Primordial odontogenic tumor: An immunohistochemical profile.

BACKGROUND: Primordial Odontogenic Tumor (POT) is a recently described odontogenic tumor characterized by a variably cellular loose fibrous tissue with areas similar to the dental papilla, covered by cuboidal to columnar epithelium that resembles the internal epithelium of the enamel organ, surrounded at least partly by a delicate fibrous capsule. The purpose of this study was to investigate the possible histogenesis and biological behavior of this rare tumor by means of a wide immunohistochemical analysis of its epithelial and mesenchymal components. MATERIAL AND METHODS: The immunoexpression of twenty-three different antibodies were evaluated in four cases of POT. RESULTS: The epithelial cells that cover the periphery of the tumor showed immunopositivity for Cytokeratins 14 and 19, while Amelogenin, Glut-1, MOC-31, Caveolin-1. Galectin-3, PITX2, p53, Bax, Bcl-2, Survivin and PTEN were variably expressed in focal areas. The mesenchymal component of the tumor was positive for Vimentin, Syndecan-1, PITX2, Endoglin (CD105), CD 34, Cyclin D1, Bax, Bcl-2, Survivin and p53. PTEN and CD 90 showed a moderate positivity. BRAF V600E and Calretinin were negative in all samples. Cell proliferation markers (Ki-67, MCM-7) were expressed in <5% of the tumor cells. CONCLUSIONS: According to these immunohistochemical findings, we may conclude that POT is a benign odontogenic tumor in which there is both epithelial and mesenchymal activity during its histogenesis, as there is expression of certain components in particular zones in both tissues that suggests this tumor develops during the immature (primordial) stage of tooth development, leading to its inclusion within the group of benign mixed epithelial and mesenchymal odontogenic tumours in the current World Health Organization classification of these lesions.

Comparative histological and immunohistochemical study of ameloblastomas and ameloblastic carcinomas.

BACKGROUND: This study aimed to compare the histological and immunohistochemical characteristics of ameloblastomas (AM) and ameloblastic carcinomas (AC). MATERIAL AND METHODS: Fifteen cases of AM and 9 AC were submitted to hematoxilin and eosin (H&E) and immunohistochemical analysis with the following antibodies: cytokeratins 5,7,8,14 and 19, Ki-67, p53, p63 and the cellular adhesion molecules CD138 (Syndecan-1), E-cadherin and ß-catenin. The mean score of the expression of Ki-67 and p53 labelling index (LIs) were compared between the groups using the t test. A value of p<0.05 was considered to be statistically significant. RESULTS: All cases were positive for CKs 5, 14 and 19, but negative for CKs 7 and 8. CKs 5 and 19 were positive mainly in the central regions of the ameloblastic islands, while the expression in AC was variable in intensity and localization. CK14 was also variably expressed in both AM and AC. Ki-67 (P=.001) and p53 (P=.004) immunoexpression was higher in AC. All cases were positive for p63, but values were higher in AC. CD138 was mainly expressed in peripheral cells of AM, with a weak positivity in the central areas, while it was positive in most areas of ACs, except in less differentiated regions, where expression was decreased or lost. E-cadherin and ß-catenin were weakly positive in both AM and AC. CONCLUSIONS: These results shows that Ki-67, p53 and p63 expression was higher in AC as compared to AM, suggesting that these markers can be useful when considering diagnosis of malignancy, and perhaps could play a role in malignant transformation of AM. Pattern of expression of CKs 5 and 19 in AC were different to those found in AM, suggesting genetic alterations of these proteins in malignant cells. It was confirmed that CK19 is a good marker for benign odontogenic tumors, such as AM, but it is variably expressed in malignant cases.

ESEM Detection of Foreign Metallic Particles inside Ameloblastomatous Cells.

Ameloblastoma is a borderline tumor of odontogenic origin, with a high recurrence rate and possible local aggressiveness. The etiopathogenetic factors involved in its occurrence are not still defined and our study has been precisely aimed to search for novel factors associated with its development. Sections cut from paraffin blocks, containing the representative specimens of 18 different ameloblastomas, collected in a 15-year period (1999-2014), have been observed by an environmental scanning electron microscope, in order to search micro- and nano-sized particles and to identify their composition. In all the neoplastic cases, micro- and nano-sized metallic debris, differing in size and composition, have been detected inside the ameloblastomatous cells. On the contrary, the total absence of metallic particles in the healthy control cases has been emerged. Our results reveal a relationship between ameloblastoma and metallic particulate. The cigarette smoke and the routine dental practice appear the most probable source for the presence of these biopersistant inorganic particles inside the neoplastic cells.

Expression of CD34 and maspin in ameloblastoma from a West African subpopulation.

Ameloblastoma is a locally invasive odontogenic tumor with a high recurrence rate. Its local invasiveness is aided by angiogenesis, which can be correctly estimated by CD34. On the other hand, maspin decreases the local invasive and metastatic capability of cancer cells and functions as an angiogenesis inhibitor. We aim to assess the association between maspin expression and microvessel density in ameloblastoma. Twenty-five formalin-fixed paraffin-embedded (FFPE) blocks of ameloblastoma cases were prepared for antibody processing to CD34 and maspin. Positive immunohistochemical staining was marked by brown cytoplasmic/membrane coloration for CD34 and by nuclear/cytoplasmic coloration for maspin. At the ×40 magnification, we counted blood vessels in two areas of dimension; 300 × 400 µm (area A) and 150 × 200 µm (area B) adjacent to the tumor region to assess relative dispersion of the vessels bordering the tumor. The overall approximate microvessel density (MVD) for area A = 11 (minimum 2, maximum 21) and that for area B = 5 (minimum 1, maximum 10). The MVD in the area A of plexiform ameloblastoma was similar to that of the unicystic, while the hemangiomatous variant had the highest MVD for area A. Maspin positivity was present only in the cytoplasm of ameloblast, stellate reticulum, and the fibrous connective tissue in varying proportions. There was no evidence of the anti-angiogenesis effect of maspin in ameloblastoma from this study. The significance of cytoplasmic localization of maspin in the ameloblasts and stellate reticulum cells needs further investigation.

Differential expression of transcription factors Snail, Slug, SIP1, and Twist in ameloblastoma.

BACKGROUND: 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. MATERIALS AND METHODS: Four transcription factors, namely Snail, Slug, SIP1, and Twist, were examined immunohistochemically in 64 ameloblastoma [18 unicystic (UA), 20 solid/multicystic (SA), 4 desmoplastic (DA), and 22 recurrent (RA)]. RESULTS: All four transcription factors were differentially expressed in ameloblastoma [Snail: n = 60/64 (94%); Slug: n = 21/64 (33%); SIP: n = 18/64 (28%); Twist: n = 26/64 (41%)] (P < 0.05). Their distribution patterns were heterogeneous and were not significantly different between the tumor invasive front and central area (P > 0.05). Intracellular protein localization was predominantly nuclear for Snail, cytoplasmic>nuclear for Slug and SIP1, and cytoplasmic/nuclear for Twist. Overexpression of Snail in most subsets (UA = 18/18; SMA = 19/20; DA = 4/4; RA = 19/22) compared with the other transcription factors (P < 0.05) and selective expression for Slug, SIP1, and Twist in squamous/keratinous foci and at sites of epithelial cystic degeneration were among the main observations made. Stromal cells surrounding immunoreactive tumor cells tended to stain positive. CONCLUSIONS: Present findings suggest that these transcription factors probably play differential roles in mediating local invasiveness in ameloblastoma. Overexpression of Snail in most subsets suggests that this molecule is most likely the prototype transcription factor involved in inducing EMT in the ameloblastoma.

[Primary intra-osseous carcinoma]. / Carcinoma primario intraóseo.

Primary intra-osseous carcinoma (PIOC) is a rare tumor, defined as squamous cell carcinoma that develops in the jaw bones, having no initial connection to adjacent skin or mucosa. It is locally aggressive, with metastases to regional lymph nodes, (28% of cases) and lung (5% of cases) at the time of diagnosis. Its origin may be di novo or from other odontogenic tumors. The maxillary bones have epithelial tissues; therefore this neoplasm is located exclusively on this site, predominantly in the jaw. PIOC diagnostic criteria are strict and include: squamous cell carcinoma histopathology, lack of commitment and sinus mucosa, ruling out the possibility of metastasis from a distant site with a thorough clinical study and complementary methods. The treatment is, whenever possible, oncologic resection, additional radio and / or chemotherapy. Reconstructive surgery with graft and / or prostheses for aesthetic and functional are also required. We report the case of a 72 years old man who consulted for sore jaw three months after molar extraction. Curettage biopsy was performed and then resected mandible with lymphadenectomy. Histopathological examination showed a poorly differentiated squamous cell carcinoma, infiltrating jawbone with morphological findings linking him to residual odontogenic cyst and metastatic lymph nodes in 15 of 48 isolates. Postoperative radiotherapy was performed, he died at 30 months of diagnosis by progressive deterioration.

LINE-1 methylation difference between ameloblastoma and keratocystic odontogenic tumor.

OBJECTIVE: Global hypomethylation is a common epigenetic event in cancer. Keratocystic odontogenic tumor (KCOT) and ameloblastoma are different tumors but posses the same tissue in origin. Here, we investigated long interspersed nuclear element-1 (LINE-1 or L1) methylation status between ameloblastoma and KCOT. MATERIALS AND METHODS: We studied the methylation levels of the long interspersed nucleotide element-1 (LINE-1) in ameloblastoma and KCOT. After collecting ameloblastoma cells and epithelium lining cells of KCOT by laser capture microdissection from paraffin embedded tissue, combined bisulfite restriction analysis of LINE-1 (COBRALINE-1) was performed to measure LINE-1 methylation levels. RESULTS: The LINE-1 methylation level in KCOT (53.16 +/- 12.03%) was higher than that in ameloblastoma (36.90 +/- 16.52%), with a statistical significance of P = 0.001. The ranges of LINE-1 methylation of both lesions were not associated with either age or sex. CONCLUSION: We found LINE-1 hypomethylation levels between ameloblastoma and KCOT are different. Therefore, global methylations between these tumors are processed differently.

Detection of Notch signaling molecules in ameloblastomas.

BACKGROUND: To evaluate the roles of Notch signaling in the oncogenesis and cytodifferentiation of odontogenic tumors, expression of Notch receptors and ligands was analyzed in ameloblastomas as well as in tooth germs. METHODS: Tissue specimens of nine tooth germs and 32 ameloblastomas were examined by reverse transcriptase polymerase chain reaction and by in situ hybridization to determine the expression of Notch1, Notch2, Notch3, Delta1, and Jagged1. RESULTS: mRNA expression of Notch1, Notch2, Notch3, Delta1, and Jagged1 was detected in all samples of normal and neoplastic odontogenic tissues. In tooth germs, Notch receptors were expressed in odontogenic epithelium (except for inner enamel epithelium), and expression of Notch ligands was lower in inner enamel epithelium than in other epithelial components. Odontogenic mesenchymal components were weakly reactive with these Notch signaling molecules. Ameloblastomas showed expression of Notch receptors and ligands in central polyhedral neoplastic cells. Notch2, Delta1, and Jagged1 were expressed in some neoplastic cells neighboring the basement membrane. Expression of Notch receptors and ligands was not found in keratinizing cells or granular cells in ameloblastoma variants. Stromal cells were weakly reactive with these Notch signaling molecules. CONCLUSION: Expression of Notch receptors and ligands in tooth germs and ameloblastomas suggests that Notch signaling might control cell differentiation and proliferation of normal and neoplastic odontogenic epithelium.

Perlecan-rich epithelial linings as a background of proliferative potentials of keratocystic odontogenic tumor.

BACKGROUND: The intraepithelial deposit of perlecan, a basement membrane-type heparan sulfate (HS) proteoglycan, has been demonstrated in neoplastic conditions such as salivary gland tumors, odontogenic tumors, and oral carcinoma in situ. Our aim was to determine whether perlecan turnover was enhanced in the lining cells of keratocystic odontogenic tumor (KCOT), which had been recently renamed from odontogenic keratocyst because of its accumulated evidence of neoplasm, as a possible background for neoplastic proliferation. METHODS: Ten surgical specimens from each of KCOT, dentigerous cyst, and radicular cyst were examined for the expressions of perlecan core protein, HS chains, heparanase, and Ki-67 by immunohistochemistry and in situ hybridization. RESULTS: In KCOT, perlecan core protein and HS chains were localized on the cell border from the parabasal to subkeratinized layers of the lining epithelium. Heparanase was localized in a similar fashion to those for perlecan and HS chains but was within the cytoplasm. mRNA signals for perlecan core protein and heparanase were mostly compatible with their protein signals. Ki-67-positive cells were localized mainly in the second basal cell layers with definitely higher labeling indices (approximately 31.3%, second layer). In contrast to KCOT, dentigerous cysts and radicular cysts had no perlecan, HS chains, and heparanase deposition in their linings with extremely lower Ki-67 indices (0.4-0.8%). CONCLUSION: The result suggests that the characteristic intra-lining-epithelial deposit of perlecan in KCOT, which has never been seen in other cystic jaw lesions, is a new evidence supporting the neoplastic nature of KCOT.

Perivascular myoid tumors of the oral region: a clinicopathologic re-evaluation of 35 cases.

BACKGROUND: Myopericytoma (MPC) is a generic denomination to describe tumors showing differentiation toward perivascular myoid cells /myopericytes. It has been suggested that MPC forms a morphologic continuum with glomus tumor (GT), solitary myofibroma (SMF), and angioleiomyoma (ALM). This proposed relationship has not yet been assessed in the oral region. METHODS: We reviewed our 28-year experience with 35 oral tumors, originally diagnosed as ALM (n = 28), SMF (n = 4), GT (n = 2), and MPC (n = 1) to analyze their overlapping microscopic features, with the assistance of immunohistochemistry. RESULTS: Myopericytoma showed a wide range of growth patterns; concentric perivascular whorls, hemangiopericytomatous areas, glomangiopericytoma (GPC)-type vessels and leiomyomatous foci. Intravascular growth was also seen. Among 28 cases studied, three ALM were reclassified as MPC (n = 2) and SMF (n = 1), based on the present diagnostic criteria. Additional MPC-type components, at varying degrees, were similarly found in four ALM and three SMF, at least focally. One GT featured intravascular whorls of spindle cells. These four interrelated groups of tumors had in common GPC-type vasculature and intraluminal cellular proliferation was nearly ubiquitously present. Diffuse immunoreactivity for alpha-smooth muscle actin and less staining intensity of muscle-specific actin were observed in all tumors. Only ALM displayed desmin positivity of variable extent. Neither case tested expressed CD34. CONCLUSIONS: Our data matches with the recent results in extraoral sites that MPC, GT, SMF, and ALM exhibit histologic and immunohistochemical overlap with each other. A common perivascular myoid differentiation between these tumor types is further reinforced by the present oral series.

Ultrastructural studies of jaw lymphomas and apoptosis.

Research on ultrastructural cytopathological changes and apoptosis that occur in jaw lymphoma were done by using electron microscopy and ground sections. The author described this tumor in 1977-1978 as a highly malignant and lethal condition affecting children between 2 and 8 years (mean age 5 years). A duration of illness between 2 and 3 weeks is common and with a general condition of severe toxicity, anemia, and high body temperature. Clinical and pathological features of 24 children with jaw lymphoma seen in the Maxillofacial Unit, Surgical Specialized Hospital, Medical city, Baghdad, are described. Thirteen males and 11 females were included, with a death rate at 91.1%. The morphological characteristics were examined by ground sections. Lymphoblastic lymphoma features were observed and apoptotic changes were seen in some of the cells. Electron microscopy showed a high number of mitotic figures and lymphoblast transformation to plasma cells with high nucleo-cytoplasmic ratio. Some cells had double nuclei and some nuclei were more convoluted. Apoptotic changes were seen in some cells; chromatin clumps aggregated near the nuclear membrane. Cytoplasmic processes and mitochondria showing degeneration and virus-like particles were seen in both nuclei and cytoplasm. The presence of a high mitotic figure with active oncogenic virus growth and reduced apoptosis is a poor prognostic feature in jaw lymphoma.

Differential expression of apoptosis-related proteins in various cellular components of ameloblastomas.

To evaluate the expression patterns of apoptosis-related proteins, including Fas, Fas-ligand (FasL), caspase-3 and Bcl-2, in various cellular components of ameloblastomas, 39 cases of ameloblastoma were examined using immunohistochemistry. The staining intensity of the antigens in the 4 types of tumour cellular component, peripheral basal cells of tumour nests, central stellate reticulum-like cells, and foci of squamous and granular cells, was scored using a semi-quantitative scale, and comparisons were made by statistical analysis. Expression of Fas, FasL and caspase-3 was detected in the majority of cases, with a similar pattern of strong staining in the foci of squamous metaplasia and granular cells usually situated in the central area of tumour islands. In contrast, expression of Bcl-2 was predominantly seen in the peripheral basal cell layer. There were significant differences in the staining intensity of Fas, caspase-3 and Bcl-2 among the 4 types of tumour cell. The differential expression of apoptosis-related proteins in various cellular components of ameloblastomas, with pro-apoptotic proteins, Fas, FasL and caspase-3 being closely associated with squamous metaplasia and granular transformation of the tumour cells, suggests that Fas/FasL-induced apoptotic cell death may play a role in the disposal of terminally differentiated or degenerative tumour cells in ameloblastomas.

Immunohistochemical characteristics of cystic odontogenic lesions: a comparative study.

OBJECTIVE: Cystic ameloblastoma, keratocystic odontogenic tumor, dentigerous cyst, and radicular cyst are the most commonly encountered cystic odontogenic lesions. The aim of this study was to investigate the expressions of survivin, E-cadherin, CD138, and CD38 in these lesions and their potential diagnostic usage. MATERIAL AND METHOD: A total of 20 cases, consisting 5 radicular cysts, 5 dentigerous cysts, 5 keratocystic odontogenic tumors and 5 cystic ameloblastomas were included in our series. For all cases, sections from the selected blocks were stained against the antibodies for survivin, E-cadherin, CD138, and CD38 on an automated device. RESULTS: All cystic ameloblastomas and keratocystic odontogenic tumors showed diffuse and strong nuclear survivin expression. No specific survivin immunoreactivity was observed in the dentigerous and radicular cysts. E-cadherin expression was stronger in all dentigerous cysts and radicular cysts when compared to others. CD138 expression in stromal cells was prominent in cystic ameloblastomas, but gradually decreased in the other three lesions. All cases were negative for CD38. CONCLUSION: In the present study, loss of E-cadherin expression in epithelial cells, strong CD138 expression in stromal cells and strong nuclear survivin expression both in epithelial and stromal cells in cystic ameloblastomas and keratocystic odontogenic tumors were the most remarkable findings. These findings are also reinforced by the studies suggesting their role in the aggressiveness and pathogenesis of these tumors.

beta-Catenin is expressed aberrantly in tumors expressing shadow cells. Pilomatricoma, craniopharyngioma, and calcifying odontogenic cyst.

We studied the beta-catenin immunohistochemical profile in tumors expressing shadow cells: pilomatricoma, 10 cases; calcifying odontogenic cyst, 6 cases; and craniopharyngioma, 9 cases. There was strong membranous, cytoplasmic, and nuclear staining of the immature basaloid cells in all of these tumors. Shadow cells were negative in all tumors. It has been documented that rising levels of free beta-catenin drive the formation of complexes with T-cell factor/lymphoid enhancer factor (TCF-Lef) and up-regulate the wingless-Wnt cell-cell signals. The end result is an abnormality of beta-catenin degradation and, thus, a buildup of free beta-catenin in the cytoplasm and/or nucleus, resulting in the stimulation of cellular proliferation and/or inhibition of cell death. beta-Catenin seems to have an important role in the oncogenesis of these tumors. The similar pattern of keratinization in these tumors and the similar pattern of beta-catenin immunoreactivity in the cytoplasm and the nucleus are important findings. It seems that the activation of a common cellular pathway, namely Wnt-beta-catenin-TCF-Lef, has a role in the pathogenesis of these tumors. The latter could be related to their shared method of keratinization or shared dysfunction of the cellular adhesion complex leading to tumorigenesis.

Clear-cell odontogenic carcinoma with pulmonary metastases resembling pulmonary meningothelial-like nodules.

Clear-cell odontogenic carcinoma (CCOC) is a rare neoplasm with malignant potential and unknown cytogenetic alterations. We describe the case of a 43-year-old woman who presented with an unusual odontogenic epithelial tumor. Histologically, the tumor was composed of clear-cell areas and exhibited a squamous pattern with little nuclear pleomorphism similar to benign squamous odontogenic tumor. Multiple small pulmonary nodules occurring 3 years after primary surgical treatment histologically closely resembled benign minute pulmonary meningothelial-like nodules (MPMN) with clear-cell features. Comparative genomic hybridization (CGH) and immunohistochemistry, performed as diagnostic adjuncts, revealed in the odontogenic tumor and the pulmonary lesions a very similar pattern of chromosomal aberrations (loss of 9, gains of 14q, 19 and 20 in both, and additional loss of 6 in the odontogenic tumor) and the same pattern of expression (positive for cytokeratin 5, 6, 8, 19 and negative for cytokeratin 18, epithelial membrane antigen, and vimentin), differing from that of MPMN. These findings confirmed the final diagnosis of metastasizing CCOC with partial squamous differentiation, substantiated the unfavorable prognosis of the clear-cell component, and highlighted the diagnostic impact of CGH and immunohistochemistry for classification of these morphologically peculiar pulmonary CCOC metastases.

Spindle-cell ameloblastic carcinoma: A case report with immunohistochemical, ultrastructural, and comparative genomic hybridization analyses.

Spindle-cell ameloblastic carcinoma is a classification proposed for a group of rare odontogenic carcinomas with sarcomatoid components and is distinguished from odontogenic carcinosarcoma. We report a case of spindle-cell ameloblastic carcinoma of the right mandible that occurred in a 67-year-old Japanese man. Growth of the tumor was destructive, there was extensive lung metastasis, and the outcome was unfavorable. Ultrastructural and immunohistochemical examination showed the spindle-cell component of the tumor to be epithelial in character. A gain of 5q with amplification of 5q13 was detected in the tumor by comparative genomic hybridization.

Epidermal growth factor receptor expression in ameloblastoma.

UNLABELLED: Ameloblastoma is a locally aggressive tumor with possible lethal potential. Currently extensive surgery is the most acceptable treatment modality. AIM: To investigate the presence of EGFR in ameloblastoma in order to consider using newly developed anti-EGFR therapeutic agents in cases of unresectable tumors. The study consisted of 58 formalin-fixed, paraffin-embedded specimens of ameloblastoma that were immunohistochemically stained with a monoclonal anti-EGFR antibody (clone 31G7). Positive and negative controls determined specificity of the antibody. A staining score based on the staining intensity and the proportion of stained cells was established, ranging between 0 and 2. All specimens were EGFR positive; 8 (14%) exhibited the maximum score of 2 and 19 (33%) scored between 1 and 2. Since ameloblastomas are EGFR-positive tumors, anti-EGFR agents could be considered to reduce the size of large tumors and to treat unresectable tumors that are in close proximity to vital structures.

Comparative immunohistochemical analysis between jaw myxoma and mesenchymal cells of tooth germ.

The histogenesis of jaw myxoma is still debated. According to some authors it arises from the primitive mesenchymal components of developing teeth. In this study, we have studied the expression of S-100 protein and vimentin in dental follicle, dental papilla and periodontal ligament cells using monoclonal and polyclonal antibodies. Myxoma of the jaw expresses vimentin and S-100 protein. On the contrary, as compared to jaw myxoma, the normal developmental structures were immunonegative for S-100 protein but stained for vimentin. These results could indicate a difference in the derivation other than tooth mesenchyma.

Different keratin profiles in craniopharyngioma subtypes and ameloblastomas.

Craniopharyngiomas are generally considered to arise from the remnants of Rathke's pouch or a misplaced enamel organ. We tried to refine these hypotheses, comparing the subtypes of craniopharyngioma with Rathke's cleft cyst, a known Rathke's pouch derivative, and with ameloblastoma, an enamel organ derivative. Nineteen craniopharyngiomas (14 adamantinomatous and 5 papillary type tumors) and 17 ameloblastomas were immunostained for cytokeratin (CK) 7, CK 8, CK 14, and human hair keratin (HHK). All cases of adamantinomatous craniopharyngioma were CK 7+/CK 8+/CK 14+. Two cases (40%) of papillary craniopharyngioma were CK 7+/CK 8+/CK 14+, whereas the remaining three cases (60%) were CK 7+/CK 8-/CK 14+. Fifteen cases (88%) of ameloblastoma were CK 7-/CK 8+/CK 14+. Only the shadow cells present in adamantinomatous craniopharyngiomas were positive for HHK, which may indicate their follicular differentiation. In Rathke's cleft cyst, ciliated cuboidal cells were CK 7+/CK 8+/CK 14- and metaplastic squamous cells were CK 7+/CK 8/CK 14+. These findings suggest that both subtypes of craniopharyngioma may differ from ameloblastoma in histogenesis, although cytokeratin expression patterns may change during tumor development. Adamantinomatous craniopharyngioma may be related to a heterotopic ectodermal tissue which can differentiate into hair follicles, while papillary craniopharyngioma may arise from Rathke's cleft cyst.

Transferrin receptor in oral tumors.

The transferrin receptor (TfR) appears in vigorously proliferating cells. We did an immunohistochemical study of TfR in oral tissues and a quantitative analysis by flow cytometry of TfR in a cancer cell line after an anticancer drug treatment. TfR was found in the parabasal and basal layers of the normal epithelium, but rarely in benign tumors. Generally, in the malignant tumors, the poor prognostic cases showed strong staining regardless of the differentiation of the tumor. In the flow cytometric analysis, the amount of TfR decreased according to the reduction of the proliferative ability of cancer cells. These results suggest that TfR expression may be useful as a prognostic marker.