ameloblastoma/phosphatase

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Role of phosphatase and tensin homolog in pathogenesis of ameloblastoma: An immunohistochemical study

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Background: Altered molecular signaling pathways in ameloblastoma have been identified to play a pivotal role in the mechanism of oncogenesis, differentiation, and tumor progression. Phosphatidylinositol 3-kinase/protein kinase

[Growth phenomena of jaw ameloblastomas].

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Jaw ameloblastomas produce most frequently (62%) multilocular translucences. An unilocular translucence was observed in 28% of the cases. In both forms, secondary cysts were present. This radiomorphologic finding is of pathognomonic value. Conchiform or finger-shaped translucences were seen in 10%

Histoenzymological features of epithelial cells in lesions of oral mucosa in cysts and ameloblastomas of jaws.

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A histoenzymological study was carried out on 41 tissue specimens removed at biopsy and for surgical operations of the following lesions: benign hyperkeratosis, lichen planus, severe epithelial dysplasia, carcinoma in situ, epidermoid carcinoma, radicular cyst, odontogenic keratocyst and

Surface vacuolar ATPase in ameloblastoma contributes to tumor invasion of the jaw bone.

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Ameloblastoma is the most common benign odontogenic tumor in Japan. It is believed that it expands in the jaw bone through peritumoral activation of osteoclasts by receptor activator of nuclear factor kappa-B ligand (RANKL) released from the ameloblastoma, as in bone metastases of cancer cells.

Expression and alterations of the PTEN / AKT / mTOR pathway in ameloblastomas.

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OBJECTIVE Recently, an allelic loss of phosphatase and tensin homologue (PTEN) was shown to occur in ameloblastomas. In carcinogenesis, loss of PTEN allows for overactivity of the phosphatidylinositol-3-kinase/protein kinase B (PI3K / AKT) pathway inducing an upregulation of mammalian-target of

[Odontogenic induction and ameloblastoma. Histoenzymological and ultrastructural studies (author's transl)].

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The ameloblastoma is usually thought to be devoid of any odontogenic capacity. However, the histological, ultrastructural and histoenzymological study of 5 cases demonstrates the fairly high level of differentiation of some ameloblastic cells in such neoplasms. Furthermore, it suggests very early

Osteogenic genes related to the canonic WNT pathway are down-regulated in ameloblastoma.

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OBJECTIVE The aim of this study was to determine the expression of essential osteogenic genes related to the canonic WNT pathway, i.e., WDR5, sFRP-2, and their downstream genes, in ameloblastoma and to clarify their biologic impact on this neoplasm. METHODS Forty-six paraffin-embedded ameloblastoma

Genetic alteration of Exon 5 of the PTEN gene in Indian patients with ameloblastoma.

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The PI3K/Akt/mTOR pathway is one of the signaling pathways associated with the pathogenesis of ameloblastoma. The phosphatase and tensin (PTEN) homologue controls cell migration and proliferation. It monitors the level of Akt and maintains cellular integrity. The aim of the present

Giant cell reaction to ameloblastoma: an immunohistochemical and ultrastructural study of a case.

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Histopathologic, immunohistochemical, and ultrastructural features of the giant cells appearing in the tissue surrounding an ameloblastoma are presented. These giant cells exhibited strong activity of a highly stable form of acid phosphatase, and were positive for alpha-1-antichymotrypsin.

Histoenzymological features of epithelial cells in epidermoid carcinomas of oral mucosa and in ameloblastomas of jaws.

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An histoenzymological study comprising oxidative enzymes, diaphorases, acid and alkaline phosphatases, naphtolesterases, referred to 60 biopsy and operation specimens. It showed interesting arguments for diagnosis and understanding of precancerous and cancerous lesions of the oral mucosa and also of

An electron-microscopic and cytochemical study of follicular ameloblastoma.

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The ultrastructural and enzyme cytochemical features of two follicular ameloblastomas were investigated. The peripheral cells of the follicular areas in both lesions had several types of tall columnar cells which were highly polarized and showed varying degrees of cellular differentiation. These

Ultrastructural and histochemical studies of granular-cell ameloblastoma.

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Four cases of granular-cell ameloblastoma were studied by light and electron microscopy, histochemistry and electron enzyme histochemistry. Microscopically, granular cells commonly occurred in a follicular pattern, but, in one case, they were in a plexiform pattern. The high activity of acid

Investigation of PTEN promoter methylation in ameloblastoma.

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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

Secreted frizzled related protein (sFRP)-2 inhibits bone formation and promotes cell proliferation in ameloblastoma.

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Secreted frizzled related protein (sFRP)-2, a Wnt antagonist, was strongly expressed by both stromal and tumor cells of ameloblastoma. The aim of this study is to evaluate whether sFRP-2 secreted from tumor cells have any direct role in suppressed bone formation or not. A pre-osteoblastic cell line,

Isozyme phenotypes of polyoma virus tumors in mice.

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Isozyme profiles for 32 enzyme systems were studied in tumors induced by two strains of polyoma virus (2PTA and LID1), in two conventional mouse strains (C3H/BiDa and NIH), and in athymic (nude) mice of two genetic backgrounds (C3H/Hes nu/nu and NIH nu/nu). Tumors studied were: primary and

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