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Displaying publications 21 - 29 of 29 in total

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Patterns of expression of intermediate filaments and S-100 protein in desmoplastic ameloblastoma

Siar CH, Ng KH

J Nihon Univ Sch Dent, 1993 Jun;35(2):104-8.
PMID: 7692015

Seventeen cases of desmoplastic ameloblastoma were examined immunohistochemically. Immunoperoxidase techniques were applied for detection of keratin, desmin, vimentin and S-100 protein expression in these tumors. The tumor epithelium of desmoplastic ameloblastoma exhibited weak, focal, inconstant keratin staining, weak, variable expression of S-100 protein, desmin immunoreactivity of mild to moderate intensity and vimentin non-reactivity. The pertinent literature on the immunohistochemistry of ameloblastomas is briefly reviewed.

Matched MeSH terms: Ameloblastoma/pathology
Fulltext Ameloblastomas--a clinicopathologic study of 133 cases in peninsular Malaysia

Ramanathan K, Chelvanayagam PI, Ng KH, Ramanathan J

Med J Malaysia, 1982 Mar;37(1):18-24.
PMID: 7121342

Ameloblastomas formed 1.1 percent of all oral pathology cases reported. The race, sex and age group distribution of 133 cases are shown. The peak age incidence (70.6 percent) was between 11-40 years. The mandible was involved 9 times more commonly than the maxilla. The anatomical sites of distribution, clinical and radiological features, histological variants and their correlation are discussed. Twenty two patients (15 percent) had ameloblastomas associated with a dentigerous cyst and/or unerupted teeth. Ameloblastomas with the above clinical features represented a much less aggressive form of neoplasm. The authors could not correlate histological variants of ameloblastoma with recurrence rates. The various treatment methods and the respective recurrence rates are outlined. Radiotherapy and marsupialization as treatment of ameloblastoma are not recommended. The indications for enucleation curettage, resection en bloc, segmental resection and hemimandibulectomy
are emphasized. Ameloblastomas involving the maxilla should be treated by complete removal en bloc with a margin of normal tissue. Since ameloblastoma has the capacity to recur after several years of apparent cure patients who have been treated for ameloblastoma must be followed up periodically during their life time. So far no case of ameloblastoma in this study has shown evidence
ofmetastasis.

Matched MeSH terms: Ameloblastoma/pathology*
Premolar Cystic Ameloblastoma in a Child

Pathak S, Sonalika WG, Hs V, Tegginammani AS

J Coll Physicians Surg Pak, 2017 Jan;27(1):47-48.
PMID: 28292369 DOI: 2521

Mandibular swellings may occur as a result of many benign lesions of odontogenic or non-odontogenic origin. Ameloblastomas are benign tumours of odontogenic origin, whose importance lies in its potential to grow into enormous size with resulting bone deformity, it is a slow-growing, persistent, and locally aggressive neoplasm. The unicystic ameloblastoma (UA) represents an ameloblastoma variant, presenting as a cyst clinically and radiographically, but showing typical ameloblastomatous epithelium lining histologically. It commonly occurs in second and third decades of life and is rare in children under 12 years of age, and better response to conservative treatment. It shares many clinical and radiographic features with odontogenic cysts/tumours and/or periapical disease of endodontic origin. Reported here is an unusual case of unicystic ameloblastoma involving the crown of an unerupted mandibular first premolar in a 9-year boy in an uncommon location, which was misdiagnosed as periapical lesion of inflammatory origin clinically, and as a dentigerous cyst radiographically. This highlights the importance to routinely submit the removed surgical specimen for histopathological examination.

Matched MeSH terms: Ameloblastoma/pathology*
Podoplanin, E-cadherin, β-catenin, and CD44v6 in recurrent ameloblastoma: their distribution patterns and relevance

Siar CH, Ishak I, Ng KH

J Oral Pathol Med, 2015 Jan;44(1):51-8.
PMID: 25059841 DOI: 10.1111/jop.12203

Ameloblastoma is a benign but locally infiltrative odontogenic epithelial neoplasm with a high risk for recurrence. Podoplanin, a lymphatic endothelium marker, putatively promotes collective cell migration and invasiveness in this neoplasm. However, its role in the recurrent ameloblastoma (RA) remains unclear. As morphological, signaling, and genetic differences may exist between primary and recurrent tumors, clarification of their distribution patterns is of relevance.

Matched MeSH terms: Ameloblastoma/pathology
Differential expression of transcription factors Snail, Slug, SIP1, and Twist in ameloblastoma

Siar CH, Ng KH

J Oral Pathol Med, 2014 Jan;43(1):45-52.
PMID: 23560539 DOI: 10.1111/jop.12065

Epithelial-to-mesenchymal transition (EMT) via the mechanism of transcription repression is a crucial process for the induction of invasiveness in many human tumors. Ameloblastoma is a benign odontogenic epithelial neoplasm with a locally infiltrative behavior. Twist, an EMT promoter, has been implicated in its invasiveness. The roles of the other transcription factors remain unclarified.

Matched MeSH terms: Ameloblastoma/pathology
Notch4 overexpression in ameloblastoma correlates with the solid/multicystic phenotype

Siar CH, Nagatsuka H, Chuah KS, Rivera RS, Nakano K, Ng KH, et al.

Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2010 Aug;110(2):224-33.
PMID: 20659700 DOI: 10.1016/j.tripleo.2010.03.009

Notch signaling has been implicated in cell fate decisions during odontogenesis and tumorigenesis of some odontogenic neoplasms; however, its role in solid/multicystic (SA), unicystic (UA), and recurrent (RA) ameloblastoma remains unclear. The aim of this study was to determine Notch receptor and ligand expressions in these subtypes and to speculate on their significance.

Matched MeSH terms: Ameloblastoma/pathology
Differential expression of Notch receptors and their ligands in desmoplastic ameloblastoma

Siar CH, Nakano K, Han PP, Nagatsuka H, Ng KH, Kawakami T

J Oral Pathol Med, 2010 Aug 1;39(7):552-8.
PMID: 20337864 DOI: 10.1111/j.1600-0714.2009.00871.x

In mammals, the Notch gene family encodes four receptors (Notch1-4), and all of them are important for cell fate decisions. Notch signaling pathway plays an essential role in tooth development. The ameloblastoma, a benign odontogenic epithelial neoplasm, histologically recapitulates the enamel organ at bell stage. Notch has been detected in the plexiform and follicular ameloblastoma. Its activity in the desmoplastic ameloblastoma is unknown.

Matched MeSH terms: Ameloblastoma/pathology*
Parenchyma-stromal interactions induce fibrosis by secreting CCN2 and promote osteoclastogenesis by stimulating RANKL and CD68 through activated TGF-β/BMP4 in ameloblastoma

Takebe Y, Tsujigiwa H, Katase N, Siar CH, Takabatake K, Fujii M, et al.

J Oral Pathol Med, 2017 Jan;46(1):67-75.
PMID: 27327904 DOI: 10.1111/jop.12467

BACKGROUND: Tumor parenchyma-stromal interactions affect the properties of tumors and their dynamics. Our group previously showed that secreted frizzled related protein (sFRP)-2 impairs bone formation and promotes bone invasion in ameloblastoma. However, the effects of the secreted growth factors CCN2, TGF-β, and BMP4 on stromal tissues in ameloblastoma remain unclear.
MATERIALS AND RESULTS: Thirty-five paraffin-embedded ameloblastoma cases, ameloblastoma-derived cell lines (AM-1), and primary cultures of ameloblastoma stromal fibroblasts (ASF) were used. Immunohistochemistry, MTT assay, Western blotting, and RT-PCR were performed on these samples. Parenchyma-stromal CCN2 overexpression correlated significantly with fibrous-type stroma, but not with myxoid-type stroma, suggesting a role of CCN2 in fibrosis (P < 0.05). Recombinant CCN2 induction of enhanced ASF proliferation in AM-1 medium supports this view. Conversely, BMP4 and TGF-β were expressed in myxoid-type fibroblasts, but little expression was found in parenchyma. RANKL-positive and CD68-positive stromal cell populations were significantly greater in myxoid-type tumor areas than in fibrous-type tumor areas, while a higher Ki-67 labeling index was recorded in ameloblastoma with fibrous-type stroma. These data suggest that stromal properties influence bone resorption-related activities and growth rates, respectively.
CONCLUSIONS: These results suggest that the effects of secreted growth factors are governed by ameloblastoma parenchyma-stromal interactions. CCN2 promotes fibrogenesis independent of TGF-β signaling. Absence of CCN2 expression is associated with a phenotypic switch to a myxoid-type microenvironment that is conducive for TGF-β/BMP4 signaling to promote osteoclastogenesis.

Matched MeSH terms: Ameloblastoma/pathology
Invadopodia proteins, cortactin, N-WASP and WIP differentially promote local invasiveness in ameloblastoma

Siar CH, Rahman ZA, Tsujigiwa H, Mohamed Om Alblazi K, Nagatsuka H, Ng KH

J Oral Pathol Med, 2016 Sep;45(8):591-8.
PMID: 26752341 DOI: 10.1111/jop.12417

BACKGROUND: Cell migration and invasion through interstitial tissues are dependent upon several specialized characteristics of the migratory cell notably generation of proteolytic membranous protrusions or invadopodia. Ameloblastoma is a benign odontogenic epithelial neoplasm with a locally infiltrative behaviour. Cortactin and MMT1-MMP are two invadopodia proteins implicated in its local invasiveness. Other invadopodia regulators, namely N-WASP, WIP and Src kinase remain unclarified. This study addresses their roles in ameloblastoma.
MATERIALS AND METHOD: Eighty-seven paraffin-embedded ameloblastoma cases (20 unicystic, 47 solid/multicystic, 3 desmoplastic and 17 recurrent) were subjected to immunohistochemistry for expression of cortactin, N-WASP, WIP, Src kinase and F-actin, and findings correlated with clinicopathological parameters.
RESULTS: Invadopodia proteins (except Src kinase) and F-actin were widely detected in ameloblastoma (cortactin: n = 73/87, 83.9%; N-WASP: n = 59/87; 67.8%; WIP: n = 77/87; 88.5%; and F-actin: n = 87/87, 100%). Protein localization was mainly cytoplasmic and/or membranous, and occasionally nuclear for F-actin. Cortactin, which functions as an actin-scaffolding protein, demonstrated significantly higher expression levels within ameloblastoma tumoral epithelium than in stroma (P < 0.05). N-WASP, which coordinates actin polymerization and invadopodia-mediated extracellular matrix degradation, was overexpressed in the solid/multicystic subtype (P < 0.05). WIP, an upstream regulator of N-WASP, and F-actin were significantly upregulated along the tumour invasive front compared to tumour centres (P < 0.05). Except for males with cortactin overexpression, other clinical parameters (age, ethnicity and anatomical site) showed no significant correlations.
CONCLUSIONS: Present results suggest that local invasiveness of ameloblastoma is dependent upon the migratory potential of its tumour cells as defined by their distribution of cortactin, N-WASP and WIP in correlation with F-actin cytoskeletal dynamics.

Matched MeSH terms: Ameloblastoma/pathology