Immunohistochemical detection of amelogenin and cytokeratin 19 in epithelial odontogenic tumors

Kumamoto, Hiroyuki; Yoshida, Mitsuhide; Ooya, Kiyoshi

doi:10.1034/j.1601-0825.2001.70306.x

Cited by 61 publications

(44 citation statements)

References 27 publications

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“…CK19 is thought to be an odontogenic epithelium marker as it is used frequently in tumors of odonotogenic origin, such as ameloblastoma, odontogenic myxoma and clear cell odontogenic carcinoma (23,26). In this study, OKC showed an intense expression of CK19 in the parakeratinized cells and upper suprabasal cells of the epithelial lining, but CK19 did not found in OOC and EDC.…”

Section: Discussionmentioning

confidence: 63%

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Odontogenic Keratocyst, Orthokeratinized Odontogenic Cyst and Epidermal Cyst: An Immunohistochemical Study Including Markers of Proliferation, Cytokeratin and Apoptosis Related Factors

Koizumi

2004

Int J Oral-Med Sci

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Objective: There are microscopic similarities among odontogenic keratocyst (OKC), orthokeratinized odontogenic keratocyst (DOC) and epidermal cyst (EDC). This study was to compare with cell proliferation, cell differentiation and apoptosis related factors in OKC, DOC and EDC in order to clarify the characters and category of three hitstopathologically similar cysts.Material and Methods: Fourteen cases of OKC, nine cases of DOC and eighteen cases ofEDC were examined immunohistochemically using antibodies against cytokeratins (CK7,10, 10/13,17,18,19,20) and apoptosis related factors (bcl-2 and Bax).Results: Ki-67 labeling index in OKC was statistically higher than that in DOC and EDC (p<0.05). And that in DOC was higher in EDC (p<0.05). In OKC, CKs and bcl-2 expression patterns were different from DOC and EDC, while both DOC and EDC showed similar reactivity with CKs and bcl-2.Conclusions: The present results suggested that OKC had high cellular proliferation and was relatively low differentiation as compare with DOC and EDC. In addition, there was participation of apoptosis suppressor in OKC. The character of DOC occupied an intermediate position between OKC and EDC. Therefore, it was possible to consider DOC as a distinct entity from OKC. EDC had the lowest cellular activity in the three cysts and it was comparatively maturated lesion.

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Section: Discussionmentioning

confidence: 63%

“…Overexpression of Bax homodimers increases the susceptibility of the cells to apoptosis (26,31). Since the present results indicate that Bax was expressed in most cases of OKC, OOC and EDC, Bax might contribute of keratinization.…”

Section: Discussionmentioning

confidence: 99%

Odontogenic Keratocyst, Orthokeratinized Odontogenic Cyst and Epidermal Cyst: An Immunohistochemical Study Including Markers of Proliferation, Cytokeratin and Apoptosis Related Factors

Koizumi

2004

Int J Oral-Med Sci

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“…9,11,14 The origin of amyloid in human CEOT and animal APOT has been studied. 19,20,29,32,37,42,43 The amyloid of canine and feline APOT did not react immunohistochemically with antibodies to human cytokeratins, human vimentin, chicken desmin, laminin, human collagen (types I, III, IV), or amyloid A; the neoplastic epithelial cells reacted only with anti-human cytokeratins. 29 Breuer et al 2 evaluated animal APOTs immunohistochemically with a panel of antibodies to amyloid A (AA protein), immunoglobulin light chain protein in amyloidosis (AL protein), amyloid protein in familial amyloidotic polyneuropathy (AF protein), amyloid fibril proteins in senile cardiac amyloid (ASc1 protein), amyloid b protein in senile plaque amyloid (AB protein), cytokeratins, vimentin, desmin, and laminin and suggested that the amyloid in CEOT was epithelial in origin based on the exclusive immunoreaction to anticytokeratin and antilaminin 2 Another investigator reported that the neoplastic epithelial cells expressed cytokeratins AE1/AE3, neuron-specific enolase, and S-100 protein but that the amyloid deposits did not express cytokeratins AE1/AE3.…”

Section: Discussionmentioning

confidence: 99%

“…32 Immunohistochemical detection of amelogenin in the human CEOT showed only feeble reactivity to intercellular amyloid-like material. 20,27 Takata et al 42 examined the immunohistochemical localization of sheathlin in 5 cases of the human CEOT; neither the amyloid nor the neoplastic cells reacted with antisheathlin antibody. 42 In the present study, the immunohistochemical characteristics of amyloid in canine APOT are clearly different from those in human CEOT.…”

Section: Discussionmentioning

confidence: 99%

Biochemical and Immunohistochemical Characterization of the Amyloid in Canine Amyloid-Producing Odontogenic Tumor

Hirayama

Miyasho

Ohmachi³

et al. 2010

Vet Pathol

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The amyloid of canine amyloid-producing odontogenic tumor (APOT) was evaluated biochemically and immunohistochemically. The N-terminal amino-acid sequence of purified amyloid protein from a canine APOT was strikingly similar to the sequence in both rat ameloblastin and porcine sheathlin. Immunohistochemically, the amyloid in APOT from 9 dogs was strongly reactive with anti-rat ameloblastin, anti-porcine sheathlin, and anti-canine APOT amyloid and weakly reactive with anti-porcine amelogenin but negative for antibodies to cytokeratins, vimentin, desmin, a-smooth muscle actin, amyloid A, glial fibrillary acidic protein, or S100 protein. The neoplastic epithelial cells of APOT were focally reactive with antibodies to ameloblastin, sheathlin, amelogenin, and canine APOT amyloid. The similarity in amino-acid sequence of the amyloid protein of canine APOT to that of enamel proteins, such as ameloblastin, sheathlin, and amelogenin, and the expression of these antigens in both APOT amyloid and in the neoplastic cells suggest that the amyloid of canine APOT is derived from enamel proteins secreted by ameloblasts. Keywords ameloblasts, amyloid, dogs, enamel proteins, odontogenic tumorAmyloidosis is a heterogeneous group of disorders characterized by the deposition of amyloid proteins derived from any of at least 25 different precursor molecules. Amyloid is considered a pathologic substance that appears histologically as an extracellular, amorphous, congophilic protein with applegreen birefringence under polarized light. Amyloidosis can be categorized as systemic or localized. Common human types of localized amyloidosis include amyloidosis of endocrine organs associated (or not) with neoplastic conditions and cerebral amyloidosis of Alzheimer's disease. 21,51 Localized amyloid deposits with or without association with neoplasia also have been described in the human mammary gland, 41,52 respiratory tract, 26,34 gastrointestinal tract, 5,38 genitourinary tract, 13,17 skin, 24,25 and bone. 23 In animals, localized amyloidosis has been associated with neoplastic conditions such as calcifying epithelial odontogenic tumor (CEOT), 2,29 pancreatic endocrine tumor, 28 medullary thyroid carcinoma, 15 ameloblastoma, 10 mammary carcinoma, 43 intestinal carcinoid, 40 extramedullary plasmacytoma, 31,36 and myeloma. 12 CEOT is a rare neoplasm of the tooth-forming apparatus that produces a mineralized substance and amyloid. 30 The origin of the amyloid in human and animal CEOT is often debated but is still unknown. 2,19,27,29,37,42,46 Recent studies indicate that the amyloid in human CEOT is secreted by the neoplastic epithelial cells, but its precise nature remains unclear. 27,39,42 CEOT in veterinary medicine is classified as amyloidproducing odontogenic tumor (APOT). 9,14 In the present study, we partially sequenced the amino acids of the major amyloid protein of canine APOT and compared the amino-terminal sequence with that of the enamel proteins rat ameloblastin and porcine sheathlin, which are transcribed in cells of the epi...

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“…3,12 Although the molecular and genetic characteristics of ameloblastomas are poorly understood, the cloning and characterization of expression of the ameloblastin and amelogenin genes in these tumors supports the hypothesis that ameloblastomas arise from the from dental lamina, the outer enamel epithelium or the inner enamel epithelium. 13,14 Chromosomal imbalances in ameloblastomas are reported to be rare with losses in chromosomes 22 and 10 being most frequently described. 15,16 Aneuploidy is more common in ameloblastic carcinomas than ameloblastomas and may predict malignant potential.…”

Section: Discussionmentioning

confidence: 99%

Allelic loss of tumor suppressor genes in ameloblastic tumors

et al. 2004

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Ameloblastoma is an odontogenic tumor with a variety of histologic appearances and an unpredictable biologic behavior. Little is known about allelic losses of tumor suppressor genes in ameloblastomas. This study surveyed DNA damage in ameloblastomas and correlated this with histologic sub-type and clinical outcome. There were 12 ameloblastomas (two peripheral, eight solid, and two unicystic) and three ameloblastic carcinoma studied for loss of heterozygosity of tumor suppressor genes on chromosomes 1p, 3p, 9p,10q, and 17p (L-myc, hOGG1, p16, pten, and p53). The frequency of allelic loss and the intratumoral heterogeneity were calculated. L-myc (71% frequency of allelic loss) and pten (62% frequency of allelic loss) had the most frequent allelic losses. Overall frequency of allelic loss and intratumoral heterogeneity were higher in mandibular and in unicystic tumors and lower in tumors that recurred/metastasized. The rate of allelic loss in the three carcinomas was similar to that seen in benign tumors. The frequency of allelic loss and intratumoral heterogeneity did not correlate with age, gender, histologic subtype, or prognosis. Since tumors that behaved aggressively did not harbor more allelic losses, it is likely that DNA damage in ameloblastomas and ameloblastic carcinomas is sporadic and cumulative. We conclude that other genetic or epigenetic mechanisms may be responsible for malignant behavior in ameloblastic carcinomas.

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Immunohistochemical detection of amelogenin and cytokeratin 19 in epithelial odontogenic tumors

Abstract: Diverse types of epithelial odontogenic tumors express amelogenin and CK19, suggesting that these tumors have ameloblastic differentiation or odontogenic epithelial properties.

Cited by 61 publications

References 27 publications

Odontogenic Keratocyst, Orthokeratinized Odontogenic Cyst and Epidermal Cyst: An Immunohistochemical Study Including Markers of Proliferation, Cytokeratin and Apoptosis Related Factors

Odontogenic Keratocyst, Orthokeratinized Odontogenic Cyst and Epidermal Cyst: An Immunohistochemical Study Including Markers of Proliferation, Cytokeratin and Apoptosis Related Factors

Biochemical and Immunohistochemical Characterization of the Amyloid in Canine Amyloid-Producing Odontogenic Tumor

Allelic loss of tumor suppressor genes in ameloblastic tumors

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