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)

Serum samples from 27 patients infected with human T-cell lymphotropic virus type III (14 with acquired immune deficiency syndrome [AIDS] and 13 with AIDS-related complex) were examined for antibodies to viral proteins by the Western blot method and with four different commercial solid-phase enzyme-linked immunosorbent assays (ELISAs). Virus-specific bands on blots at molecular masses of 64, 55, 53, 41, 31, 24, and 17 kilodaltons were observed. Rank correlation matrices were calculated to relate the intensity of viral bands, stage of illness, and ELISA kit optical densities (ODs). Groups of bands tended to covary in intensity: p17, p24, and p55 (gag gene products); p53 and p64 (pol gene products); and p31 (pol/endonuclease gene product) and p41 (env gene product). Blots of sera from AIDS-related complex patients usually showed strong activity against all viral proteins, while those of sera from AIDS patients characteristically showed strong reactivity only at the pol/endonuclease and env bands. For one ELISA kit (Abbott Laboratories, North Chicago, Ill.), ODs correlated well with the env and pol band intensity scores, while ELISA ODs with other kits (from Litton Industries, Sunnyvale, Calif.; Electro-Nucleonics, Inc., Fairfield, N.J.; and E.I. du Pont de Nemours & Co., Inc., Wilmington, Del.) correlated closely with gag band intensity scores. We conclude that human T-cell lymphotropic virus type III Western blot patterns are determined by (i) viral protein processing pathways and (ii) the stage of illness of the patient and may reflect (iii) the ELISA method used for serum screening.
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PMID:Variations in Western blot banding patterns of human T-cell lymphotropic virus type III/lymphadenopathy-associated virus. 354 2

The recent results obtained from investigations based on molecular biological techniques have led to a better understanding of recurrent genetic causes important for the pathogenesis of tumors. Several genes have been identified as being involved in the development of cancer. In many cases, the activation of oncogenes or the inactivation of tumor-suppressor genes is the predominant reason for cancerogenic cell transformation. Functional dysregulation is frequently the consequence of mutations, resulting in an alteration of the primary structure of the DNA. As our understanding of the nature, function, and interaction of these genes evolves, new opportunities for early diagnosis, classification, prevention, and treatment of malignant tumors will arise. The present report summarizes the current molecular biological aspects of several oncogenes (erbB, ras, myc, raf, fos, jun, bcl, mdm2, myb, kit CSF1R, met) and tumor suppressor genes (p53, rb, mts) involved in lung-cancer development with respect to the pathology of lung tumors, including the importance of these genes as far as the clinical course of the disease is concerned.
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PMID:[Oncogenes and tumor suppressor genes in the pathogenesis of lung tumors]. 785

We analyzed the levels of p53 protein in 10 frozen astrocytoma specimens by using an ELISA kit. p53 protein was detected in seven of ten specimens, and ranged from 0.4 to 18.0ng/ml. To confirm that the p53 protein detected in this study actually represented mutations occurring within the p53 gene, we determined the nucleotide sequence in five of six positive cases, and in three of four negative cases. We amplified exons 5 to 9 by the PCR and sequence analysis was carried out by the dideoxy chain termination method. Point mutations resulting in amino acid substitutions were found in four of five positive cases but not in negative cases. Then we analyzed the presence of p53 protein in sera of 42 patients with malignant astrocytoma and 34 healthy donors, by the same method. p53 protein was detected in sera of 7 of 42 patients and 6 of 34 healthy donors, suggesting that this result may be due to non-specific responses. In conclusion, using the ELISA kit, overexpression of p53 protein, resulting from p53 mutations, in frozen astrocytoma specimens can be detected. This may be a good screening method for the detection of overexpression of p53 protein.
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PMID:[Overexpression of p53 protein in gliomas]. 811 6

We have studied by immunohistochemistry the nuclear expression of p53 and the finding of oncoprotein c-erbB-2 in a series of 85 breast carcinomas. The tissue was fixed in buffered formalin and embedded in paraffin. The primary antisera were obtained from Biogenex (USA), Bp53-12, monoclonal, used in a dilution of 1:100 for p53 and from Triton Diagnostics (USA), pAB-1, polyclonal, used in a dilution of 1:200 for c-erbB2. The detection system was the Vectastain Elite kit obtained from Vector Laboratories (USA). The results were compared with several morphological features of the tumors such as size and type of the tumor, extension of the intraductal component, nuclear grade, axillary lymph node metastasis and estrogen receptor data as well as with total and disease free survival. The oncoprotein p53 was detected in the nuclei in 25 (29.4%) of our cases (Fig 1). Its presence was correlated with tumor size (p < 0.01), high nuclear grade (p < 0.0001) and estrogen receptor negative tumors (p < 0.0001). There was an inverse relationship between p53 expression and 5 year disease free survival (p < 0.005). In 21 (24.7%) of the cases we found amplification of c-erbB-2. The staining pattern was membranous (Fig. 2). It was correlated significantly with the ductal type of invasive carcinoma (p < 0.05), an associated extensive intraductal component (p < 0.001), estrogen receptor negative tumors (p < 0.0001) and shortening of disease free survival in the patients with positive axillary lymph nodes (p < 0.005). In 9 cases we found staining for both markers without statistically significant relationship with the other features studied. We conclude that the presence of these genetic alterations demonstrated by immunohistochemistry were, in our series, unfavourable prognostic factors in invasive breast cancer.
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PMID:[Immunohistochemical analysis of p53 and c-erbB-2 in breast cancer]. 872 71

Wilms' tumour (nephroblastoma) has been associated with chromosomal abnormalities at the 11p13, 11p15 and 16q regions. A study into the possibility of mutations occurring within p53, the ubiquitous adult tumour suppressor gene, in Wilms' tumour was carried out. Thirty-eight cases were studied. Of these 36 were categorised into the favourable histology group and two into the unfavourable histology group based on the National Wilms' Tumour Study criteria. Archival formalin-fixed, paraffin-embedded tissue sections from each case were stained with a polyclonal (AB565:Chemicon) and a monoclonal (DO7:Dako) antibody raised against p53 protein using a peroxidase-labelled streptavidin biotin kit (Dako). 'Cure' (disease-free survival of 60 months or longer) was documented in 39% of cases with favourable histology tumours. Eleven percent in this group succumbed to the disease. Both cases with unfavourable histology died. Four out of 36 (11%) tumours with favourable histology demonstrated weak to moderate staining with both AB565 and DO7 in more than 75% of tumour cells. In contrast, p53 protein expression in unfavourable histology tumours was significantly increased compared with the favourable histology group (P = 0.021) with both cases demonstrating immunopositivity in > 75% of tumour cells when stained with AB565 and DO7. The intensity of staining ranged from moderate to strong in both cases. It appears from this preliminary study that the immunohistochemical expression of p53 protein in Wilms' tumour, presumably a result of mutation in the p53 tumour suppressor gene, correlates with histological classification, histological categorisation being one of the useful features in the prognostic assessment of Wilms' tumours.
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PMID:Immunohistochemical expression of p53 proteins in Wilms' tumour: a possible association with the histological prognostic parameter of anaplasia. 883 20

Increasing evidence from experimental studies indicates that apoptosis may be related to angiogenesis in tumor progression. To explore how spontaneous apoptosis correlates with tumor angiogenesis, we measured the apoptotic index (AI) using the ApopTag kit (Oncor) and intratumoral microvessel density using an anti-CD34 monoclonal antibody in 101 cases of gastric carcinoma. Immunohistochemical staining for Ki-67 labeling index and the expression of p53 were conducted simultaneously. Statistical analysis revealed an inverse correlation between AIs and intratumoral microvessel densities (r = -0.4066, P < 0.0001) and failed to find significant correlations between AI and Ki-67 labeling index, as well as the expression of p53. The results of this study demonstrated for the first time that the incidence of apoptosis in gastric carcinoma is significantly influenced by the extent of neovascularization and suggests that tumor angiogenesis may contribute to a reduction of apoptosis in tumor cells.
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PMID:Spontaneous apoptosis is inversely related to intratumoral microvessel density in gastric carcinoma. 900 May 58

p53 mutations are amongst the most prevalent alterations in human cancer. Overexpression of p53 is usually caused by mutation and is observed in a high percentage of squamous cell carcinomas of the head and neck (SCCHN). Fifty two fresh samples of SCCHN were examined for p53 overexpression and 23 tumor-free tonsils served as controls. Using the monoclonal antibody Pab 1801 a refined ELISA technique was employed. In contrast to established ELISA procedures tumor tissue was pulverized at -80 degrees C prior to the actual ELISA (ELISA I). Comparative p53 detection was carried out by immunohistochemistry (IHC) and a commercially available ELISA kit (ELISA II). The modified ELISA I revealed p53 overexpression in 48 tumor samples (92%). p53 detection was obtained in 26 cases (50%) with ELISA II and with IHC 39 stained positive for p53 (75%). All of the controls were negative for p53 with ELISA and IHC. The p53 staining in IHC showed a significant correlation with the grading of the tumor. The ELISA results of the p53 overexpression did not show any correlation with tumor size or stage and rate of metastasis or other clinical parameters. This ELISA represents a more sensitive detection method of p53 than any other technique so far. It improves on former ELISA and IHC results on p53 overexpression in squamous cell carcinoma of the head and neck and underlines the involvement and the importance of the p53 tumor suppressor protein in carcinogenesis of head and neck cancer.
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PMID:High rate of p53 overexpression in head and neck carcinomas detected with a refined ELISA. 906 97

A good prognosis is often achieved in patients who have undergone treatment for human papillary carcinoma of the thyroid. On the assumption that this may be partly attributable to an apoptotic tendency of this special type of tumor, we measured DNA fragmentation, cell death by enzyme-linked immunosorbent assay (ELISA), and the expression of apoptosis-related genes. DNA fragmentation occurred more extensively in malignant tumor cells than in benign thyroid tumors or normal thyroid tissue, as examined by agarose gel electrophoresis and confirmed by the quantitative method using an ELISA kit. Although only expression of the tumor suppressor gene, p53, was increased in the tumor tissue, no expression of other genes, such as Fas, TNF, c-myc, c-fos or bcl-2, was observed in the normal, benign, or malignant tumor tissues, indicating that the roles of these gene functions, if any, were minimal in these tissues. Since p53 is closely related to cellular apoptosis and no point mutation was observed in the transcripts expressed by malignant cells, apoptosis and/or the production of an angiogenesis inhibitor induced by wild-type p53 molecules may be related to the favorable prognosis of patients treated for papillary carcinoma of the thyroid.
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PMID:Expression of wild-type p53 tumor suppressor gene and its possible involvement in the apoptosis of thyroid tumors. 906 3

P53 gen mutations play significant role in neoplastic transformation of colorectal mucosa. We investigated p53 immunostaining in 80 cases of spontaneous human colorectal adenocarcinomas (with monoclonal DO7 antibody and LSAB+ kit). We found positive, nuclear p53 immunostaining in 64% of nonmucinous adenocarcinoma tissues and in 19% of mucinous adenocarcinomas tissues. P53 protein deposits were most often found in colorectal adenocarcinomas localised in rectum (66.67%) and in advanced (Dukes C, D) colorectal adenocarcinomas (59.38%) as well. There was no statistical significance between the p53 positive immunostaining and the histological differentiation of the colorectal adenocarcinomas. The overall survival of patients with tumours positive for p53 protein was significantly shorter than that of patients with colorectal cancers negative for p53 protein. We conclude that p53 immunohistochemical analysis may be treated as a supplementary prognostic marker for patients with colorectal adenocarcinoma, especially it may be useful for adjuvant therapy selection.
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PMID:[P53 protein in adenocarcinoma of the large intestine]. 944 10

Alteration of the tumour-suppressor gene p53 is the commonest genetic change encountered in human malignant tumours. A study was undertaken to ascertain the prognostic value of p53 immunoexpression in nephroblastomas. A series of 93 consecutive cases was analysed. Archival formalin-fixed, paraffin wax-embedded tissue sections were stained with monoclonal anti-p53 antibody (DO-7, Dako) using a peroxidase-labelled streptavidin biotin kit. Five of seven tumours (71.4%) with unfavourable histology, but only 3 of 86 favourable histology tumours, showed 'high' p53 immunoexpression (P < 0.001). p53 expression in unfavourable histology tumours was present in both anaplastic and non-anaplastic components. Moreover, there was uniform staining of blastema, epithelium and stroma in unfavourable histology tumours. No statistical difference in p53 expression was found between patients who had received and those who had not received preoperative chemotherapy (P = 0.678). Similarly, no statistical difference was found in the groups of patients who were disease free, who had residual/recurrent disease or who had died (P = 0.238). The mean survival period for patients with tumours that had 'low' and 'high' expressions was 24.8 months and 12.6 months respectively (P = 0.0003). In conclusion, p53 immunoexpression in nephroblastomas was found to be an important determinant of poor prognosis as it identifies those patients with a shorter survival period and also those with unfavourable histology tumours. It may also be of practical value to the practising pathologist by identifying those tumours that require careful assessment for the presence of anaplasia.
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PMID:p53 protein expression in nephroblastomas: a predictor of poor prognosis. 946 Oct 3


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