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PloS One 2015Malignant ameloblastoma, comprising metastasizing ameloblastoma and ameloblastic carcinoma, represents 1.6-2.2% of all odontogenic tumors. Due to its rare nature,...
BACKGROUND
Malignant ameloblastoma, comprising metastasizing ameloblastoma and ameloblastic carcinoma, represents 1.6-2.2% of all odontogenic tumors. Due to its rare nature, malignant ameloblastoma has only been reported in the literature in small case series or case reports. Using the Surveillance, Epidemiology and End-Results (SEER) database, we have performed a population-based study to determine the incidence rate and the absolute survival of malignant ameloblastoma.
METHOD
Using the International Classification of Diseases for Oncology (ICD-O) codes 9310/3 and 9270/3, data from the SEER database were used to calculate the incidence rate and absolute survival rate of population with malignant ameloblastoma.
RESULTS
The overall incidence rate of malignant ameloblastoma was 1.79 per 10 million person/year. The incidence rate was higher in males than females and also higher in black versus white population. The median overall survival was 17.6 years from the time of diagnosis and increasing age was associated with a statistically significant poorer survival.
CONCLUSIONS
To our best knowledge, we report the largest population-based series of malignant ameloblastoma. The incidence rate was 1.79 per 10 million person/year and the overall survival was 17.6 years.
Topics: Adolescent; Adult; Ameloblastoma; Child; Child, Preschool; Cohort Studies; Databases, Factual; Epidemiological Monitoring; Female; Humans; Incidence; Infant; Infant, Newborn; Jaw Neoplasms; Male; Middle Aged; Survival Rate; Young Adult
PubMed: 25692490
DOI: 10.1371/journal.pone.0117789 -
Archives of Oral Biology Feb 2019Ameloblastoma is an aggressive odontogenic jaw neoplasm. Its unlimited growth confers high potential for malignant transformation and recurrence. It is unclear why...
OBJECTIVES
Ameloblastoma is an aggressive odontogenic jaw neoplasm. Its unlimited growth confers high potential for malignant transformation and recurrence. It is unclear why ameloblastoma is highly recurrent despite surgical resection with a wide margin of normal tissue. While canonical autophagy can be used to degrade and eliminate damaged cellular components, it is also a protective mechanism that provides energy and vital metabolites for cell survival. We used ameloblastoma-derived cells to test the hypothesis that autophagic processes play a role in survival and reactivation of ameloblastoma.
METHODS
Primary epithelial (EP-AMCs) and mesenchymal (MS-AMCs) ameloblastoma-derived cells were established from tissue samples of solid multicystic ameloblastoma. Clonogenic capacity and basal autophagic capacity were assessed in ameloblastoma-derived cells relative to human odontoma-derived cells (HODCs) and maxilla-mesenchymal stem cells (MX-MSCs). Ability of ameloblastoma-derived cells to survive and form new ameloblastoma was assessed in mouse tumor xenografts.
RESULTS
EP-AMCs were highly clonogenic (p < 0.0001) and demonstrated enhanced basal levels of autophagic proteins microtubule-associated protein 1-light chain 3 (LC3) (p < 0.01), p62 (Sequestosome 1, SQSTM1) (p < 0.01), and the LC3-adapter, melanoregulin (MREG) (p < 0.05) relative to controls. EP-AMCs xenografts regenerated solid ameloblastoma-like tumor with histological features of columnar ameloblast-like cells, loose stellate reticulum-like cells and regions of cystic degeneration characteristic of follicular variant of solid multicystic ameloblastoma. The xenografts also displayed stromal epithelial invaginations strongly reactive to LC3 and p62 suggestive of epithelial-mesenchymal transition and neoplastic odontogenic epithelium.
CONCLUSIONS
EP-AMCs exhibit altered autophagic processes that can support survival and recurrence of post-surgical ameloblastoma cells.
Topics: Adaptor Proteins, Vesicular Transport; Ameloblastoma; Ameloblasts; Animals; Autophagy; Carrier Proteins; Cell Survival; Disease Models, Animal; Epithelial-Mesenchymal Transition; Epithelium; Female; Heterografts; Humans; Intracellular Signaling Peptides and Proteins; Mesenchymal Stem Cells; Mice; Microtubule-Associated Proteins; Neoplasm Recurrence, Local; Odontogenic Tumors; Sequestosome-1 Protein; Xenograft Model Antitumor Assays
PubMed: 30465934
DOI: 10.1016/j.archoralbio.2018.11.013 -
Journal of Oral Science Jun 2011Although ameloblastoma and adenomatoid odontogenic tumor (AOT) belong to the same group according to the World Health Organization, they show different biologic... (Comparative Study)
Comparative Study
Although ameloblastoma and adenomatoid odontogenic tumor (AOT) belong to the same group according to the World Health Organization, they show different biologic behaviors. PCNA, an amplifier of cell proliferation, and p53, a tumor suppressor protein, are overexpressed in some odontogenic lesions. The purpose of this study was to immunohistochemically evaluate the expression of p53 and PCNA to clarify the possible role of these proteins in different behaviors of ameloblastoma and AOT. The immunohistochemical expression of PCNA and p53 was determined in 30 solid ameloblastomas and 12 AOTs. Statistical tests including one-way ANOVA, t-test, chi-square, Mann-Whitney U and Kendall were used to analyze the data. All tissue sections (except one specimen of plexiform ameloblastoma) exhibited immunoexpression for p53. PCNA was expressed in all specimens. There was no significant difference in PCNA expression between ameloblastomas and AOTs (P > 0.05). For p53, there was no statistical difference between subtypes of ameloblastomas (P > 0.05), whereas statistical differences were observed between ameloblastomas and AOTs (P < 0.001). There was no statistical difference in PCNA intensity of staining between ameloblastomas and AOTs (P > 0.05), whereas the p53 intensity in ameloblastomas was stronger than AOTs (P < 0.05). Positive correlation between PCNA and p53 was observed. We concluded that PCNA overexpression is not responsible for the difference in clinical behavior of these two lesions, whereas the expression of p53 in ameloblastoma may explain the more aggressive nature of this tumor compared with AOT.
Topics: Adenocarcinoma; Adult; Ameloblastoma; Female; Gene Expression Regulation, Neoplastic; Humans; Immunohistochemistry; Lymphoma; Male; Odontogenic Tumors; Proliferating Cell Nuclear Antigen; Tumor Suppressor Protein p53; Young Adult
PubMed: 21712626
DOI: 10.2334/josnusd.53.213 -
Head and Neck Pathology Dec 2020Peripheral ameloblastoma (PA) is a prototype form of extraosseous odontogenic tumor. As knowledge of PA has accumulated on the basis of more than 200 cases reported... (Review)
Review
Peripheral ameloblastoma (PA) is a prototype form of extraosseous odontogenic tumor. As knowledge of PA has accumulated on the basis of more than 200 cases reported worldwide over a 60-year timeframe, it is important to comprehend the historical evolution of this entity. In 2018, we summarized the American history of PA, stressing the important early strides made by Bloodgood in 1904 with his many original observations of the "epulis form of ameloblastoma". During the preparation of our previous report, we were able to find several earlier and interesting descriptions in the literature. This review covers the early history of PA since the nineteenth century, chronologically focusing on meritorious articles published in the United States and Europe.
Topics: Ameloblastoma; History, 19th Century; History, 20th Century; History, 21st Century; Humans
PubMed: 32451874
DOI: 10.1007/s12105-020-01168-6 -
Medicina Oral, Patologia Oral Y Cirugia... Mar 2021Desmoplastic Ameloblastoma (DA) is a rare, true neoplasm of jaws with reported incidence of 4-13% among other variants of Ameloblastoma, however this appears distinct... (Review)
Review
BACKGROUND
Desmoplastic Ameloblastoma (DA) is a rare, true neoplasm of jaws with reported incidence of 4-13% among other variants of Ameloblastoma, however this appears distinct than the classic Ameloblastoma in anatomical distribution and clinical presentation. This is often mistaken as a fibro-osseous lesion because of its similar radiological appearance.
MATERIAL AND METHODS
To describe the clinical, radiographic and histopathological characteristics through a series of new cases of histologically proven DA including a case of an exceptionally large, recurrent lesion along with retrospective analysis of cases from literature available for an improved understanding of the behaviour and prognosis of DA. A total of 50 cases were analysed for the anatomical distribution, radiographic presentation and management. Out of the 50 cases, 47 cases were from the English literature reported from 2011 to 2019 and 3 were new cases.
RESULTS
DA showed a slight male predilection (male: female=1.17:1) with a predominance in the fourth and fifth decade of life. Mandibular involvement (52%) was more commonly seen with a marked tendency for the anterior region. Radiographically, most of the lesions presented mixed radiopacity with radiolucency(80%) and root displacement was observed in only 70.27 % cases. Recurrence rate of 26 .47 % was observed. Cases treated with resection resulted in lesser recurrence as compared to those treated with enucleation and curettage.
CONCLUSIONS
DA is distinguished by a peculiar display of clinicalopathological parameters. DA has tendency of local disposition and propensity of recurrence, which thus necessitates its aggressive management. It is not possible to conclude or report on the aggressive/recurrent nature and appropriate treatment modality for DA due to inadequate follow-up results.
Topics: Ameloblastoma; Female; Humans; Male; Mandible; Mandibular Neoplasms; Neoplasm Recurrence, Local; Radiography; Retrospective Studies
PubMed: 33037797
DOI: 10.4317/medoral.24152 -
Head and Neck Pathology Jun 2022Adenoid ameloblastoma is a hybrid odontogenic tumour showing histopathological features of both ameloblastoma and adenomatoid odontogenic tumour (AOT), with... (Review)
Review
Adenoid ameloblastoma is a hybrid odontogenic tumour showing histopathological features of both ameloblastoma and adenomatoid odontogenic tumour (AOT), with approximately 40 cases reported in the literature. The aims of the report are to illustrate the diagnostic challenges of adenoid ameloblastoma using three new cases and to analyze evidence in literature to consider adenoid ameloblastoma as a new sub type of ameloblastoma. A literature review was performed with the key words-adenoid ameloblastoma, hybrid/composite odontogenic tumours, hybrid ameloblastoma and adenomatoid odontogenic tumour, ameloblastoma with inductive changes, dentinoid and dentinoma to select the cases compatible with the diagnosis of adenoid ameloblastoma. Out of the 40 cases reported in literature, 31 cases with sufficient information and 3 new cases were analyzed. Out of the 34 adenoid ameloblastomas majority of tumours (76.5%) occurred in adults with age ranging from 25 to 55 years. Slight female predilection with a male:female ratio of 0.9:1 was observed. Approximately, 64.7% occurred in the mandible. Radiologically, 82.4% of adenoid ameloblastomas presented as radiolucent lesions while 47.1% occurred with ill-defined margins and cortical perforation at diagnosis. Histopathologically, 70.8% of tumours presented as plexiform ameloblastomas, while duct like structures/glandular structures were the commonest feature supportive of adenomatoid odontogenic tumour observed in overwhelming majority of 95.9% of adenoid ameloblastomas. 91.6% of tumours showed inductive change in the form of dentinoid. Further, 45.4% of the tumours developed at least one recurrence following surgical excision. The report presents literature review based evidence to show the existence of adenoid ameloblastoma, which is demographically similar to conventional ameloblastoma but with histopathological differences and presenting with higher rate/multiple recurrences, indicating its biological aggressiveness. Thus, we would like to propose the inclusion of adenoid ameloblastoma as a sub type of ameloblastoma in the next revision of the WHO odontogenic tumour classification.
Topics: Adenoids; Adult; Ameloblastoma; Female; Humans; Male; Mandible; Middle Aged; Odontogenic Tumors
PubMed: 34282559
DOI: 10.1007/s12105-021-01358-w -
BMC Oral Health Aug 2023Ameloblastic carcinoma and metastasising ameloblastoma are rare epithelial odontogenic tumours with aggressive features. Distinguishing between these two lesions is... (Review)
Review
BACKGROUND
Ameloblastic carcinoma and metastasising ameloblastoma are rare epithelial odontogenic tumours with aggressive features. Distinguishing between these two lesions is often clinically difficult but necessary to predict tumour behaviour or to plan future therapy. Here, we provide a brief review of the literature available on these two types of lesions and present a new case report of a young man with an ameloblastoma displaying metastatic features. We also use this case to illustrate the similarities and differences between these two types of tumours and the difficulties of their differential diagnosis.
CASE PRESENTATION
Our histopathological analyses uncovered a metastasising tumour with features of ameloblastic carcinoma, which developed from the ameloblastoma. We profiled the gene expression of Wnt pathway members in ameloblastoma sample of this patient, because multiple molecules of this pathway are involved in the establishing of cell polarity, cell migration or for epithelial-mesenchymal transition during tumour metastasis to evaluate features of tumor behaviour. Indeed, we found upregulation of several cell migration-related genes in our patient. Moreover, we uncovered somatic mutation BRAF p.V600E with known pathological role in cancerogenesis and germline heterozygous FANCA p.S858R mutation, whose interpretation in this context has not been discussed yet.
CONCLUSIONS
In conclusion, we have uncovered a unique case of ameloblastic carcinoma associated with an alteration of Wnt signalling and the presence of BRAF mutation. Development of harmful state of our patient might be also supported by the germline mutation in one FANCA allele, however this has to be confirmed by further analyses.
Topics: Male; Humans; Ameloblastoma; Proto-Oncogene Proteins B-raf; Odontogenic Tumors; Mutation; Carcinoma
PubMed: 37573343
DOI: 10.1186/s12903-023-03259-6 -
Scientific Reports Dec 2021Ameloblastoma is a benign, epithelial cancer of the jawbone, which causes bone resorption and disfigurement to patients affected. The interaction of ameloblastoma with...
Ameloblastoma is a benign, epithelial cancer of the jawbone, which causes bone resorption and disfigurement to patients affected. The interaction of ameloblastoma with its tumour stroma drives invasion and progression. We used stiff collagen matrices to engineer active bone forming stroma, to probe the interaction of ameloblastoma with its native tumour bone microenvironment. This bone-stroma was assessed by nano-CT, transmission electron microscopy (TEM), Raman spectroscopy and gene analysis. Furthermore, we investigated gene correlation between bone forming 3D bone stroma and ameloblastoma introduced 3D bone stroma. Ameloblastoma cells increased expression of MMP-2 and -9 and RANK temporally in 3D compared to 2D. Our 3D biomimetic model formed bone nodules of an average surface area of 0.1 mm and average height of 92.37 [Formula: see text] 7.96 μm over 21 days. We demonstrate a woven bone phenotype with distinct mineral and matrix components and increased expression of bone formation genes in our engineered bone. Introducing ameloblastoma to the bone stroma, completely inhibited bone formation, in a spatially specific manner. Multivariate gene analysis showed that ameloblastoma cells downregulate bone formation genes such as RUNX2. Through the development of a comprehensive bone stroma, we show that an ameloblastoma tumour mass prevents osteoblasts from forming new bone nodules and severely restricted the growth of existing bone nodules. We have identified potential pathways for this inhibition. More critically, we present novel findings on the interaction of stromal osteoblasts with ameloblastoma.
Topics: Ameloblastoma; Animals; Bone Resorption; Core Binding Factor Alpha 1 Subunit; Gene Expression; Humans; Jaw Neoplasms; Matrix Metalloproteinase 2; Neoplasm Invasiveness; Osteoblasts; Osteogenesis; RANK Ligand; Rats; Stromal Cells; Tissue Engineering; Tumor Cells, Cultured; Tumor Microenvironment
PubMed: 34916549
DOI: 10.1038/s41598-021-03484-5 -
CA: a Cancer Journal For Clinicians 1968
Topics: Ameloblastoma; Humans; Mandibular Neoplasms; Radiography
PubMed: 4992869
DOI: 10.3322/canjclin.18.4.205 -
Canadian Medical Association Journal Dec 1950
Topics: Adamantinoma; Ameloblastoma; Jaw; Neoplasms
PubMed: 14792442
DOI: No ID Found