontoma; Mouth Neoplasms; Carcinoma
PubMed: 36629457
DOI: 10.1111/jop.13401 -
Oral Radiology Jan 2021To describe the radiographic features of odontogenic keratocysts (OKCs) and ameloblastomas and to compare the radiographic findings between these 2 lesions.
OBJECTIVES
To describe the radiographic features of odontogenic keratocysts (OKCs) and ameloblastomas and to compare the radiographic findings between these 2 lesions.
METHODS
Radiographs of OKCs and ameloblastomas were retrospectively reviewed. Location, border, shape, association with impacted tooth, tooth displacement, root resorption, and bone expansion were evaluated. Chi-squared or Fisher's exact tests were used for statistical analysis. A p value < 0.05 was considered to indicate statistical significance.
RESULTS
One hundred OKCs and 101 ameloblastomas were reviewed. The ratios of maxilla to mandible were 1:1.4 and 1:9.1 in OKCs and ameloblastomas, respectively. All evaluated features significantly differed between OKCs and ameloblastomas (p ≤ 0.001). Most OKCs showed smooth border (60%) and unilocular shape (82%), while most ameloblastomas showed scalloped border (77.2%) and multilocular shape (68.3%). Association with impacted tooth was found in 47% of OKCs and 18.8% of ameloblastomas. Adjacent tooth displacement was found in 33.7% of OKCs and 55.8% of ameloblastomas. Root resorption was more common in ameloblastomas (66.7%) than in OKCs (7%). Bone expansion was also more common in ameloblastomas (96.3%) than in OKCs (63.6%).
CONCLUSION
A unilocular radiolucent lesion with smooth border, no adjacent tooth displacement, no root resorption and causing mild or no bone expansion is suggestive of an OKC rather than an ameloblastoma.
Topics: Ameloblastoma; Humans; Jaw Neoplasms; Odontogenic Cysts; Odontogenic Tumors; Retrospective Studies
PubMed: 32030659
DOI: 10.1007/s11282-020-00425-2