Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adamantinoma of long bones is a rare malignant tumor composed of cells with epithelial characteristics in various differentiation patterns surrounded by fibrous cells. Evidence as to whether this neoplasm should be designated as an epithelial bone tumor or a biphasic sarcoma with both epithelial and mesenchymal features is lacking. In this study the nature of the mesenchymal and epithelial components of adamantinoma was investigated by DNA flow cytometry, DNA image cytometry, p53 immunohistochemistry, and polymerase chain reaction-based loss of heterozygosity detection at the p53 locus. Specimens from 6 of 15 patients (40%) analyzed by flow cytometry had an aneuploid DNA index. Image cytometry analysis of Feulgen-stained paraffin sections of 6 aneuploid and 2 diploid tumors revealed that aneuploid nuclei were detected in cells with an epithelial phenotype only, whereas all fibrous cells were diploid. Immunohistochemistry for p53 on specimens from 25 patients revealed moderate or strong immunoreactivity in 12 tumors (48%) restricted to the epithelial cells. Loss of heterozygosity at the p53 locus could be confirmed in the epithelial component of an immunohistochemically p53-positive tumor. Additionally, sections of 7 lung metastases were studied histologically. Only keratin-positive epithelial cells, predominantly in the spindle cell pattern, were present in these metastases, whereas the osteofibrous tissue present in the primary tumors was not detected. These results suggest that either adamantinoma consists of a malignant epithelial part with a reactive osteofibrous stroma or that the malignant epithelial cells develop next to a proliferating benign fibrous component. Additional analysis of common genetic abnormalities in the fibrous and epithelial cells of adamantinoma is therefore indicated.
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PMID:DNA aberrations in the epithelial cell component of adamantinoma of long bones. 749 1

To clarify the possible role of apoptosis in odontogenic epithelium, apoptosis-related factors and apoptotic cells were examined by immunohistochemistry and an in situ DNA nick end-labelling method. Expression of bcl-2 protein was detected in both normal and neoplastic odontogenic epithelium, whereas expression of p53 protein was detected only in neoplastic but not in normal odontogenic epithelium. The prevalence of cases positive for Lewis(y) antigen in ameloblastomas was significantly lower than in enamel organs. Correlation between these factors and apoptotic cells presented by an in situ DNA nick end-labelling method was not clear. The number of apoptotic cells in ameloblastomas was significantly greater than in normal odontogenic epithelium, and apoptotic reactions in the granular cell type ameloblastoma tended to be more frequently detected than in other types of ameloblastomas. These results suggested that apoptotic cell death might play an important role in oncogenesis and/or tissue differentiation in odontogenic epithelium.
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PMID:Detection of apoptosis-related factors and apoptotic cells in ameloblastomas: analysis by immunohistochemistry and an in situ DNA nick end-labelling method. 938 80

Overexpression of p53 protein in unicystic ameloblastoma (uAB) is denser than in the conventional ameloblastoma (cAB) type, indicating increased wild type p53--suppressing the growth potential of uAB and denoting the early event of neoplastic transformation, probably of a previous odontogenic cyst. Overexpression of p53 in borderline cAB and malignant ameloblastoma (mAB) types might reflect a mutational p53 protein playing an oncogenic role, promoting tumour growth. Overexpression of p53 protein could be a valid screening method for predicting underlying malignant genetic changes in AB types, through increased frequency of immunoreactive cells or increased staining density.
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PMID:Immunohistochemical detection of p53 protein in ameloblastoma types. 1079 27

The botryoid odontogenic cyst (BOC) is considered a rare multilocular variant of the lateral periodontal cyst. The origin of the BOC can be seen in aberrant odontogenic tissue. The BOC is found especially in the premolar region of the mandible, as well as in the frontal region of the maxilla of patients aged between 60 and 70 years. Most of the 11 published articles of BOC have shown high rates of recurrence. Histopathologically the BOC is marked by multilocular cysts lined by a thin, nonkeratinized epithelium. Clusters of glycogen-rich epithelial cells may be noted in nodular thickenings of the cyst lining. For the clinician, the differentiation of the BOC from the keratocyst and ameloblastoma is relevant. One case of a large BOC (65-year-old male, BOC regio 33-45, diameter 5 cm, radiographically and histologically multilocular) is presented with a review of the literature, including the therapeutic management, and the possible diagnostic criteria are discussed. The immunohistochemically determined expression of cytokeratin (CK) 13 implicates the histogenetic origin of the BOC from the squamous epithelium of the oral cavity and excludes the origin from the small salivary glands. The expression of CK 19 and the lack of expression of p53, as well as the higher proliferation rate of the basal epithelial cell layer by the BOC, may be useful for distinction between the keratocyst.
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PMID:[Cytokeratin expression in botryoid odontogenic cyst. A rare differential keratocyst and ameloblastoma diagnosis]. 1109 84

Ameloblastoma is a unique tumor in the oral and maxillofacial region with various levels of proliferative activity in each type. p53 is most commonly found to be mutated in human cancer and sometimes is overexpressed also in other lesions, such as ameloblastoma. Murine Double Minute 2 (MDM2) is able to physically associate with the p53 tumor suppressor and therefore block the growth suppressive functions of p53. In the present study, immunohistochemistry, western blotting and enzyme-linked immunosorbent assay for p53 mutant selective test were done. MDM2 was overexpressed in ameloblastoma and the results showed different numbers of MDM2 labeling index based on both WHO classification and cytological pattern of outer layer cells. Basal ameloblastoma, which has a high proliferative activity, had the highest MDM2 labeling index. We suggest MDM2 protein caused the high proliferative activity of ameloblastoma, especially in basal cell ameloblastoma.
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PMID:The role of MDM2 in the proliferative activity of ameloblastoma. 1290 16

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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PMID:Allelic loss of tumor suppressor genes in ameloblastic tumors. 1513 74

In this study, proliferating cell nuclear antigen (PCNA) and p53 protein expressions were analyzed in 16 cases of ameloblastoma and 8 cases of adenomatoid odontogenic tumor (AOT). The cases of ameloblastoma consisted of solid type tumors and histologic arrangements of different subtypes were observed. In some specimens, more than one histologic subtype was identified in the same lesion, and each tumor was categorized according to the predominant cell pattern. The odontogenic tumors were grouped as follows: follicular ameloblastoma (n=7), plexiform ameloblastoma (n=4), acanthomatous + follicular ameloblastoma (n=3), basal cell ameloblastoma (n=2), adenomatoid odontogenic tumor (n=8). PCNA immunohistochemical expression revealed stronger quantitative labeling index for the follicular ameloblastoma, while for p53 protein the strongest quantitative labeling index was detected in the plexiform type. Nevertheless, statistical analysis using ANOVA and Tukey's test did not detect significant differences (p>0.05) among the histologic subtypes of ameloblastoma. The findings of this study suggest that the different histologic patterns of ameloblastoma did not show a direct correlation with their clinical behavior and consequently with the prognosis of the cases. The results also indicated that the ameloblastoma has greater proliferative potential than the AOT, which can contribute to explain its more aggressive and invasive characteristics.
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PMID:Proliferating cell nuclear antigen (PCNA) and p53 protein expression in ameloblastoma and adenomatoid odontogenic tumor. 1611 35

Ameloblastic carcinoma is described in the updated World Health Organization (WHO) classification as a rare malignant lesion. Ameloblastic carcinoma meeting the WHO criteria may arise either as a result of malignant change in a pre-existing benign ameloblastoma (carcinoma ex ameloblastoma) or as a primary malignant ameloblastoma not preceded by an ordinary ameloblastoma (de novo carcinoma). We report a case of ameloblastic carcinoma ex ameloblastoma and examine how this case underwent malignant transformation. The DNA was extracted separately from benign and malignant areas in paraffin sections of the tumor. Direct sequencing showed no genetic mutation of exons 5-8 of the p53 gene. Hypermethylation of CpG islands of the p16 gene was detected in the malignant parts of the tumor. The results indicate that hypermethylation of p16 may have been involved in the malignant transformation of the ameloblastoma in the present case.
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PMID:Ameloblastic carcinoma ex ameloblastoma: report of a case-possible involvement of CpG island hypermethylation of the p16 gene in malignant transformation. 1717 97

Ameloblastoma is the most common odontogenic tumor. It can exhibit a variety of histological patterns, a great infiltrative potential and a high recurrence rate. Mutations in microsatellite sequences are a hallmark of neoplastic transformation but little is known about their role in ameloblastoma development. In this study DNA was extracted from laser-microdissected samples of 24 ameloblastomas and was analyzed for the status of 22 microsatellite loci. The occurrence and the pattern of microsatellite alterations, in form of loss or length variation, was evaluated and correlated with the Ki67 labeling index and with other clinicopathologic parameters. The prognostic significance of these alterations was also evaluated. High Ki67 expression was significantly associated with a shorter disease-free survival (p=0.003 by log-rank test). Alterations of at least one of the selected loci was observed in all (100%) the ameloblastomas analyzed with a mean of 4 altered microsatellites for each tumor. The microsatellites most frequently altered were D9S747 and D11S488 (42%). All the other loci analyzed were altered in less than 40% of cases and some of them (D3S1312, D3S1300, IFNA, D9S164, D13S176 and TP53) did not show alterations in any of the ameloblastomas analyzed. No relationship was observed between the occurrence of microsatellite alterations and other parameters, such as patients age and gender, tumor size, localization and histotype. The occurrence of microsatellite alterations was more frequent in tumors displaying a high Ki67 labeling index (p=0.03) and in a univariate analysis was predictor of an increased risk of disease recurrence (p=0.039 by log-rank test). These findings demonstrate that microsatellite alterations are frequent event in ameloblastomas. They also suggest that evaluation of tumor cells proliferative activity and microsatellite alterations may be helpful to stratify ameloblastomas prognostically and to predict the clinical behavior of these tumors.
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PMID:Tumor cell proliferation and microsatellite alterations in human ameloblastoma. 1730 20

Ameloblastoma (AM) is recognized as a benign tumour but locally invasive with a high risk of recurrence. In vitro model systems for studying AM are limited due to the fact that AM cells grow poorly and begin to senesce early. Japanese researchers have reported the construction of an AM cell line, AM-1, by exposing cells to human papillomavirus 16 (HPV16) but retaining the potential of transformation. In this study, we used a retroviral infection method to over-express the human telomerase reverse transcriptase (hTERT) gene to acquire immortality of hTERT(+)-AM cells. Furthermore, it was revealed both by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot that the pathway of immortalization was loss of p16, not p53 or p21. Also, there was no evidence indicating that the hTERT(+)-AM cells underwent malignant transformation by the nude mouse tumorigenicity assay. Taken together, this hTERT-immortalized cell line may be a potentially valuable and reliable cell model for further study of the invasive properties of AM in vitro.
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PMID:Immortalization of ameloblastoma cells via reactivation of telomerase function: Phenotypic and molecular characteristics. 1983 45


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