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)

We assessed the immunohistochemical profile of an unusual case of multiple similarly looking tumors in the jawbone of a young patient. Histologically, the tumors exhibited features of adenomatoid odontogenic tumor (AOT) and adenomatoid dentinoma but showed no resemblance to any other defined odontogenic tumor entities. They expressed high amounts of cytokeratin (CK) 8 and 14 together with some Vimentin. A small rim of peripheral cells showed CK 5, 17, and 19 reactivity. Also, these lesions expressed some bcl-2 as well as p53 and Ki67. Histologically and immunohistochemically, the unusual multiple lesions differed in details from a simultaneously examined group of 24 classical AOT cases, suggesting that they may represent a hitherto less well-defined odontogenic tumor entity.
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PMID:A case of multiple AOT-like jawbone lesions in a young patient--a new odontogenic entity? 1255 60

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

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

Clear cell odontogenic carcinoma (CCOC) is a rare odontogenic tumor associated with aggressive clinical behavior, metastasis, and low survival. We report a case of CCOC affecting the mandible of a 39-year-old man. The tumor presented a biphasic pattern composed of clear cell nests intermingled with eosinophilic cells and separated by collagenous stroma. Immunoreactivity to cytokeratin (CK), specifically AE1/AE3 and CK 8, 14, 18, and 19 was found, as well as to epithelial membrane antigen (EMA). The tumor cells were negative for S100 protein, CK 13, vimentin, smooth muscle actin, laminin and type IV collagen. Low labeling indices for the proliferation markers Ki-67 and proliferating cell nuclear antigen and to p53 protein might predict a favorable prognosis for the lesion. A surgical resection was performed, followed by adjuvant radiotherapy. A 2-year follow-up has shown no signs of recurrence. The significance of histochemical and immunohistochemical resources in the correct diagnosis of CCOC is analyzed.
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PMID:Clear cell odontogenic carcinoma: case report with immunohistochemical findings adding support to the challenging diagnosis. 1860 8

The central granular cell odontogenic tumor (CGCOT) is a rare lesion that usually affects the posterior region of the mandible of young adults. We present a case of CGCOT involving the mandible of a 20-year-old white woman, emphasizing the immunohistochemical characteristics using a large panel of antibodies. The lesion was removed surgically, and after 4 years of follow-up, there are no evidences of recurrences. The odontogenic epithelium (OE) showed positivity for cytokeratins (CKs) AE1/AE3, 34betaE12, CK5, CK7, CK8, CK14, CK19, E-cadherin, beta-catenin, CD138, and p63. The granular cells were positive for vimentin, CD68, lysozyme, muscle-specific actin, alpha-smooth muscle actin, calponin, neuron-specific enolase (NSE), CD138, and bcl-2. Dendritic-like cells surrounding the OE displayed positivity for vimentin, CD1a, S100, CD68, and bcl-2, but it was negative for factor XIIIa, supporting a Langerhans cell phenotype. Ki-67 labeling index was 1.8%, whereas p53 was negative. These data confirm the benign nature of CGCOT, the association of OE with Langerhans cells, and a variable phenotype of the granular cells.
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PMID:Central granular cell odontogenic tumor: a histopathologic and immunohistochemical study. 1991 79

Ameloblastoma is the most frequently encountered odontogenic tumor, characterized by a locally invasive behavior, frequent recurrences, and, although rare, metastatic capacity. Loss or inactivation of tumor suppressor genes (TSGs) allows cells to acquire neoplastic growth. The ING family proteins are tumor suppressors that physically and functionally interact with p53 to perform important roles in apoptosis, DNA repair, cell cycle regulation, and senescence. TP53 genetic alterations were reported to infrequently occur in ameloblastoma. Considering that other TSGs related to TP53 could be altered in this tumor, we focused our study on the ING family genes. We analyzed the loss of heterozygosity (LOH) status of the ING family (ING1-ING5) chromosomal loci in a group of ameloblastomas by microsatellite analysis, and correlated the ING LOH status with clinicopathological characteristics. By using specific microsatellite markers, high frequency of LOH was found at the loci of each ING gene family member (33.3-72.2%). A significant relationship was shown between LOH of D2S 140 (ING5 locus) and solid tumor type (p = 0.02). LOH of ING3MS (ING3 locus) was also high in solid type tumors, showing a near significant association. In addition, a notable tendency toward higher LOH for half of the markers was observed in recurrent cases. LOH of ING family genes appears as a common genetic alteration in solid ameloblastoma. The current study provides interesting novel information regarding the potential prognostic significance of the allelic loss of the ING gene family loci in ameloblastoma tumorigenesis.
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PMID:Allelic loss of the ING gene family loci is a frequent event in ameloblastoma. 2068 10

The adenomatoid odontogenic tumor (AOT) is a clinically benign lesion. Discussions about the AOT hamartomatous or neoplastic nature, and the probable odontogenic epithelial cell it originates from still exist. This research aimed to study and discuss the subject by the immunohistochemical detection of cytokeratins, laminin, collagen IV, PCNA and p53 in 8 tumor samples and 8 dental follicle samples containing reduced enamel epithelium. The results have shown that CK14 labelling indicated differentiation grades for secreting ameloblasts or ameloblasts in the post-secreting stage in the adenomatoid structure of AOT. Laminin, found on the luminal surface of adenomatoid structures, was compatible with the reduced enamel epithelium during the "protective stage of amelogenesis". PCNA specifically labelled the spindled areas and peripheral cords of the AOT, indicating that these areas are responsible for tumor growth. After considerations about pathogenesis, the authors suggested that the nature of AOT is hamartomatous with histogenesis from the reduced enamel epithelium.
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PMID:Study on the origin and nature of the adenomatoid odontogenic tumor by immunohistochemistry. 2086 28

Although ameloblastoma and adenomatoid odontogenic tumor (AOT) belong to the same group according to the World Health Organization, they show different biologic behaviors. PCNA, an amplifier of cell proliferation, and p53, a tumor suppressor protein, are overexpressed in some odontogenic lesions. The purpose of this study was to immunohistochemically evaluate the expression of p53 and PCNA to clarify the possible role of these proteins in different behaviors of ameloblastoma and AOT. The immunohistochemical expression of PCNA and p53 was determined in 30 solid ameloblastomas and 12 AOTs. Statistical tests including one-way ANOVA, t-test, chi-square, Mann-Whitney U and Kendall were used to analyze the data. All tissue sections (except one specimen of plexiform ameloblastoma) exhibited immunoexpression for p53. PCNA was expressed in all specimens. There was no significant difference in PCNA expression between ameloblastomas and AOTs (P > 0.05). For p53, there was no statistical difference between subtypes of ameloblastomas (P > 0.05), whereas statistical differences were observed between ameloblastomas and AOTs (P < 0.001). There was no statistical difference in PCNA intensity of staining between ameloblastomas and AOTs (P > 0.05), whereas the p53 intensity in ameloblastomas was stronger than AOTs (P < 0.05). Positive correlation between PCNA and p53 was observed. We concluded that PCNA overexpression is not responsible for the difference in clinical behavior of these two lesions, whereas the expression of p53 in ameloblastoma may explain the more aggressive nature of this tumor compared with AOT.
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PMID:Immunohistochemical detection of p53 and PCNA in ameloblastoma and adenomatoid odontogenic tumor. 2171 26

Odontogenic myxoma (OM) is an ectomesenchymal benign odontogenic tumor characterized by spindle or stellate-shaped cells embedded in an abundant myxoid or mucoid extracellular matrix. DNA methylation is characterized by the addition of methyl groups in cytosines within CpG islands in the promoter gene. DNA methylation can decrease the expression of tumor suppressor genes and contribute to the development of neoplastic lesions. The aim of study was to evaluate the methylation pattern of the tumor suppressor genes P16 (CDKN2A), P21 (CDKN1A), P27 (CDKN1B), P53 (TP53) and RB1 in OM and dental pulp. Methylation was evaluated using methylation-specific polymerase chain reaction (PCR). The transcription was studied in some cases by using reverse transcription quantitative PCR. A higher frequency of unmethylated P27, P53, and RB1 samples was observed in the OM when compared with the dental pulp. OM expressed mRNA of all the genes evaluated. Considering all the samples together, the expression of Rb was higher in the unmethylated samples compared with the partially methylated samples. This investigation revealed hypomethylation of the genes P27, P53, and RB1 in OM. In addition, methylation of tumor suppressor genes was found to be an usual event in normal dental pulp.
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PMID:Hypomethylation of tumor suppressor genes in odontogenic myxoma. 2201


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