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Medicina Oral, Patologia Oral Y Cirugia... Sep 2022Ep-CAM, a transmembrane glycoprotein expressed in most epithelium in normal conditions, has diverse roles in these tissues, including in cell adhesion, proliferation,...
BACKGROUND
Ep-CAM, a transmembrane glycoprotein expressed in most epithelium in normal conditions, has diverse roles in these tissues, including in cell adhesion, proliferation, differentiation, cell cycle regulation, migration and intracellular signaling. It is also over-expressed in most malignant neoplasia, participating in the initiation, progression, and metastatic dissemination of the tumor. The expression and roles of this protein in oral neoplasia, particularly in odontogenic tumors, remain unestablished. The objective of this study consisted in analyzing the expression of this protein in ameloblastoma and tooth germ.
MATERIAL AND METHODS
Ep-CAM (MOC-31) expression was evaluated by immunohistochemistry in tooth germs (TG) (n = 16) ameloblastomas (AM) (n = 60) and 2 ameloblastic carcinomas. Sections were visualized in their totality with an optical microscope, and positivity observed in cell membrane and cytoplasm was graded according to the following semi-quantitative scale: Neg, "essentially unstained", for negative sections or staining <5% of cells; + for staining of 5-50% of cells; ++ for staining >50% of cells.
RESULTS
Most tooth germs expressed MOC-31 (81.3%), strong staining was observed both in the inner epithelium of the enamel organ and in the adjacent stellate reticulum. 16.7% of the AM cases showed MOC-31 expression, the immunoexpression expression was diffuse at the cytoplasmic and membrane level. The only two cases of ameloblastic carcinoma included were strong positive to MOC-31. No correlation was observed between protein expression and gender, age, clinical variants, or histological subtypes.
CONCLUSIONS
Overexpression was found in TG and ameloblastic carcinoma compared to AM; further studies with different experimental strategies are suggested to clarify the biological significance of this finding.
Topics: Ameloblastoma; Carcinoma; Epithelial Cell Adhesion Molecule; Humans; Odontogenic Tumors; Tooth Germ
PubMed: 35975801
DOI: 10.4317/medoral.25145 -
Internal Medicine (Tokyo, Japan) Jun 2020A 78-year-old man with a history of surgical resection for ameloblastoma 31 years earlier visited our hospital for prolonged cough. Chest computed tomography showed... (Review)
Review
A 78-year-old man with a history of surgical resection for ameloblastoma 31 years earlier visited our hospital for prolonged cough. Chest computed tomography showed multiple nodules in both lungs. Although there was no local recurrence in the mandible, the specimen taken from a transbronchoscopic bronchial biopsy showed recurrent ameloblastoma. Despite receiving no treatment, the disease in our patient remained clinically stable for 8.4 years. Chest physicians should be aware that pulmonary malignant ameloblastoma can first relapse several decades after curative surgery. In addition, pulmonary malignant ameloblastoma without local recurrence may be associated with a good prognosis.
Topics: Adult; Aged; Ameloblastoma; Female; Humans; Jaw Neoplasms; Lung Neoplasms; Male; Middle Aged; Neoplasm Metastasis; Neoplasm Recurrence, Local; Tomography, X-Ray Computed; Treatment Outcome
PubMed: 32132332
DOI: 10.2169/internalmedicine.3716-19 -
Head and Neck Pathology Jun 2020The goal of this study was to investigate the immunolocalization of inositol 1,4,5-trisphosphate receptor (IP3R) and vacuolar ATPase (V-ATPase) in ameloblastomas with...
The goal of this study was to investigate the immunolocalization of inositol 1,4,5-trisphosphate receptor (IP3R) and vacuolar ATPase (V-ATPase) in ameloblastomas with special attention to the invasive front. Thirty-seven cases of previously diagnosed formalin-fixed paraffin-embedded (FFPE) human ameloblastoma samples were selected for this study. The samples were grouped according to the predominant histologic pattern and comprised twelve plexiform, eighteen follicular, and seven unicystic ameloblastomas. Of the unicystic variants, six demonstrated purely luminal and intraluminal growth, and one displayed mural extension. One granular cell variant was included in the follicular ameloblastoma group. All specimens were evaluated for IP3R and V-ATPase expression by immunohistochemistry (IHC). IP3R was positive in columnar cells, similar to ameloblasts, and non-peripheral cells in all samples. In the area of tumor protrusion and front of invasion, membranous and cystoplasmic IP3R expression was observed. In contrast, areas adjacent to tumoral protrusion demonstrated only membranous staining patterns. V-ATPase was not expressed in peripheral columnar cells of the unicystic and granular cell variants of ameloblastoma; however, strong staining was present in these cells in plexiform ameloblastomas, follicular ameloblastomas, and areas of mural growth of unicystic ameloblastomas. In areas of tumor protrusion, reactivity for V-ATPase was observed with both membranous and cytoplasmic staining, while other areas showed only membranous V-ATPase. These findings suggest that concomitant immunolocalization of IP3R and V-ATPase, with both cytoplasmic and membranous expression in the peripheral columnar cells, may indicate the invasive potential of ameloblastomas. Furthermore, these results suggest the tumoral spread of ameloblastomas may be correlated with the autophagy process and channelopathy. The expression of these proteins could establish a baseline for future research and provide therapeutic targets for treatment of ameloblastomas.
Topics: Ameloblastoma; Biomarkers, Tumor; Humans; Immunohistochemistry; Inositol 1,4,5-Trisphosphate Receptors; Jaw Neoplasms; Vacuolar Proton-Translocating ATPases
PubMed: 31183746
DOI: 10.1007/s12105-019-01044-y -
Medicina Oral, Patologia Oral Y Cirugia... Jul 2020Phosphatase and tensin homolog (PTEN) acts as a tumor suppressor gene. Inactivation of PTEN has been reported in various types of cancers. PTEN promoter methylation...
BACKGROUND
Phosphatase and tensin homolog (PTEN) acts as a tumor suppressor gene. Inactivation of PTEN has been reported in various types of cancers. PTEN promoter methylation possibly underlies PTEN inactivation, which results in tumorigenesis. The aim of this study was to investigate whether PTEN promoter methylation contributes to PTEN inactivation in ameloblastoma and its associated protein expression.
MATERIAL AND METHODS
In total, 20 fresh-frozen ameloblastoma samples were evaluated for PTEN promoter methylation using methylation-specific polymerase chain reaction (MS-PCR). A subset of 10 paraffin-embedded ameloblastoma samples was examined for PTEN expression through immunohistochemistry. Four primary cultured ameloblastoma cells were investigated for PTEN promoter methylation and PTEN transcriptional expression via reverse transcription PCR.
RESULTS
PTEN promoter methylation was detected in 65% (13/20) of the ameloblastoma samples. Of 10 ameloblastoma samples, 4 exhibited reduced PTEN expression. Of 5 samples with methylated PTEN, 3 (60%) were associated with loss of PTEN expression. However, PTEN expression was detected in 4 (80%) of 5 samples with unmethylated PTEN. In addition, 3 (75%) of 4 primary ameloblastoma cell cultures exhibited an inverse correlation between PTEN promoter methylation and PTEN transcription level.
CONCLUSIONS
PTEN promoter methylation is found in a number of ameloblastomas but not significantly correlated with loss of PTEN expression. Genetic or epigenetic mechanisms other than PTEN promoter methylation may contribute to PTEN inactivation in ameloblastoma tumor cells.
Topics: Ameloblastoma; DNA Methylation; Humans; Immunohistochemistry; PTEN Phosphohydrolase; Polymerase Chain Reaction; Promoter Regions, Genetic
PubMed: 32134893
DOI: 10.4317/medoral.23498 -
BMJ Case Reports Sep 2013Desmoplastic ameloblastoma is one of the six histopathological subtypes of ameloblastoma. The age and gender groups affected by desmoplastic are similar to those...
Desmoplastic ameloblastoma is one of the six histopathological subtypes of ameloblastoma. The age and gender groups affected by desmoplastic are similar to those affected by the conventional ameloblastoma. It usually presents as a painless enlargement of the jaw. Owing to its deceptive radiological appearance as a mixed radiopaque-radiolucent lesion, it is often mistaken as a fibro-osseous lesion. Histologically, desmoplastic ameloblastoma has a densely collagenised and hypocellular stroma, where the epithelium tends to proliferate in the form of cords and nests instead of cellular islands. Most desmoplastic ameloblastomas display occasional classic islands of follicular ameloblastoma among the predominant strands and cords. Studies have shown that desmoplastic ameloblastoma shows a tendency to recur. We present a rare case of a tumour occurring in the anterior mandibular region in a 60-year-old man over a period of 11/2 months.
Topics: Ameloblastoma; Humans; Male; Mandibular Neoplasms; Middle Aged; Radiography
PubMed: 24045759
DOI: 10.1136/bcr-2013-200082 -
Frontiers in Immunology 2023Ameloblastoma is a locally invasive and aggressive epithelial odontogenic neoplasm. The BRAF-V600E gene mutation is a prevalent genetic alteration found in this tumor...
BACKGROUND
Ameloblastoma is a locally invasive and aggressive epithelial odontogenic neoplasm. The BRAF-V600E gene mutation is a prevalent genetic alteration found in this tumor and is considered to have a crucial role in its pathogenesis. The objective of this study is to develop and validate a radiomics-based machine learning method for the identification of BRAF-V600E gene mutations in ameloblastoma patients.
METHODS
In this retrospective study, data from 103 patients diagnosed with ameloblastoma who underwent BRAF-V600E mutation testing were collected. Of these patients, 72 were included in the training cohort, while 31 were included in the validation cohort. To address class imbalance, synthetic minority over-sampling technique (SMOTE) is applied in our study. Radiomics features were extracted from preprocessed CT images, and the most relevant features, including both radiomics and clinical data, were selected for analysis. Machine learning methods were utilized to construct models. The performance of these models in distinguishing between patients with and without BRAF-V600E gene mutations was evaluated using the receiver operating characteristic (ROC) curve.
RESULTS
When the analysis was based on radiomics signature, Random Forest performed better than the others, with the area under the ROC curve (AUC) of 0.87 (95%CI, 0.68-1.00). The performance of XGBoost model is slightly lower than that of Random Forest, and its AUC is 0.83 (95% CI, 0.60-1.00). The nomogram evident that among younger women, the affected region primarily lies within the mandible, and patients with larger tumor diameters exhibit a heightened risk. Additionally, patients with higher radiomics signature scores are more susceptible to the BRAF-V600E gene mutations.
CONCLUSIONS
Our study presents a comprehensive radiomics-based machine learning model using five different methods to accurately detect BRAF-V600E gene mutations in patients diagnosed with ameloblastoma. The Random Forest model's high predictive performance, with AUC of 0.87, demonstrates its potential for facilitating a convenient and cost-effective way of identifying patients with the mutation without the need for invasive tumor sampling for molecular testing. This non-invasive approach has the potential to guide preoperative or postoperative drug treatment for affected individuals, thereby improving outcomes.
Topics: Humans; Female; Ameloblastoma; Proto-Oncogene Proteins B-raf; Retrospective Studies; Machine Learning; Mutation
PubMed: 37646022
DOI: 10.3389/fimmu.2023.1180908 -
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 -
Frequency of Odontogenic Tumors: A Single Center Study of 1089 Cases in Japan and Literature Review.Head and Neck Pathology Jun 2022Several attempts have been made to classify odontogenic tumors; however, the need for a uniform international classification system led the World Health Organization... (Review)
Review
Several attempts have been made to classify odontogenic tumors; however, the need for a uniform international classification system led the World Health Organization (WHO) to present a classification of odontogenic tumors in 1971. We aimed to evaluate the number and types of odontogenic tumors examined at the Tokyo Dental College Hospital in Japan to determine the frequency and types of odontogenic tumors, based on the 2017 WHO classification system, as this information has not been reported previously in Japan. We also compared the results of our evaluation with those reported in previous studies. We conducted a clinicopathological evaluation of odontogenic tumors examined at the Tokyo Dental College Hospital between 1975 and 2020. This included an analysis of 1089 cases (malignant, n = 10, 0.9%; benign, n = 1079, 99.1%) based on the 2017 World Health Organization Classification of Head and Neck Tumors. We identified 483 (44.3%), 487 (44.7%), and 109 (10.0%) benign epithelial odontogenic, mixed odontogenic, and mesenchymal tumors, respectively. The most common tumor types were odontoma (42.5%) and ameloblastoma (41.9%). Of the 1089 cases, 585 (53.7%) and 504 (46.3%) were male and female patients, respectively. Ameloblastoma and ameloblastic fibroma occurred more commonly in male patients, whereas odontogenic fibroma and cemento-ossifying fibroma affected female patients primarily. The age at diagnosis ranged from three to 87 (mean, 29.05) years. In 319 (29.3%) patients, the age at diagnosis ranged from 10 to 19 years. Ameloblastoma and odontoma were the most common tumor types among patients in their 20s and those aged 10-19 years, respectively. In 737 (67.7%) and 726 (66.7%) patients, the tumors were located in the mandible and posterior region, respectively. Ameloblastoma was particularly prevalent in the posterior mandible. Odontogenic tumors are rare lesions and appear to show a definite geographic variation.
Topics: Ameloblastoma; Female; Fibroma, Ossifying; Humans; Japan; Male; Odontogenic Tumors; Odontoma; Retrospective Studies
PubMed: 34716904
DOI: 10.1007/s12105-021-01390-w -
International Journal of Environmental... Apr 2021Ameloblastic carcinoma is a rare malignant odontogenic neoplasm with a poor prognosis. It can arise de novo or from a pre-existing ameloblastoma. Research into stemness...
Ameloblastic carcinoma is a rare malignant odontogenic neoplasm with a poor prognosis. It can arise de novo or from a pre-existing ameloblastoma. Research into stemness marker expression in ameloblastic tumours is lacking. This study aimed to explore the immunohistochemical expression of stemness markers nestin, CD138, and alpha-smooth muscle actin (alpha-SMA) for the characterisation of ameloblastic tumours. Six cases of ameloblastoma and four cases of ameloblastic carcinoma were assessed, including one case of ameloblastic carcinoma arising from desmoplastic ameloblastoma. In all tumour samples, CD138 was positive, whilst alpha-SMA was negative. Nestin was negative in all but one tumour sample. Conversely, the presence or absence of these markers varied in stroma samples. Nestin was observed in one ameloblastic carcinoma stroma sample, whilst CD138 was positive in one ameloblastoma case, one desmoplastic ameloblastoma case, and in two ameloblastic carcinoma stroma samples. Finally, alpha-SMA was found positive only in the desmoplastic ameloblastoma stroma sample. Our results suggest nestin expression to be an indicator for ameloblastic carcinoma, and CD138 and alpha-SMA to be promising biomarkers for the malignant transformation of ameloblastoma. Our data showed that nestin, CD138, and alpha-SMA are novel biomarkers for a better understanding of the origins and behaviour of ameloblastic tumours.
Topics: Actins; Ameloblastoma; Biomarkers; Humans; Mandibular Neoplasms; Nestin
PubMed: 33917771
DOI: 10.3390/ijerph18083899