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)

This study investigated a total number of 120 colorectal malignant tumor tissues by applying a new quantitative luminometric assay (LIA)-mat, immunohistochemistry (IHC) (n=100), PCR/SSCP (n=42), and sequencing (n=7). Sera were collected from 235 patients suffering from colorectal carcinoma in addition to 195 healthy individuals as a control group. Manual ELISA kit was developed to detect p53 autoantibodies in the sera of those patients. Our data demonstrated that the LIA-mat yields reliable estimates of p53 expression in soluble cell extracts as compared with results obtained by immunohistochemistry which showed positive immunostaining in 63% of the studied cases. Using a cut-off value of 1.8 ng/mg protein, 65 tumors out of 120 (54%) were classified to be positive by LIA-mat, manifesting protein overexpression, while 22 out of 42 (52%) tumor samples showed p53 gene alteration when applying single strand conformation polymorphism (SSCP) analysis on polymerase chain reaction products. In tumor samples without a p53 gene alteration, the median soluble p53 protein level was 4.3 ng/mg protein, whereas the median p53 protein level for tumor samples with p53 gene alteration was 7.5 times higher. Despite a significant correlation between the outcome of LIA and SSCP, a disagreement was found in 30% of cases. We found no significant correlation between p53 protein overexpression and clinicopathological findings except for distant metastasis (p=0.33), indicating p53 immunoreactivity to be an independent prognostic factor. Our data showed that 18% of patients suffering from colorectal cancer developed autoantibodies against p53 in their sera which might be an early indicator for tumor development and distant metastasis.
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PMID:p53 genetic alterations, protein expression and autoantibodies in human colorectal carcinoma: A comparative study. 949 37

This project was undertaken to study the survival properties of various prostate cells, including normal (NHP), BPH (benign prostate hyperplasia), primary carcinoma (PCA), and metastatic prostate cancer cells (LNCaP, PC3, and Du145), in the absence of trophic factors. Cell proliferation and cell death were quantitated by enumerating the number of live cells using MTS/PMS kit and of dead (apoptotic) cells using 4',6-diamidino-2-phenylindole dihydrochloride nuclear staining. These cells demonstrated an overall survivability in the order of BPH < NHP < LNCaP < PC3 < PCA < Du145. Upon growth factor deprivation, NHP/BPH cells rapidly underwent apoptosis, leading to a decreased number of live cells. PCA/PC3/Du145 cells, in contrast, demonstrated an initial phase of aggressive growth during which apoptosis rarely occurred, followed by a "plateau" phase in which cell loss by apoptosis was compensated by cell proliferation, followed by a later phase in which apoptosis exceeded the cell proliferation. LNCaP cells demonstrated survival characteristics between those of NHP/BPH and PCA/PC3/Du145 cells. We concluded that the increased survivability in prostate cancer cells results from enhanced cell proliferation as well as decreased apoptosis. The molecular mechanisms for evasion of apoptosis in prostate cancer cells were subsequently investigated. Quantitative Western blotting was used to examine the protein expression of P53 and P21WAF-1, Bcl-2 and Bcl-X(L) (anti-apoptotic proteins), and Bax, Bak, and Bad (proapoptotic proteins). The results revealed that, upon trophic factor withdrawal, NHP and BPH cells upregulated wild-type p53 and proapoptotic proteins Bax/Bad/Bak and down-regulated the expression of P21. Furthermore, NHP and BPH cells endogenously expressed little or no Bcl-2. In sharp contrast, prostate cancer cells expressed nonfunctional P53 and various amounts of Bcl-2 proteins. Upon deprivation, these cancer cells up-regulated P21 and Bcl-2 and/or BclX(L), lost response to withdrawal-induced up-regulation of Bax/Bad/Bak or decreased or even completely lost Bax expression and expressed some novel proteins such as P25 and P54/55 complex. These data together suggest that prostate cancer cells may use multiple molecular mechanisms to evade apoptosis, which, together with increased proliferation, contribute to extended survivability of prostate cancer cells in the absence trophic factors.
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PMID:Extended survivability of prostate cancer cells in the absence of trophic factors: increased proliferation, evasion of apoptosis, and the role of apoptosis proteins. 969 82

We describe a method of in situ hybridization (ISH) to assess numerical chromosome abnormalities on alcohol-fixed smears obtained by fine-needle aspiration from breast cancer patients, using a commercially available amplification kit to demonstrate numerical chromosome alterations of chromosome 17. In this staining procedure after detection of the biotin-labeled alpha-satellite probe for chromosome 17 with avidin-biotin-peroxidase, we incorporated a signal amplification based on the peroxidase-catalyzed deposition of a biotinylated phenolic compound followed by a secondary reaction with peroxidase. The reactions are revealed by deposition of diaminobenzidine and can be analyzed in an optical microscope, with total preservation of the morphology, allowing a direct morphologic-cytogenetic correlation. A series of 25 cases of aspirates from breast cancer were analyzed with this methodology. Aneusomy was found in 14 cases (56%), whereas 11 (44%) had a normal number of chromosome 17 copies. Polysomy occurred in all aneusome cases except one. We did not find concordance between numerical chromosome abnormalities of chromosome 17 and nuclear grading as well as with the immunoexpression of p53 and c-erbB2 studied in the smears. We conclude that the application of the ISH signal amplification method on alcohol-fixed smears will eliminate the need for fresh material and will provide several advantages, such as improvement of morphological concomitant analysis without the need for a fluorescence microscope; utilization, whenever malignancy is found, without necessity to reaspirate the patient; and adequacy of archival material.
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PMID:Detection of numerical chromosome 17 abnormalities in fine-needle aspirates of breast cancer using a novel in situ hybridization signal amplification method. 970 95

Scooter exhaust particulate matter emissions were found to be mutagenic and to induce potential carcinogenicity. To further explore the mechanisms of mutagenicity and potential carcinogenicity of scooter exhaust particulate matter emissions, immunohistochemistry assays were carried out to detect the expression of some oncogenes and tumor suppressor genes in human diploid cell strain (KMB-13) cells, which were morphologically transformed by the organic extracts of scooter exhaust particulate matter emissions. An ABC diagnostic kit was used to investigate the expression of c-myc, p21, p53, and p16 proteins in the transformed cells. The c-myc and p21 proteins showed marked positive staining compared to control. The data suggest that the mutagenicity and potential carcinogenicity of the scooter exhaust particulate matter emissions correlate with the activation of some cellular oncogenes.
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PMID:Activation of cellular oncogenes in human diploid cell strain (KMB-13) cells by scooter exhaust particulate matter emissions. 980 Nov 90

Activation of the angiogenic process occurs during tumorigenesis, as does disturbance of cell proliferation and apoptosis. Seeking a potential correlation, we investigated tumor cell apoptosis, proliferation, and angiogenesis in the adenoma-carcinoma sequence of colorectal carcinogenesis using an in situ apoptosis detection kit and MIB-1 and anti-CD34 antibodies in 27 adenomas with low dysplasia, 17 adenomas with high dysplasia, and 26 carcinomas in adenoma, as well as assessed p53 and bcl-2 expressions. The results showed that the potential for apoptosis was augmented, paralleling the increment of proliferation, in adenomas with low dysplasia but diminished when adenomas progressed from low dysplasia to high dysplasia and cancer. A gradual increment of microvessel density was observed during the progression with an increase during transition from low dysplasia to high dysplasia and cancer. Correlation coefficient test showed an inverse correlation between apoptotic index and microvessel density when all of the lesions were taken into account. No apparent impact of aberrant p53 on angiogenesis or bcl-2 on apoptosis was observed in this study. These results suggest that the angiogenesis initiates during transition from low dysplasia to high dysplasia and cancer, which may, in turn, contribute to the reduction of tumor cell apoptosis during colorectal carcinogenesis.
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PMID:Changes of angiogenesis and tumor cell apoptosis during colorectal carcinogenesis. 991 11

We investigated the expression of apoptosis-related factors, p53, Bax, Bcl-2, and spontaneous apoptosis in 57 cases of oral and oropharyngeal squamous cell carcinoma (SCC) by immunochemical staining and ApopTag kit. Positive expression of Bax was inversely associated with advanced tumor stage (P = 0.0225), lymph node metastasis (P = 0.0225), clinical stage (P = 0.0083) and poor prognosis (P = 0.0478). Positive expression of p53 was related to poor prognosis (P = 0.0445) and was associated with negative expression of Bax (P = 0.0439). The apoptosis index did not correlate with clinical outcome. These results suggest that abnormality of Bax expression plays an important role in tumor progression in oral and oropharyngeal SCC.
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PMID:Decreased expression of Bax is correlated with poor prognosis in oral and oropharyngeal carcinoma. 1040 45

The results of immunohistochemical expression of p53 protein in 106 invasive breast cancers were correlated with conventional pathologic prognostic parameters. Archival formalin-fixed, paraffin-embedded tissue sections of these cases were stained with a monoclonal antibody (Ab-2), raised against p53 protein using a peroxidase-labelled streptavidin biotin kit. Fifty-six (53%) showed positive nuclear staining; 31 were considered weakly, 21 moderately and 4 strongly positive. Forty-three (77%) of these positive cases stained less than 50% of the tumor cells, with a significant association between intensity and proportion of nuclei stained (p<0. 05). p53 staining also correlated with histologic grade (p<0.005) but not with tumor size nor clinical stage (p>0.05). The follow-up data did not reveal any statistically significant survival advantage for patients with p53 negative tumors.
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PMID:Immunohistochemical expression of p53 protein in invasive breast carcinoma: clinicopathologic correlations. 1042 20

The purpose of this study was to determine whether point mutations and loss of the p53 gene take place in ulcerative colitis which is histologically negative for dysplasia. DNA was extracted from 13 frozen rectal or colon biopsies and blood samples. Ulcerative colitis was classified histologically as active (10 cases) and inactive (3 cases). Exons 5-8 were amplified by PCR, treated with exonuclease and shrimp alkaline phosphatase and sequenced by the dideoxy chain termination method with the Sequenase Version 2.0 DNA sequencing kit. PCR products of intron 6 and exon 4 were digested with MspI and AccII, respectively, for RFLP analysis. No p53 gene mutation was detected in these cases. The number of informative patients for loss of heterozygosity (LOH) at the p53 intron 6 was high, 11 out of 12 (92%), whereas no LOH was observed. LOH affecting p53 exon 4 was not detected in lesions from 5 of 12 patients (42%). In ulcerative colitis, tumor progression is similar to that in sporadic colon cancer, and other oncogenes and tumor suppressor genes are likely to be mutated before the p53 gene.
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PMID:Infrequent p53 gene alterations in ulcerative colitis. 1046 83

The purpose of this study was to clarify which factors are important as predictors not only of patient survival but also of hematogenic metastasis in 15 patients with stage I lung adenocarcinoma who underwent curative operation. The relationship between tumor angiogenesis, apoptosis, and p53 oncogene was also studied. A total of 15 patients were divided into two groups: surviving group (n = 7) and nonsurviving (metastasis) group (n = 8). We studied the medical charts, operative records, pathologic reports, and tumor specimens taken at surgical resection. We measured the apoptotic index using the ApopTag kit and the intratumoral microvessel count using an anti-CD34 monoclonal antibody. In addition, immunohistochemical staining for the expression of p53 was conducted simultaneously. The clinicopathological characteristics, including age, sex, tumor size (pT), and histological differentiation, were not significantly different between the surviving and the nonsurviving group. The microvessel count was significantly higher in nonsurviving group than in the surviving group. The apoptotic index and the expression of p53 was not significantly different between the two groups. An inverse correlation between the apoptotic index and microvessel count, and a positive correlation between the expression of p53 and microvessel count, were observed. Angiogenesis may be an important prognostic factor in patients with stage I lung adenocarcinoma.
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PMID:Tumor angiogenesis, apoptosis, and p53 oncogene in stage I lung adenocarcinoma. 1055 32

Tumor cell apoptosis, proliferation and p27 expression using an in situ apoptosis detection kit, anti-Ki67 antibody and anti-p27 antibody were investigated in 171 colorectal adenocarcinoma specimens, together with the assessment of mutated p53 expression. No apparent association was observed among p27 expression, mutated p53 accumulation, the Ki67 labeling index and the apoptotic index (AI). In the multivariate analysis using the median values as the cut-off points (46.8% for p27 expression and 0.89% for AI), p27 expression was identified as an independent and significant predictor for overall survival. When the present series of patients were dichotomized by these cut-off points to categorize the cases into 4 subgroups, the patients in the group with low p27 expression and a low AI had the poorest prognosis. The assessment of p27 expression and AI therefore may prove valuable in identifying patients with colorectal adenocarcinoma who may have a poor prognosis.
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PMID:Prognostic significance of p27(kip1) protein expression and spontaneous apoptosis in patients with colorectal adenocarcinomas. 1064 40


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