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)

Paraffin embedded, formalin fixed tissue sections from patients suffering from a primary oral squamous cell carcinoma were immunohistochemically investigated for the presence of p53 expression using the Bp53-11 antibody. The aim of this study was to determine the predictive value of p53 expression as a biomarker for the development of a second primary tumour (SPT) in the respiratory and upper digestive tract. In a nested case control study, neoplastic and normal tissue sections of 44 patients who had a previous history of cancer were used. 15 of the 44 had developed a SPT, while the other 29 were minimally 7 years free of disease. Additionally, nine SPTs were included in this study to establish whether concordance exists in tumours that develop in the same field. 10 of the 29 patients (34%) free of tumour during follow-up had p53 positive tumours. 8 of 15 patients (53%) who developed a SPT had a p53 positive primary tumour. This difference is not statistically different (chi 2-test). Forty percent of the total group of primary oral cavity tumours showed p53 positivity. When comparing the first and the second tumours, discordance in p53 expression between the first and second tumours was seen in 4 out of 9 cases. None of the cases showed p53 positivity in adjacent normal mucosa. In conclusion, p53 immunoreactivity in neoplasia, dysplasia and normal tissue does not predict the development of a SPT. In addition, multiple primary tumours do not have identical p53 expression.
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PMID:Value of p53 expression in oral cancer and adjacent normal mucosa in relation to the occurrence of multiple primary carcinomas. 874 70

The expression of the p53 protein in photodamaged skin from the face, forearm and neck of 18 subjects was compared to non-exposed skin taken at autopsy from the abdomens of 9 subjects of the same age. Paraffin sections and the polyclonal antibody CM1 were used with the ABC technique. The p53 protein was expressed in the nuclei of keratinocytes in 7 of the 18 samples obtained from sun-exposed skin and in 1 of 9 samples from non-exposed skin. The expression in sun-exposed skin can be due either to its overexpression due to DNA damage or to the appearance of mutant forms.
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PMID:Expression of the p53 protein in sun-damaged skin. 880 Feb 99

Reactive atypia of alveolar epithelium occurs in many types of lung injury and may sometimes raise suspicions of adenocarcinoma or bronchioloalveolar carcinoma. To assess whether there is sufficient difference in the frequency of p53 protein immunopositivity in these lesions to provide a practical basis for differentiating malignancy from reactive atypia, we immunostained 110 malignant and inflammatory/fibrotic lung specimens for p53 protein. Paraffin-embedded sections were immunostained with p53 protein antibody (clone BP53-12; BioGenex, San Ramon, CA) and standard capillary gap (Microprobe; Fisher Scientific, Fairlawn, NJ) avidin- biotin complex technique with antigen retrieval solution. Percent of immunopositive cells was semiquantitatively categorized as follows: 0%, less than 1%, 1% to 10%, 10% to 50%, more than 50%. Of reactive atypias, 94% are negative or show p53 immunopositivity in less than 10% of cells. Of p53 positive malignancies, 86% are positive in more than 10% of cells. When p53 immunopositivity occurs in more than 10% of atypical cells, the lesion is usually a malignancy, primarily adenocarcinoma. Most reactive atypias are immunopositive in less than 10% of atypical cells. Important caveats were noted. Rare reactive atypias are p53 immunopositive in greater than 10% of cells. Bronchioloalveolar carcinomas are infrequently p53 immunopositive. Therefore, this approach would be less useful in their differentiation from reactive atypias.
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PMID:Potential utility of p53 immunopositivity in differentiation of adenocarcinomas from reactive epithelial atypias of the lung. 891 31

The aim of the study was to investigate whether nuclear immunopositivity for p53 is a factor of prognostic significance in astrocytomas of childhood and adolescence. Paraffin-embedded tissues of astrocytomas (10 WHO grade II, 11 WHO grade III) from 21 patients under 18 years of age, when operated for the first time, were studied immunohistochemically. We used a set of 6 different antibodies against p53, suitable for paraffin section (PAb1801, PAb240, DO-1, DO-7, BP53-12, CM-1). The intensity of the nuclear staining was scored and the percentage of stained nuclei counted. A tumor was scored positive if at least 10% of nuclei showed at least medium staining intensity with at least 1 primary antibody. No single antibody detected all cases designated immunopositive. This shows the advantage of using a set of antibodies. The time of survival in the immunopositive cases was significantly shorter, but immunopositivity was correlated with grade III (WHO). Comparing the time of survival between p53-immunopositive and -immunonegative grade III (WHO) astrocytomas no significant difference was found. We conclude that p53 immunoreactivity is not an independent unfavorable prognostic factor in astrocytomas of childhood and adolescence.
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PMID:Accumulation of nuclear p53 protein and prognosis of astrocytomas in childhood and adolescence. 892 99

We investigated the p53 protein expression in gastrointestinal lymphomas (GIL). Paraffin-embedded samples of 52 patients were examined for this purpose. The avidin-biotin Complex method was used for immunostaining. Nine of the 52 samples (17.3%) showed p53 staining. There was no relationship between the p53 protein expression and clinical characteristics, such as stage, disease localization and tumor burden. Complete remission was higher in patients not expressing this protein, and the p53 protein was more frequently expressed in intermediate and high grade histopathology than low grade lymphomas, but there was no statistically significant difference between the two groups (p = 0.008). Interestingly, patients expressing the p53 protein were younger than the ones not expressing it (30.7 +/- 14.1 vs. 43.6 +/- 15.7 years). We conclude that the p53 protein expression in GILs may be a poor prognostic indicator due to a lower response rate to chemotherapy.
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PMID:p53 protein expression in gastrointestinal lymphomas. 897 99

Research on Neurofibromatosis (NF) has been directed at understanding what determines disease quiescence, exacerbation, and the possible malignant evolution. Studies on NF have examined the role of genetic oncosuppression in the evolution of the defence against the non-self. Paraffin fixed specimens of benign and malignant neoplasia, occurring in patients with NF1 and NF2, were tested for the presence of p53: a reliable marker of genetic oncosupression. The wild type variant of p53 is expressed in malignant neoplasia, and is usually not expressed in benign tumors. Contrariwise, an immune reaction it is seen in benign tumors and is practically absent in malignant tumors. Evidence of protein p53 in the various malignant neoplasias studied by our group seems to reflect the up-regulation on the oncosuppresive genetic potential that occurs while there is a lack of immunological defence. In the presence of an immunological defence, the expression p53 is normally not seen e.g. plexiform neurofibromas. The evolution of the various neoplastic types here reported was the same as that reported by current clinical and experimental models: the cell's defective genes are no longer suppressed and after activation the genes undergo initiation, promotion, and the cell sustains inflammatory-immune reactions that lead to fibrosis; what follows is a variable period of apparent quiescence. Severe pathogenic stimuli may act on predisposed cells and deteriorate pre-existing genetic damage, casting the cell into a phase of dysplastic or neoplastic proliferation that overcomes the body's defences. Hope for future therapy lies in the development of drugs that can either mimic the immune system or the proteins encoded by the oncosuppressor genes.
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PMID:Tumour suppressor genes, immunology and local manifestations of neurofibromatosis phenotypes. 900 79

Abnormalities in the p53 tumour suppressor gene and in the expression of its protein are common in colorectal carcinoma. The prognostic significance of these p53 abnormalities was studied in 66 patients with colorectal cancer, followed for more than 10 years. Single-strand conformation polymorphism (SSCP) analysis was used to detect alterations in exons 5-8 of the p53 gene. Paraffin sections were examined immunohistochemically for p53 overexpression with the monoclonal antibody DO-7 (Dako) both with and without microwave antigen retrieval. Abnormalities of the p53 gene were found in 41 per cent of cases by SSCP analysis. Outcome was unrelated to SSCP abnormalities (P = 0.19), except for the Dukes' A and B subgroup, where decreased survival was found in cases with abnormal SSCP (P = 0.01). Overexpression of p53 protein was seen by immunohistochemistry in 47 per cent of cases without, and in 52 per cent of cases with microwave antigen retrieval. Immunohistochemical overexpression of p53 protein either with or without microwave antigen retrieval was an independent prognostic indicator of poor survival. These results suggest that for routine purposes, immunohistochemical detection of the p53 protein product may be more useful than SSCP analysis of the encoding p53 gene in identifying those at high risk of colorectal cancer recurrence and death.
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PMID:Prognostic significance of p53 abnormalities in colorectal carcinoma detected by PCR-SSCP and immunohistochemical analysis. 901 55

Cell proliferation indices of 31 primary intracranial haemangiopericytomas (HPC) and their recurrences and metastases were correlated with the long-term recurrence, metastasis and survival rates. Paraffin-embedded specimens were used for K-67, PCNA and p53 immunostainings and for estimation of S-phase fraction (S-PF) in flow cytometry. The median Ki-67 and PCNA indices and S-PFs were 10.4, 3.2, and 4.0 for primary HPCs and 14.1, 14.1, and 5.5 for recurrences, respectively. High indices were associated with higher recurrence, metastasis and death rates, but not at the p < or = 0.5 level. Consequently, these indices do not seem useful in planning of treatment and follow-up of meningeal HPCs. Meningeal HPCs, in contrast to meningiomas, recur almost always despite seemingly complete removal and often metastasize elsewhere in the body. This difference between two sharply demarcated tumours must reflect particularly adhesive and infiltrative properties of HPC cells and not just higher proliferation potential.
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PMID:Outcome of 31 intracranial haemangiopericytomas: poor predictive value of cell proliferation indices. 903 Mar 46

Paraffin embedded tissue of 84 oligodendrogliomas (63 primary tumours, 21 recurrences), 21 glioblastomas with oligodendroglial growth pattern (15 primaries, 6 recurrences) and 17 mixed gliomas was investigated for the presence of mutations in exons 5-9 by means of single stranded conformation polymorphism (SCCP), temperature gradient gel electrophoresis (TGGE) and direct DNA sequencing. In parallel, p53 protein accumulation was determined by means of immunohistochemistry. The percentage of mutations was found to be higher than previously reported (6 of 44 grade II oligodendrogliomas, 4 of 19 grade III oligodendrogliomas, 4 of 15 glioblastomas). In 4 cases, the mutations lead to distinct changes in the primary or secondary structure of the protein (cysteine-->tyrosine, proline-->leucine) and were associated with marked accumulation of p53 protein. A significant correlation between p53 protein accumulation and TP53 gene aberrations was found (P < 0.001), although p53 protein accumulation was detected more often than TP53 gene anomalies, indicating that factors other than TP53 gene mutation may also lead to a p53 protein accumulation in the tumour cells. A significant correlation was found for p53 protein accumulation and tumour grade but not TP53 gene mutations. In conclusion, evaluation of p53 protein accumulation reflected the clinical course of oligodendrogliomas better than the mere presence of TP53 gene mutations.
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PMID:Demonstration of p53 protein and TP53 gene mutations in oligodendrogliomas. 903 5

The purpose of the present study was to investigate the role of p53 in tumor progression of colorectal adenomas and early carcinomas, while especially focusing on flat tumors (depressed adenomas and non-polypoid carcinomas). Paraffin sections of 61 pure adenomas (33 polypoid, 28 depressed), 26 carcinomas in polypoid adenoma (CIA) and 63 pure carcinomas (36 polypoid, 27 non-polypoid) were examined for immunostaining using p53 monoclonal antibody (PAb 1801). All of the carcinomas were restricted to the mucosa. The number and distribution of the p53 positive tumor cells was evaluated, and then compared with tumor growth patterns and histological features. The incidence of p53 expression in carcinomas (58% in CIA and 51% in pure carcinomas) was significantly higher than that in polypoid adenoma (27% in CIA and 21% in pure adenomas). However, the same incidence in depressed adenomas (51%) was significantly higher than in polypoid adenomas. No correlation in carcinomas was observed between p53 expression and clinicopathologic data except for age. The distribution of p53 positive cells was different between adenomas and carcinomas. There tended to be fewer p53 positive cells in adenomas, even in depressed ones, than in carcinomas and they also tended to be confined to the superficial areas in adenomas, while they were diffusely distributed in carcinomas. Interestingly, the p53 positive cells were more frequently present in the deep mucosal areas than in the superficial areas of some non-polypoid carcinomas. In conclusion, the following hypotheses are suggested: (i) the increase of p53 expression from adenoma to carcinoma supports the hypothesis of an adenoma-carcinoma sequence in a polypoid tumor; (ii) the unique p53 expression in non-polypoid carcinoma suggests the existence of another type of carcinogenesis; and (iii) depressed adenomas are thus considered to have a high potential risk of carcinoma.
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PMID:p53 expression patterns in colorectal adenomas and early carcinomas: a special reference to depressed adenoma and non-polypoid carcinoma. 911 Mar 48


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