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)

Simian virus 40 (SV40) large-T antigen and the cellular protein p53 were phosphorylated in vivo by growing cells in the presence of 32Pi. The large-T/p53 complex was isolated by immunoprecipitation and used as a substrate for protein phosphatase 2A (PP2A) consisting of the catalytic subunit (C) and the two regulatory subunits, A and B. Three different purified forms of PP2A, including free C, the AC form, and the ABC form, could readily dephosphorylate both proteins. With both large-T and p53, the C subunit was most active, followed by the AC form, which was more active than the ABC form. The activity of all three forms of PP2A toward these proteins was strongly stimulated by manganese ions and to a lesser extent by magnesium ions. The presence of complexed p53 did not affect the dephosphorylation of large-T antigen by PP2A. The dephosphorylation of individual phosphorylation sites of large-T and p53 were determined by two-dimensional peptide mapping. Individual sites within large-T and p53 were dephosphorylated at different rates by all three forms of PP2A. The phosphates at Ser-120 and Ser-123 of large-T, which affect binding to the origin of SV40 DNA, were removed most rapidly. Three of the six major phosphopeptides of p53 were readily dephosphorylated, while the remaining three were relatively resistant to PP2A. Dephosphorylation of most of the sites in large-T and p53 by the AC form was inhibited by SV40 small-t antigen. The inhibition was most apparent for those sites which were preferentially dephosphorylated. Inhibition was specific for the AC form; no effect was observed on the dephosphorylation of either protein by the free C subunit or the ABC form. The inhibitory effect of small-t on dephosphorylation by PP2A could explain its role in transformation.
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PMID:Dephosphorylation of simian virus 40 large-T antigen and p53 protein by protein phosphatase 2A: inhibition by small-t antigen. 184 68

We studied p53 gene at the DNA and protein level in human gastric cancer tissues and corresponding normal gastric mucosae from 20 cases of patients undergone radical surgery. By Southern blotting, the p53 gene was found to be partially deleted in 30% (6/20) of gastric cancer tissues. ABC immunohistochemical study of p53 expression was carried out on cryostat sections using monoclonal antibodies (PAb 1801) to p53. High level expression of mutated p53 protein was detected in 55% (11/20) gastric cancer tissues. The staining pattern was intranuclear and/or intracytoplamic. There was no detectable staining of any of the normal gastric tissues with 1801 antibody. The positive rate of p53 overexpression was higher in poorly-differenciated glandular carcinomas than well-differenciated cancer (P = 0.0116). Highly significant association exists between high level p53 expression and allele deletion (r = 0.59). The date indicate that inactivation of p53 gene is important in human gastric carcinogenesis and tumor progression. The assay of p53 gene structure and products may provide new biologically relevant tumor marks for predicting the behavior of gastric carcinomas, identifying more aggressive tumors, determining prognosis of the patients and guiding treatment.
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PMID:[p53 gene deletion and abnormal expression in gastric carcinoma]. 765 19

Mutational changes in the p53 tumor suppressor gene are the most frequent genetic alterations in human malignant tumors. Studies have shown a correlation of p53 expression in breast cancer with tumor prognosis. In contrast to mutational activation of ras and GSP in thyroid tumors, little is known about the role of p53 in thyroid tumor development. Therefore thyroid tumors and thyroid tumor cell lines were studied for the presence of p53 mutations. Snap-frozen tissues from 57 differentiated thyroid carcinomas (DTCs) and 5 goiters were studied by immunohistochemical methods. A panel of six antibodies (pAb 240, 421, 1620, 1801, DO7, and CM1) was employed by using the ABC technique. Five cell lines from DTCs (FTC133, 236, 238, PTC337, MTC164) were examined by the same technique. Additionally, genomic DNA from the cells was amplified by the polymerase chain reaction (PCR) and the PCR product studied for p53 mutations (R273H) by mutation-specific oligonucleotide hybridization (MOH) and temperature gradient gel electrophoresis (TGGE) for the p53 exon 8. None of the benign thyroid tumors and 7 of 57 (12%) DTCs strongly express p53 with a heterogeneous distribution in the tumor tissue. All seven patients have metastatic disease or dedifferentiated tumors G3 (three of seven). CM1 was positive in two cell lines (FTC-133, PTC-337), questionable in FTC-238, and negative in FTC-236 and MTC-164. All three follicular cell lines, however, and the original tumor tissue showed the same p53 mutation (R273H) in MOH analysis and TGGE. P53 mutations are rare in thyroid tumors, but the presence of p53 mutations indicates a poor prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of P53 in human thyroid tumors. 772 41

Loss or inactivation of p53 gene--a suppressor oncogene has been considered to be one of the important mechanisms in the development of human tumors. One of the evidences for mutation of allelic gene of p53 is the identification of p53 protein concentrated in the nuclei of related cells. By using ABC immunohistochemical method, we studied the expression of p53 in cryostatic sections of the tumor tissue and adjacent mucosa resected from 38 patients with gastric cancer. p53 was found to be positive in the nuclei with intensive staining in 24 out of 38 cases with carcinoma (63.2%). p53 positive cells were distributed diffusively in the cancer tissue. All the adjacent mucosa specimens except 10 were negatively stained with p53 monoclonal antibody. These 10 specimens including 3 with dysplasia and 4 with metaplasia were only weakly stained. p53 was also found to be positive in 18 out of 23 cancer patients with metastasis in perigastric lymph nodes (78.3%). We also studied in the same section the nucleolar organizer region-associated proteins (AgNORs) with using silver staining technique to find if there is any relationship between p53 gene mutation and the activity of rRNA transcription of tumor cells. The number of AgNORs dots per nucleus detected in gastric cancer sections with positive staining of p53 (9.9 + 2.14) was greater than those with p53 negative staining (7.2 + 1.68). There was a significant statistical difference between the two groups (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The expression of mutant p53 gene in gastric carcinoma]. 786 23

In order to investigate the expression of mutant p53 protein (Mp53) and HBxAg in chronic active hepatitis (CH) and hepatocellular carcinoma (HCC), 30 specimens of HCC with surrounding liver tissues (SL), 15 biopsy specimens from CH were examined with immunohistochemical method (ABC system). The results showed, that 13 (43.3%) specimens of HCC and 15 (50%) of SL were positive for MP53 and HBxAg staining; 3 (16.7%) of HCC and 8 (26.7%) of SL were only MP53 positive, being HBxAg staining negative. On the contrary, 4 (13.3%) of HCC and 1 (3%) of SL were negative for MP53 staining and positive for HBxAg staining (P < 0.05, chi 2 test). In 15 specimens of CH, 3 cases were positive for MP53, 2 for HBxAg. The results indicate that there is a correlation between mutant p53 protein and HBxAg, suggesting that the p53 gene mutation may be closely related with HBV infection, and the mutation of p53 gene would be one of hepatocarcinogenesis mechanisms of HBV.
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PMID:[Expression of mutant p53 in chronic HBV infection and hepatocellular carcinoma]. 795 95

The expression of tumour suppressor gene P53 products-P53 protein in patients with primary lung cancer has been studied by ABC immunohistochemical method using McAb 1801 as probe. Abnormalities in P53 expression were found in 63 of 78 carcinomas, 23 of 26 squamous cell carcinomas, 23 of 29 adenocarcinomas, 7 of 11 large cell carcinomas, 7 of 9 small cell carcinomas and all 3 cases of adenoid cystic carcinomas showing abnormal P53 expression, whereas no expression of P53 was detectable in 11 normal lung samples. These findings suggest that the pathogenesis of lung cancer may also be related with abnormalities of P53 gene.
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PMID:[The immunohistochemical study of p53 protein in primary lung cancer]. 808 21

The importance of epidermal growth factor receptor (EGF-R) as an immunohistochemical factor of prognosis has been investigated in 820 cases of breast carcinoma irrespective of subtyping. An immunohistochemical membrane positivity for EGF-R (Ab1, clone 455 and Ab2, clone 528, Oncogene Science Manhasset NY, USA, ABC-peroxidase method) has been observed in neoplastic cells of 131/820 breast carcinomas (15.9%); the percentage is lower than those of the majority of reported series, but the total number of cases is higher. A significant inverse relationship between EGF-R and estrogen/progesterone receptors has been found (ER-ICA, PgR-ICA, Abbott, PAP-method). Highly proliferating Ki67 positive (> = 20% stained nuclei-Dakopatts Denmark) and oncoprotein p53 (Pab 1801 clone, Oncogene Science) positive carcinomas are more frequently EGF-R positive (p < 0.001). No relationship exists between EGF-R expression, c-erbB-2 (3B5 clone, Oncogene Science) expression, tumor size and lymph node status. The detection of EGF-R may be a useful addition to other immunohistochemical prognosticators, but it must be related with clinical outcome in further studies.
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PMID:Relationships between epidermal growth factor receptor (EGF-R) and other predictors of prognosis in breast carcinomas. An immunohistochemical study. 817 Jul 12

Immunohistochemistry (ABC method) and in situ hybridization (DNA-RNA) were used to detect c-myc and p53 gene expression in tissues of human HCC and nearby non-tumorous liver (NT) from 23 patients. The results showed that the positive rates of P62c-myc were 87% (20/23) in HCC and 91% (21/23) in NT. The positive rates of P53 protein were 39% (9/23) in HCC as well as in NT. The positive rates of c-myc and p53 mRNA were 70% (16/23) and 56% (13/23) in HCC and NT respectively. The expression of c-myc and p53 at protein level was significantly correlated with that at mRNA level. These observations suggest a close association of c-myc and p53 gene overexpression with hepatocarcinogenesis. Immunohistochemistry (ABC method) on section of paraffin embedded tissue is a reliable method for detecting c-myc and p53 gene expression in HCC.
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PMID:[Overexpression of c-myc and p53 gene in human hepato-cellular carcinoma--a study with immunohistochemistry and in situ hybridization]. 869 90

T cell lines (Coculture-14, Coculture-5) derived from human T-cell leukemia virus type I (HTLV-I)-seronegative persons acquired interleukin-2 (IL-2)-dependent continuous growth capacity (immortalized) following in vitro HTLV-I infection. They showed structural abnormalities of chromosomes carrying proviral DNA as seen by in situ hybridization. Following ultraviolet (UV) irradiation, Coculture-5 cells achieved IL-2-independent autonomous growth (transformed) resulting in the establishment of UV-1 and UV-5 lines. They showed additional abnormalities of the same chromosomes. Cocultivation of Coculture-5 cells with IUdR-treated UV-1 cells also resulted in autonomous growth of Coculture-5 cells, giving rise to three cell lines. By ABC immunostaining with specific antibodies, expression of proteins coded for growth regulatory genes, including Ki-67, Topo II, Pol alpha, c-MYC, p53, Rb, bcl-3, bcl-2, and BM-1, was found to be variably altered in transformed cells compared with immortalized cells. These results demonstrated chromosomal instability, altered gene product expression of HTLV-I-infected human lymphocytes, and their susceptibility to transformation without exposure to an initiating carcinogen.
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PMID:Genetic instability as a basis for transformation of human lymphocytes infected with human retrovirus. 870 44

Silver staining PCR-SSCP method was used to detect point mutation of p53 gene in paraffin-embedded malignant fibrous histiocytoma (MFH) tissues. The abnormal shifting of the single-stranded DNA (ssDNA) was identified in 9 out of 16 cases. The positive figure of SSCP was 1,4,4, 3 in exon 5, 6, 7, 8, respectively. The mutant p53 protein was detected by microwave oven treatment and ABC immunohistochemistry. Positive nuclear staining was observed in 10 cases. The positive coincidence rate was 90.0% between SSCP and p53 protein expression. The mutation of p53 gene was not correlated with the subtypes of MFH. Our results indicate that detection of point mutations with silver staining PCR-SSCP is convenient, rapid and reliable in the screening of point mutation of genes.
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PMID:[Detection of point mutation of p53 gene by silver staining PCR-SSCP in paraffin-embedded malignant fibrous histiocytoma]. 873 3


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