Disease relevance of Ameloblastoma

• Beta-catenin mutations are frequent in calcifying odontogenic cysts, but rare in ameloblastomas [1].
• In addition, prostaglandin E2 assay revealed that ameloblastoma produces prostaglandin E2, which results in hypercalcemia [2].
• The term unicystic ameloblastoma refers to those cystic lesions that show clinical, radiographic, or gross features of a jaw cyst, but on histologic examination show a typical ameloblastomatous epithelium lining part of the cyst cavity, with or without luminal and/or mural tumor growth [3].
• We report an unusual case of metastatic ameloblastoma, involving lung and pleura. that repeatedly responded to systemic treatment with paclitaxel and carboplatin. suggesting principle chemosensitivity of this rare disease [4].
• No intracellular staining for enamelysin was detected in ameloblastomas or the ameloblastic portion of ameloblastic fibro-odontomas [5].

High impact information on Ameloblastoma

• No beta-catenin mutations were found in ameloblastomas, except for one case of the follicular type [1].
• Immunohistochemical analysis was performed to determine the localization of epidermal growth factor receptor (EGFR) in ameloblastomas [6].
• Positive (99mTc) diphosphonate and 67 Ga-citrate scans in ameloblastoma: case report [7].
• Technetium-99m-diphosphonate scintigrams and 67Ga citrate bone scans were performed in a patient with known ameloblastoma of the right mandible [7].
• The aim of this study was to investigate whether genetic alterations of CTNNB1 and PTCH1 are present in ameloblastoma [8].

Chemical compound and disease context of Ameloblastoma

• Metastatic malignant ameloblastoma responding to chemotherapy with paclitaxel and carboplatin [4].
• A case of metastatic ameloblastoma is presented which was resistant to treatment with adriamycin (doxorubicin), platinol (cis-platinum), cytoxan (cyclophosphamide), dacarbazine (DTIC), and 5-fluorouracil (5-FU) [9].
• METHODS AND RESULTS: Immunohistochemistry was carried out to detect different MMPs in formalin-fixed paraffin-embedded samples of human ameloblastoma [10].
• In the plexiform ameloblastoma, dental germ and lamina integrin staining was uniform [11].
• Oxytalan fibers stained by potassium monopersulfate-aldehyde fuchsin were demonstrated in the stroma of all desmoplastic ameloblastomas [12].

Biological context of Ameloblastoma

• K-Ras gene status and expression of Ras/mitogen-activated protein kinase (MAPK) signaling molecules in ameloblastomas [13].
• Cyclin D1 was expressed in epithelial cells near the basement membrane in tooth germs and ameloblastomas, suggesting that this protein participates in cell proliferation in odontogenic epithelium [14].
• Direct DNA sequencing showed a GGT to GCT point mutation at codon 12 of K-Ras gene in one ameloblastoma [13].
• BACKGROUND: To clarify the possible role of apoptotic cell death in oncogenesis and cytodifferentiation of odontogenic epithelium, apoptosis-related factors--Fas, Fas ligand (FasL), caspase-3 and single-stranded DNA (ssDNA)--were analyzed in ameloblastomas as well as in tooth germs [15].
• BACKGROUND: To clarify the roles of the p53-MDM2-p14(ARF) cell cycle regulation system in oncogenesis and cytodifferentiation of odontogenic tumors, p53 gene status and expression of p53, MDM2, and p14(ARF) proteins was analyzed in ameloblastomas as well as tooth germs [16].

Anatomical context of Ameloblastoma

• Inducible NO synthase (iNOS) and heat shock proteins (HSPs) were analyzed in ameloblastomas as well as in tooth germs [17].
• Immunoreactivity for p16 protein was observed in most epithelial cells in tooth germs and ameloblastomas [14].
• TIMP-2 reactivity was prominently found in basement membrane zones of dental laminae in tooth germs, and tumor cell islands or nests in ameloblastomas [18].
• All ameloblastoma samples were positive for telomerase activity, and TERT expression was detected in the nuclei of neoplastic cells but not in those of stromal cells [19].
• RESULTS: Immunohistochemical reactivity for beta-catenin was detected in the cell membrane and cytoplasm of most odontogenic epithelial cells in tooth germs and ameloblastomas [20].

Gene context of Ameloblastoma

• Human ameloblastomas express AMBN transcripts that contain some mutations [21].
• In ameloblastomas, expression of p53, MDM2, and p14(ARF) was significantly higher in plexiform cases than in follicular cases [16].
• MVD tended to depend on VEGF expression levels in both benign and malignant ameloblastomas [22].
• In ameloblastomas, these SHH signaling molecules were expressed more intensely in peripheral columnar or cuboidal cells than in central polyhedral cells; keratinizing cells and granular cells showed no or little reactivity [23].
• Tumor cells in plexiform ameloblastomas showed slightly higher reactivity for PTHrP and ODF/RANKL than tumor cells in follicular ameloblastomas [24].

Analytical, diagnostic and therapeutic context of Ameloblastoma

• Use of calretinin in the differential diagnosis of unicystic ameloblastomas [25].
• RT-PCR, Southern blotting and DNA sequencing have established for the first time that tuftelin mRNA is expressed in human ameloblastoma tumor [26].
• In the present study, expressions of TRAIL receptors, death receptor 4 (DR4) and DR5, were detected in all ameloblastoma tissues by immunohistochemistry as well as in AM-1 cells by immunofluorescence [27].
• Immunohistochemistry and in situ hybridization of heparanase were carried out in 23 ameloblastomas [28].
• In this study, we analyzed amelogenin gene expression in 19 samples (9 male, 10 female) of oral ameloblastomas by RT-PCR and detect the chromosomal origin of amelogenin mRNA by restriction enzyme digestion of the RT-PCR product [29].

References