Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

A study was made of the incidence of p53 mutations in Japanese males with prostate cancer or benign prostatic hyperplasia. Polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) was used as a primary screening technique with gene sequencing being carried out in positive cases. Two out of 21 prostate cancers (9.5%) were found to have p53 mutations. These were stage B2 and D2 prostate cancers. No abnormalities were found in the remaining cases or benign prostatic hyperplasia. Mutations of the p53 gene would thus appear infrequent in the tumourigenesis of primary prostate cancer.
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PMID:Infrequent involvement of p53 gene mutations in the tumourigenesis of Japanese prostate cancer. 769 Nov 45

Gene mutation and abnormal expression of ras oncogenes and p53 gene have a direct bearing on the carcinogenesis. Polymerase chain reaction (PCR), sequencing technique of ds DNA cycle and sequencing system were used to detect the gene mutation of N-ras as well as the exon 5 and 7 of p53 gene in hLA and LTEP-a2 cell lines of human lung adenocarcinoma. The result showed that mutation of both cell lines occurred on the 154th codon in exon5 of p53 gene, where GGC was displaced by GTC resulting a substitution of Val for Gly, nevertheless, N-ras oncogene and the exon7 of p53 gene are normal.
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PMID:[Sequence analysis of N--ras and p53 gene mutation in the human lung adenocarcinoma cell lines]. 772 Jan 10

Squamous carcinoma of the vulva (SCV) is an uncommon neoplasm of uncertain etiology. There is evidence that there are two subgroups of SCV, one associated with human papilloma virus (HPV) and a second HPV-negative group. The UCI-VULV-1 cell line, obtained from a lymph node metastasis of an SCV, grows with a population doubling time of approximately 60 hr. The saturation density is 10(5) cells/cm2. The cell line does not exhibit anchorage independence and is weakly tumorigenic. The cells range in appearance from an abundant spindle cell to a less common larger, flat cell. All of the cells are immunoreactive for high-molecular-weight keratin, but only the flat cells, which form squamous pearls in vivo, are immunoreactive for low-molecular-weight keratin. The cell line expresses epidermal growth factor (EGF), transforming growth factor-alpha, the EGF receptor, and p53 protein. Polymerase chain reaction revealed no HPV DNA within the cells. Early passage cells exhibited karyotypic heterogeneity with few similarities to previous described SCV karyotypes. The cells display sensitivity to cis-platinum in concentrations toxic to many ovarian and cervical carcinoma lines. UCI-VULV-1 may be helpful for studying the properties of the HPV-negative form of SCV.
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PMID:UCI-VULV-1, a vulvar squamous carcinoma cell line. 772 33

The ENU1564 tumor line originated from a rat mammary tumor induced by N-ethyl-N-nitrosourea (ENU), an alkylating chemical carcinogen which induces genetic point mutations. The oncogene abnormalities in rat mammary tumors induced by ENU have not been characterized. In this study, two highly metastatic clones (Br7-C5 and FP2-All) derived from the adenocarcinoma cell line ENU1564, were evaluated for the presence of mutational activation involving the c-Ha-ras, c-neu, and p53 oncogenes. These oncogenes were chosen for investigation based upon their involvement in other ENU-induced rat tumors (c-neu in malignant schwannomas and p53 in nephro-blastomas) or in methylnitrosourea (MNU)-induced rat mammary tumors (c-Ha-ras). Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and sequence-specific oligonucleotide hybridization analyses indicated that no c-Ha-ras codon 12 mutation was present in these tumor cells. PCR-RFLP and single-stranded conformational polymorphism (PCR-SSCP) analyses showed that no sequence changes were present over a 138 base-pair gene fragment spanning codon 664 of the c-neu protooncogene (the site of point mutation in ENU-induced rat nerve tumors). Immunoprecipitation and Western immunoblotting indicated that the p53 protein is neither over-expressed nor mutated in the tumor cells. The results failed to identify specific oncogene alterations in the ENU1564 rat mammary tumor line but ruled out mutational activation of c-Ha-ras (codon 12), c-neu (codon 664), and the p53 genes.
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PMID:Evaluation of potential oncogene alterations in the ENU1564 rat mammary tumor model. 791 94

The 3Y1 cell line, established from a rat whole embryo, is widely used as a normal immortalized fibroblast. We analyzed p53 mutations in four clonal lines derived from the 3Y1 cell line; 3Y1-B clone 1-6, 3Y1-C and two clonal lines (3Y1 cl-3 and 3Y1 cl-6) which had been transformed by the human papilloma virus E6 gene. Polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP) analysis and DNA sequencing showed that three clonal lines had a double mutation at codons 130 and 136 on the same allele and that the other clonal line, 3Y1 cl-3, had no mutations. 3Y1-B clone 1-6, which has been registered as the standard clonal line at the Japanese Cancer Research Resources Bank, demonstrated weak bands of the wild type allele, suggesting the existence of heterogeneous cell types in this "clonal" line. PCR-SSCP analysis of 25 subclones obtained by limiting dilution of 3Y1-B clone 1-6 cells revealed a mixture of two types of cells; 12 subclones showed only the bands of mutated allele, and 13 subclones showed both bands of the wild and mutated p53 alleles. These findings should be taken into consideration when using this cell line as a normal immortalized cell line.
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PMID:Presence of p53 mutations in 3Y1-B clone 1-6: a rat cell line widely used as a normal immortalized fibroblast. 801 1

Atypical fibroxanthoma (AFX) is an uncommon neoplasm of the superficial soft tissue occurring in actinically damaged skin of elderly patients. Sun-exposed skin also represents the main site of squamous and basal cell carcinomas and malignant melanoma, and a key role for ultraviolet (UV) radiation in their pathogenesis has long been suspected. UV-related mutations of the p53 gene have been identified in human skin cancers. To verify whether the pathogenesis of AFX is related to the effect of sunlight, p53 protein and gene status have been investigated in a series of 10 cases of AFX. Seven of 10 showed p53 immunoreactivity in most of the neoplastic cells. Molecular analysis of the p53 gene revealed an abnormal single strand conformation polymorphism pattern in all the p53 positive cases. Polymerase chain reaction direct sequencing revealed that all the mutations involved cytosine bases. Four cases showed C to T transitions (including two CC-TT double base substitutions) and two cases showed C to G transversion. All but one mutation took place at dipyrimidine sites. These findings provide the first objective evidence for the central role of UV radiation in the development of AFX and also represent the first in vivo demonstration of solar UV-induced mutations in a human mesenchymal neoplasm.
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PMID:Ultraviolet-induced p53 mutations in atypical fibroxanthoma. 803 Jul 43

Previous studies have shown that human rhabdomyosarcoma cells are induced to differentiate by TPA, in the absence of appreciable alterations of the muscle regulatory genes and their products (1). The question was addressed whether the tumor suppressor p53 could be a target of TPA action in these cells. Genomic analysis by a Polymerase Chain Reaction/Single-Strand Conformation Polymorphism (PCR/SSCP) and direct sequencing indicate the presence of a mutation in exon VII at codon 248 (C to T transition) and a loss of heterozygosity of p53 gene in human rhabdomyosarcoma cell line (RD). It is here shown that transcription of p53 mRNA strongly decreases in RD cells induced to growth arrest and differentiate by TPA treatment. In these cells immunoprecipitation and immunoblot analysis show that both synthesis and total cellular concentration of the protein are also reduced by TPA. Nevertheless nuclear p53 accumulation is at much higher extent, whereas 32P-orthophosphate labelling, followed by immunoprecipitation, demonstrates a decrease of phosphorylation of both cytoplasmic and nuclear p53. These results indicate that TPA causes a number of alterations of mutant p53, likely mediated through a protein kinase C dependent mechanism, which might impair the transforming ability of mutant p53 in growth-arrested and differentiating RD cells.
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PMID:TPA-induced differentiation of human rhabdomyosarcoma cells involves dephosphorylation and nuclear accumulation of mutant P53. 803 10

A cell-line (UACC 2561), was established from a biopsy specimen of a lung carcinosarcoma. The patient had Stage III non-small cell lung cancer. Characterization of this cell line revealed highly aneuploid cells containing multiple clonal chromosome alterations with growth in nude mice within 3 weeks following subcutaneous injection. The cell line UACC 2561 stained positive for vimentin and displayed resistance to a variety of chemotherapeutic agents. Polymerase chain reaction followed by single-strand conformational polymorphism analysis revealed the presence of a K-ras 12 codon mutation. This mutation was confirmed by mutation specific PCR analysis for mutant K-ras alleles and direct DNA sequencing to be a GGT to GTT at codon 12 of the K-ras gene. Examination by PCR-SSCP for p53 mutations did not reveal any point mutations in exon 5-8 of the p53 gene. This relatively rare cell line may represent a useful model to investigate human lung sarcomas.
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PMID:Establishment of a new lung sarcoma cell line from a human lung carcinosarcoma. 805 85

Paired samples of chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) and the subsequent diffuse large cell lymphoma (DLL) of six cases of Richter's syndrome were investigated to establish the clonal relationship between the CLL/SLL and the DLL components and to define the oncogene and/or tumor-suppressor gene alterations involved in the morphologic transformation of CLL/SLL. Southern blot hybridization analysis showed identical clonal immunoglobulin (Ig) gene-rearrangement patterns in the CLL/SLL and DLL components in four cases and different Ig gene-rearrangement patterns in two cases. Polymerase chain reaction (PCR) amplification, cloning, and DNA sequencing of complementary determinant region 3 (CDR3) of the Ig-heavy chain gene of one of the two cases in which the Ig gene-rearrangement patterns were different showed nonidentical sequences in the CLL/SLL and DLL components. In the other case, monomorphic Epstein-Barr virus (EBV) genome integration was detected in the DLL but not in the CLL, suggesting that the CLL and DLL components in this case of Richter's syndrome also represent unrelated clones. Single-strand conformation polymorphism (SSCP) analysis and sequencing of exons 5 through 9 of the p53 tumor-suppressor gene showed a mutation in codon 176 of the DLL but not in the CLL/SLL component in one case where the CLL/SLL and DLL represented different clones. The p53 mutation probably played a role in the development of the lymphoma rather than morphologic transformation of the CLL/SLL in this case. SSCP analysis and sequencing also showed identical mutations in codon 282 in both the CLL/SLL and DLL components in a case where the CLL and DLL represented identical clones. Thus, this p53 gene mutation was present both before and after morphologic transformation, and therefore, probably did not play a primary role in this process. Southern blot hybridization analysis failed to show evidence of bcl-1, bcl-2, c-myc proto-oncogene or retinoblastoma (Rb) tumor-suppressor gene rearrangements in these six cases of Richter's syndrome. In conclusion, the original CLL/SLL and the subsequent DLL in Richter's syndrome may or may not be derived from identical clones, and the well-known proto-oncogenes and tumor-suppressor genes do not appear to play an obvious and consistent role in the morphologic transformation of CLL/SLL to DLL.
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PMID:Molecular genetic demonstration of the diverse evolution of Richter's syndrome (chronic lymphocytic leukemia and subsequent large cell lymphoma). 811 38

Abnormalities of the p53 gene are frequently observed in human tumors, including urinary bladder carcinoma, suggesting that p53 plays an important role in human carcinogenesis. However, its role in rat bladder carcinogenesis is unclear. In this study, we investigated the presence of p53 mutations in 122 urinary bladder tumors induced in F344 rats in the following carcinogenesis models: (i) 0.2% N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT; 6 weeks) in the diet followed by 3% or 5% sodium saccharin in the diet, 5% sodium ascorbate, 3.12% calcium saccharin (CaSac), 1.34% sodium chloride (NaCl), 5.2% CaSac plus 1.34% NaCl, or basal diet alone (72 weeks); and (ii) 0.2% FANFT, 0.05% N-(4-hydroxybutyl)nitrosamine in the drinking water, N-methyl-N-nitrosourea 20 mg/kg body wt, i.p. twice per week, or basal diet alone (4 weeks), followed by 3% uracil in the diet (20 weeks). Polymerase chain reaction-single-strand conformation polymorphism analysis and direct sequencing were performed for exons 5-8 in the rat p53 gene. We found nine tumors (7.4%) with p53 mutations. Two tumors had two mutations in the p53 gene. The tumors that had p53 mutations were relatively smaller than those that did not have p53 mutations. There were no mutation clusters among the treatments or hot-spots for p53 mutations. These results indicate that p53 mutation is infrequent in bladder carcinogenesis in rats, and when it does occur, it does not appear to provide a growth advantage.
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PMID:p53 mutation is infrequent and might not give a growth advantage in rat bladder carcinogenesis in vivo. 811 28


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