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)

Carcinogenesis in human large intestine is a result of multiple, heterogeneous and random genetic changes. Deletion of tumor suppressor genes and activation of oncogenes appear to be important molecular events. These compromise the loss of chromosomes 5, 17, 18 or functional inactivation of FAP, p53 and DCC genes. Activation of Ki-ras and c-myc oncogenes seems to be crucial for both cell immortalization and morphology modification. Identification of genes involved in this process enables both a screening and a new classification. Also it is an important step towards a gene therapy.
Patol Pol 1992
PMID:Colorectal carcinoma as a genetic phenomenon. 129 35

Thirty seven cases of recurrent gliomas with survival time from 3 month to 13 years were investigated morphologically and immunohistochemically to evaluate progression and transformation of tumors. Using antibodies against PCNA and p53 the proportion of positively marked cells (nuclei) to all tumor cells was assessed at both primary and secondary surgery. This was compared with morphology and survival time between first and second surgery. In 10 cases (27.0%) there were no positively marked cells. In the remaining 27 cases (73.0% of the whole group), the following indices (percents of positive cells) were calculated: for patients with survival below 1 year (mean = 9m) 28.3% PCNA-positive cells and 30.3% p53-positive cells at first operation. For recidiving tumors both indices were lower namely for PCNA 20.9% and for protein p53-26.7%. For patients with survival over 1 year (mean = 4.8y) the index after I operation for PCNA was 25.5% and was higher than found after II operation-22.3%. In contrary, the index for protein p53 was 20.1% after I operation and was lower as compared with the index after II operation-28.2%. Eleven of twelve fibrillary astrocytomas and all five gemistocytic astrocytomas at first operation underwent changes towards malignisation. The immunocytochemical results confirm the high phenotypic differentiation what is reflected in different indices for PCNA and p53 of tumors.
Pol J Pathol 1995
PMID:PCNA and protein P53 in recurrent supratentorial glial brain tumors: studies on correlation between morphology and tumor progression. 749 34

The incidence of genetic abnormalities have been investigated in a variety of preleukaemic states RAS and FMS oncogene, p53 suppressor gene mutations and monoclonality in myelodysplastic syndromes (MDS), a paradigm for pre-leukemias have been observed. Other patients at risk of developing either secondary leukaemia or evolving into leukaemia have been similarly studied including haematologically normal patients in remission from lymphoma. Time from treatment to detection of genetic abnormalities is a significant factor in some of these patients which is consistent with the expansion of an abnormal clone. A case of non-dysplastic MDS has been identified with a 7q-karyotypic abnormality typical of therapy related MDS, abnormal progenitor growth and RAS mutations but with normal clinical features. Normal individuals have also been under investigation and found to have a low incidence of proto-oncogene mutations. A prospective study should enable us to determine if these parameters are indeed prognostic indicators.
Acta Haematol Pol 1993
PMID:Genetic lesions in preleukemia. 824 36

We analyzed the expression of p53 in 74 cutaneous adnexal tumors, with enhancement of the detection by incubation of the slides in the microwave. The immunostaining in benign tumors was almost uniformly negative as we found p53-positivity only in one poroma, one nodular hidradenoma, and one case of syringocystadenoma papilliferum (amongst 13 spiradenomas, 9 cylindromas, 12 nodular hidradenomas, 7 poromas, 6 syringomas, 7 syringocystadenomas papilliferum, 2 papillary tubular adenomas and 4 chondroid syringomas). These results contrasted with the widespread p53 overexpression, which was revealed in the sweat gland carcinomas. All spiradenocarcinomas (3), malignant nodular hidradenoma (1), apocrine hidradenocarcinoma (1), and malignant syringoadenoma (1) showed a strong reaction to anti-p53 antibody. Two of three eccrine hidradenocarcinomas, and two of three porocarcinomas presented p53 overexpression, whereas in one case of malignant cylindroma and adenoid cystic carcinoma we did not find p53-positivity. The results of the study indicate an important role, that p53 protein plays in the malignant sweat gland tumors in comparison to their benign counterparts, but reveal that its overexpression may also occur in the reactive and benign neoplastic processes.
Pol J Pathol 1996
PMID:p53 expression in sweat gland tumors. 870 67

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

Cancer is a genetic disease and the development of the techniques of molecular biology in recent 10 years contributed to the new understanding of neoplasmatic process. The mutations of gene p53 became one of the most common abnormality in human cancer. The aim of this research was to mark oncoprotein p53 in 120 cases of larynx cancer and the correlation of its appearance with clinical and histopathological parameters. The evaluate the degree of immunohistochemical staining of cell nuclei a 5 degree scale was adopted. The positive staining of cell nuclei was observed in 70% of cases. Positive correlations based on a chi-square test was observed between p53 and T and N as well as between p53 and the degree of histological differentiation.
Otolaryngol Pol 1996
PMID:[p53 oncogene in the laryngeal cancer]. 904 79

Early during the herpes simplex virus (HSV) lytic cycle or in the presence of DNA synthesis inhibitors, core viral replication machinery proteins accumulate in intranuclear speckled punctate prereplicative foci, some of which colocalize with numerous sites of host cellular DNA synthesis initiation known as replisomes. At later times, in the absence of inhibitors, several globular or large irregularly shaped replication compartments are formed; these compartments also contain progeny viral DNA and incorporate the IE175(ICP4) transcription factor together with several cellular proteins involved in DNA replication and repair. In this study, we demonstrate that several forms of both prereplication foci and active viral replication compartments that display an appearance similar to that of the compartments in HSV-infected cells can be successfully assembled in transient assays in DNA-transfected cells receiving genes encoding all seven essential HSV replication fork proteins together with oriS target plasmid DNA. Furthermore, bromodeoxyuridine (BrdU)-pulse-labeled DNA synthesis initiation sites colocalized with the HSV single-stranded DNA-binding protein (SSB) in these replication compartments, implying that active viral DNA replication may be occurring. The assembly of complete HSV replication compartments and incorporation of BrdU were both abolished by treatment with phosphonoacetic acid (PAA) and by omission of any one of the seven viral replication proteins, UL5, UL8, UL9, UL42, UL52, SSB, and Pol, that are essential for viral DNA replication. Consistent with the fact that both HSV IE175 and IE63(ICP27) localize within replication compartments in HSV-infected cells, the assembled HSV replication compartments were also able to recruit both of these essential regulatory proteins. Blocking viral DNA synthesis with PAA, but not omission of oriS, prevented the association of IE175 with prereplication structures. The assembled HSV replication compartments also redistributed cotransfected cellular p53 into the viral replication compartments. However, the other two HSV immediate-early nuclear proteins IE110(ICP0) and IE68(ICP22) did not enter the replication compartments in either infected or transfected cells.
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PMID:Assembly of complete, functionally active herpes simplex virus DNA replication compartments and recruitment of associated viral and cellular proteins in transient cotransfection assays. 906 Jun 78

Immunohistopathological staining for p53, PCNA and Ki67 was performed in 120 specimens from previously untreated laryngeal carcinomas using the avidin-biotin method with peroxidase as a marker enzyme and diaminobenzidine as a chromogen. A 5-grade staining score system was used. Statistically significant correlations (Chi-square) were seen between T- and N-stage and histopathological grading. p53 and Ki67 scoring correlated with T- and N-stage whereas PCNA with T-stage. All staining correlated with histopathological grading. The score of staining for p53, PCNA and Ki67 correlated with each other. The patients with recurrences within 3 years had mainly carcinomas with higher staining scores. Using Chi-square analysis the p53, PCNA and Ki67 staining scores were also independent prognostic indicators.
Pol J Pathol 1996
PMID:p53, PCNA and Ki67 in laryngeal cancer. 909 9

A comparison was performed of staining intensity of immunohistochemical proliferating antigens (p53, PCNA, Ki67), DNA flow cytometry and ultrastructure of the carcinoma cells in 120 cases of laryngeal cancer. Clinically very advanced tumors were in majority (T3 - 43%, T4 - 18%). A 5 graded scale was adapted to evaluate the level of immunohistochemical staining of the carcinoma cell nuclei. A positive staining was obtained in 70% for p53, 57% for Ki67 and in 80(2/3) for PCNA. 62% of the cases were DNA diploid and 38% DNA aneuploid. The DNA diploid carcinomas were accompanied by the enlargement of the cell nuclei, preserving of the nuclei's wide margins of heterochromatine, enlargement of the nuclear area and increase of the number of nuclei. In the aneuploid-polyploid cancer the nuclei had a substantial polymorphism with large cleaved nuclei and with significant variation in size, and with nuclear envelope. A frequent finding was euchromatization of chromatine. Dense chromatine appeared in the form of small clumps spread over the whole area of these irregular nuclei. Enlargement and activation of nucleoli occurred. There was a positive correlation (Chi-square) between T- and N-stage and immunohistochemical staining. There was also a positive correlation in staining intensity between p53, Ki67 and PCNA. There is also strong correlation between these markers of proliferative activity and the degree of aggressiveness of the tumour.
Otolaryngol Pol 1996
PMID:[Diagnostic and prognostic value of p53 oncogene and the selected neoplastic markers (Ki67, PCNA, DNA ploidy) of the ultrastructure in patients with laryngeal cancer]. 917 91

DNA-dependent protein kinase (DNA-PK) has been known to catalyze phosphorylation of a number of regulatory factors involved in DNA replication and transcription such as simian virus 40 T antigen, p53, c-Myc, Sp1, and RNA polymerase II (Pol II). We examined the possibility that DNA-PK phosphorylates the general transcription factors TATA-binding protein (TBP) and transcription factor (TF) IIB, which play key roles in the formation of transcription initiation complex with Pol II. By using a highly purified preparation of DNA-PK from Raji cells, both TBP and TFIIB were shown to be phosphorylated in vitro by DNA-PK. We then investigated the effect of the phosphorylation of these factors on Pol II basal transcription. Stepwise analysis of preinitiation complex formation by electrophoretic mobility shift assay revealed that the phosphorylation of TBP and TFIIB by DNA-PK did not affect the formation of promoter (P)-TBP and P-TBP-TFIIB complexes but synergistically stimulated the formation of P-TBP-TFIIB-TFIIF-Pol II complex. Similarly, combination of the phosphorylated TBP and TFIIB synergistically stimulated Pol II basal transcription from adenovirus major late promoter. These observations suggest that DNA-PK could positively regulate the Pol II basal transcription by phosphorylating TBP and TFIIB.
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PMID:Phosphorylation of human general transcription factors TATA-binding protein and transcription factor IIB by DNA-dependent protein kinase--synergistic stimulation of RNA polymerase II basal transcription in vitro. 928 44


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