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)

p53 protein accumulation, thought to be caused by p53 gene mutation, is closely related to poor prognosis of patients with certain types of carcinomas. The progression of esophageal squamous cell carcinoma (SCC) is also strongly suspected to depend on the p53 tumor suppressor gene. Formalin-fixed, paraffin-embedded sections were taken from 25 patients who underwent esophagectomy for SCC. Fourteen patients had no preoperative therapy (control group), while the other 11 patients received preoperative radiotherapy (radiation group). There was no difference in pathological TNM classification between the two groups. These sections were examined by immunostaining with monoclonal antibody PAb 1801 to determine the accumulation of p53 protein, and apoptotic frequency was determined by TdT mediated dUTP-biotin nick end-labeling (TUNEL). In the control group, well to moderately differentiated cases showed a significantly higher AI (apoptotic index which is the number of apoptotic cells among 1000 cancer cells. %0) (51.7+/-83.4) than poorly differentiated cases (AI=1.3+/-1.0) (P<0.05). Similar results were obtained in the radiation group. The former group included 4 cases of p53 grade 4 (p53 protein detected in over 70% of the tumor cells), and the latter included 2. Few apoptotic cells were observed in any of 6 tumor tissues. In each patient, tumor cells with accumulated p53 protein were very rare to be apoptotic. On the other hand, apoptosis was observed in tumor cells without p53 protein accumulation. Spontaneous apoptosis in esophageal SCC can be induced more easily in differentiated than in poorly differentiated cases. This tendency may be enhanced by preoperative radiotherapy. Extensive p53 protein may suppress apoptotic induction in esophageal squamous cell carcinomas.
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PMID:Suppressed apoptotic induction in esophageal squamous cell carcinomas expressing extensive p53 protein. 900 43

In immunohistochemistry, it is well known that the majority of monoclonal antibodies to keratins work best on fresh frozen tissue specimens, yet in clinical practice most biopsies are routinely fixed in formaldehyde. This seriously limits the range of keratins that can be reliably assessed in retrospective studies (particularly where only rare archival material exists) and where subtle changes during tissue differentiation may be important. Antigen retrieval using exposure to microwave radiation is one technique that has been applied successfully to other tumour markers (e.g., p53). However, few papers have used this method when immunolabelling for keratins, in spite of the widespread use of antikeratin antibodies as markers of differentiation. The effect of keratin antigen retrieval using microwave processing was assessed on a range of oral mucosal biopsies, since the oral cavity displays a wide range of keratins. A panel of six well characterized antibodies was chosen: LP34 (Ck1, 5, 6, 18), LH1 (Ck10), LL025 (Ck16), A53 BA2 (Ck19), AE8 (Ck13), and E3 (Ck17). For each specimen, one piece was stored in liquid nitrogen and another piece fixed in formalin. Tissue sections were cut from each and, using the peroxidase avidin biotin technique, keratin expression was recorded for a frozen section, a dewaxed section, and a microwave-heated dewaxed section. Although overall there was a 25% improvement in identification of keratins after microwaving, some antibodies performed better than others. Given that keratins have been shown to be of value in tumour diagnosis, this study suggests that microwave processing of archival material can be a valuable adjunct to such analysis.
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PMID:Keratin antigen retrieval in oral mucosal biopsies using microwave processing. 901 9

Detection of p53 expression has been reported to be associated with poor prognosis in a variety of human malignancies. The aim of the current study was to utilize immunocytochemical antigen detection techniques to search for evidence of altered p53 protein overexpression in 43 primary osteosarcomas (OS). The study was carried out on formalin fixed, paraffin-wax embedded 3 to 4 microns, previously decalcified OS tissue sections. A four step biotin-streptavidin based method was employed with peroxidase conjugation as the enzymatic label. Presence of a frequent level of p53 protein expression was detected in all 43 primary osteosarcomas, suggesting a frequent p53 gene mutation. p53 protein alterations were also associated with all grades of cell microenvironment heterogeneity in the observed OSs. Overexpression of the p53 protein was detected in 31/43 (72%) primary OS cases. Formalin fixed and paraffin-wax embedded human breast carcinoma tissue sections were employed as positive control tissue. p53 protein absence was demonstrated in normal postnatal thymus, serving as the negative control tissue. Our results lead us to the following conclusions: a) the altered p53 gene product is detectable employing the chosen mouse anti-human MoAB in decalcified, formalin fixed, paraffin-wax embedded, routine tissue sections of OSs and breast carcinomas which provides an opportunity for numerous retrospective studies and comparison with additional immunodiagnostic indicators; b) primary OSs with similar cell differentiation may be genetically heterogeneous; c) p53 gene or protein alterations represent early, immunodiagnostic markers of a malignant immunophenotype (IP) in various human neoplasms, including OSs; and d) immunomorphological techniques and in situ hybridization should be employed as methods to collect data for computerized, quantitative image analysis (IA) of the cellular accumulation and localization of the altered p53 protein.
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PMID:Immunohistochemical detection of p53 protein overexpression in primary human osteosarcomas. 906 1

Geographic differences in exposure to suspected carcinogens have been identified in esophageal carcinogenesis, and both p53 alterations and human papillomavirus (HPV) infection have been reported in esophageal squamous carcinoma (ESC) from high-risk areas, including China and South Africa. The status of p53 alterations and HPV infection in ESC has not been determined in northern Italy, where the incidence of ESC is low. Formalin-fixed paraffin-embedded esophageal samples containing normal, dysplastic, and carcinomatous tissue from 18 patients were examined for p53 protein accumulation with immunohistochemistry, p53 mutation (exons 5-8) with PCR-single-strand conformation polymorphism analysis and DNA sequencing, and HPV infection with PCR using general primers to amplify the L1 gene. Accumulation of p53 protein was observed in both precancerous and carcinomatous lesions. p53 mutations were rare in dysplastic lesions but were detected in 9 of 18 carcinomas, a finding consistent with reports from other geographic areas. Examination of the p53 mutation spectrum revealed no hot spot mutation. In contrast, HPV was not found in any of these 18 cases. This is consistent with the findings from other low ESC risk areas in which HPV infection may not play a crucial role in esophageal oncogenesis, whereas the high risk of ESC in China and South Africa may be attributed to frequent HPV infection.
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PMID:p53 alterations but no human papillomavirus infection in preinvasive and advanced squamous esophageal cancer in Italy. 913 59

Although the relationship among different biologic markers of breast cancer has been shown to be important in predicting cancer behavior, expression of these markers can be an attribute of the population under study. Breast cancer is the most common malignancy among Egyptian women. We have studied a number of prognostic tumor markers in infiltrating ductal carcinoma in a group of Egyptian women and have correlated our results with traditional histologic parameters of behavior such as tumor nuclear grade and lymph node status. Seventy-five cases of infiltrating ductal breast cancer were evaluated from pathology archives. Formalin-fixed paraffin-embedded sections were immunohistochemically stained for PCNA, p53, c-erB-2, metallothionein, cathepsin-D, and GST-pi using specific antibodies and a standard avidin-biotin method. Most high-grade tumors were associated with higher PCNA expression and p53 abnormality. There was a significant difference between node-negative and node-positive tumors with regard to their metallothionein content; other markers, however, did not differ significantly between node-negative and node-positive tumors. PCNA expression, metallothionein expression, and p53 mutation appear to be markers of aggressive tumor behavior in Egyptian women with breast cancer.
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PMID:Immunohistochemical markers of tumor prognosis in breast cancer in Egypt. 916 36

P53 is overexpressed in more than 50% of all human cancers. A previous study suggested that p53 was also overexpressed in oral papillomas. This study was carried out to investigate whether p53 expression was correlated with expression of the cellular proliferation marker Ki-67 and the epithelial differentiation marker cytokeratin-4 (CK4) in oral papillomas. Formalin-fixed paraffin-embedded sections of 30 oral papilloma specimens and 30 unmatched normal oral mucosal specimens were processed for immunohistochemistry, using an avidin-biotin-peroxidase procedure and monoclonal antibodies. A semiquantification analysis on p53 and Ki-67 labeling indices was performed. Twenty-eight of 30 (93%) papilloma specimens were positive for p53. The percentage of p53-positive cells in the basal layer was 60.4 +/- 14.8 (mean +/- SD, n = 28), and that of Ki-67-positive cells was 26.7 +/- 14.4. There was no correlation between expression of p53 and that of Ki-67. Expression of CK4 was inversely correlated with the expression of Ki-67 but not correlated with the expression of p53.
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PMID:Expression of p53, Ki-67 and cytokeratin-4 (CK4) in oral papillomas. 917 72

The aim was to investigate the pattern of expression of p53 protein and two wild-type (wt) p53-induced proteins (mdm2 and p21/waf1), as an indirect way of assessing p53 gene status in breast carcinomas. Formalin-fixed paraffin embedded tissue from 102 cases of breast carcinomas comprising mostly ductal carcinomas (88 cases) was stained by immunohistochemistry for p53, mdm2 and p21/waf1 proteins. We found p53, mdm2 and waf1/p21 protein expression in 33/102, 20/102 and 38/102 breast carcinomas, respectively. Parallel p53/mdm2 protein expression was found in 9 cases. Five were also p21/waf1 positive. Discordant p53+/ mdm2-protein expression was found in 24 cases. Nine were p21/waf1 positive and the remaining fifteen were p21/waf1 negative. The patterns mdm2+/p53-/p21- and p21+/p53-(+)/mdm2- were found in 6 and 20 cases, respectively. Parallel p53/mdm2/p21 protein expression may represent breast carcinomas with wt p53 gene since mdm2 and p21 proteins are inducible by wt p53 gene. In these cases p53 protein expression may be due to stabilisation to mdm2 protein. This could be important in the pathogenesis of these cases since mdm2 may deregulate the p53-dependent growth suppressive pathway. Discordant p53+/mdm2-/p21- protein expression may represent breast carcinomas with p53 gene mutations unable to activate expression of mdm2 and p21 proteins. Breast carcinomas with p53+/mdm2/p21+ protein expression may have either wt p53 with deregulated mdm2 gene expression or mutated p53 gene with p53-independent p21 expression. Cases with only mdm2 expression may represent tumours with mdm2 gene amplification or overexpression and cases with only p21 expression may reflect p53-independent regulation of p21 protein.
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PMID:p53 protein expression in breast carcinomas. Comparative study with the wild type p53 induced proteins mdm2 and p21/waf1. 921 75

Formalin-fixed paraffin-embedded material from 57 patients in whom curative resection of pancreatic carcinoma had been attempted was analysed by an immunohistochemical procedure to estimate proliferation and p53 protein expression. Using the monoclonal antibody (MAb) MIB-1, which recognizes a Ki-67 epitope, the proliferating cell index (PCI, percentage of immunoreactive tumour nuclei) and proliferating cell area (PCA, percentage of immunoreactive tumour nuclear area) were calculated using an interactive image analysis system and were compared with semiquantitative scoring of stainability. MAb DO-7, which recognizes both wild- and mutant-type p53 protein, was used to assess p53 expression in the same material. MIB-1 stainings were of high quality in 53 tumours. The median PCI was 29.7% (range 0.5-82.1%) and the median PCA was 10.6% (range 0.0-36.5%). There was a close correlation between PCI and PCA (P < 0.0001). PCI and PCA values were in conformity with the semiquantitative scoring (P < 0.0001). The p53 immunohistochemical stainings were successful in 48 tumours and the protein was expressed in 22 (46%). High PCI values (> 45%, n = 14) correlated with shorter survival time (P < 0.01). PCA (P < 0.05) and the expression of p53 protein (P < 0.001) were independent prognostic variables.
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PMID:Prognostic significance of Ki-67 antigen and p53 protein expression in pancreatic duct carcinoma: a study of the monoclonal antibodies MIB-1 and DO-7 in formalin-fixed paraffin-embedded tumour material. 921 33

We have performed immunohistochemical staining for p53 and c-erbB-2 on formaldehyde-fixed, paraffin-embedded primary invasive ductal carcinomas from 112 patients, with a minimal follow-up time of 60 months. All of them had received postoperative chemoradiation therapy. We have analyzed the association of these factors with epidemiologic risk factors, histopathologic features and hormonal receptor status and the influence on prognosis. Our results indicate that the expression of c-erbB-2 protein defines a group of node-negative patients with poor prognosis. The overexpression of c-erbB-2 has shown a significant association with estrogen receptor status (those tumors expressing c-erbB-2 are usually estrogen receptor negative), presence of fibrosis and lymphoplasmacytoid infiltrates. P53 expression has shown no relation either with prognosis or with any other histopathologic or clinical feature. The only factors with prognostic influence in our series have been tumor size, the presence of node metastases, TNM stage and the prognostic morphometric index (Baak's index), apart from c-erbB-2 in node-negative patients. However, only the TNM stage showed an independent association with prognosis after a multivariate analysis. In summary, in our experience the expression of p53 protein has no prognostic influence on breast carcinoma, and TNM stage remains to be as the most powerful prognostic factor in these patients.
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PMID:Immunohistochemical expression of p53 and c-erbB-2 in breast carcinoma: relation with epidemiologic factors, histologic features and prognosis. 922 51

The present study was undertaken to examine the distribution of p53, p21, mdm-2 and bcl-2 protein expression in human colorectal adenocarcinomas in order to obtain combined information about the immunophenotypes characterising these tumours. Formalin-fixed, paraffin-embedded tissue sections from 52 cases of colorectal adenocarcinomas were stained using immunohistochemical methods for the detection of p53, p21/waf1, mdm2 and bcl-2 proteins. P53, p21/waf1, mdm2 and bcl-2 proteins were expressed in 35/52, 45/52, 9/52 and 27/52 cases, respectively. All nine mdm2+ cases expressed p53 and p21 proteins as well. The three patterns observed in p53/p21 expression were: p53+/p21+, p53+/p21- and p53-/p21+ in 28, 7, and 17 cases, respectively. Consequently, p53+/mdm2-/p21+, p53+/mdm-/p21- and p53-/mdm2-/p21+ immunophenotypes were expressed in 19, 7, and 17 cases respectively. Four patterns of p53/bcl2 expression were identified: p53+/bcl2+, 20 cases; p53+/bcl2-, 15 cases; p53-/bcl2+, 7 cases; p53-/bcl2-, 10 cases. It was noteworthy that 9 of the 10 p53-/bcl2-tumours had negative lymph node status. The present results suggest that both p53 dependent and p53-independent induction of p21 expression may be involved in the molecular mechanisms controlling these tumours. High expression of the p53 protein in colorectal carcinomas could be due not only to p53 gene mutations but also to binding to mdm2 protein which leads to p53 protein stabilisation. In addition, tumours with p53-/bcl2- immunophenotype are frequently associated to negative lymph node status and seem to be less aggressive.
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PMID:Immunohistochemical expression of p53, bcl-2, mdm2 and waf1/p21 proteins in colorectal adenocarcinomas. 925 82


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