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)

The frequency of RAS and p53 mutations was investigated in 30 acute promyelocytic leukemias by single strand conformation polymorphism analysis and direct sequencing of genomic DNA. Only two cases bore N-RAS codon 12 mutations and none had p53 mutations responsible for aminoacid substitutions. It would, therefore, seem that neither RAS nor p53 are involved in acute promyelocytic leukemogenesis.
Leuk Lymphoma 1993 Nov
PMID:Frequency of RAS and p53 mutations in acute promyelocytic leukemias. 812 13

Recently striking progress has been made in molecular biology. Among the newly developed techniques, PCR (polymerase chain reaction) is making an epoch in DNA diagnosis in the field of clinical pathology and laboratory medicine. In this symposium, we discussed the available PCR methods in DNA diagnosis and also the future prospect of PCR method as a routine laboratory procedure. First, Dr. Kawabata reviewed the PCR technique and analytical procedures of PCR products. Next five symposium presented the data on DNA diagnosis for particular diseases using the PCR method. Dr. Hasebe presented the HCV genotyping data from the patients. Dr. Hirose showed us the difference in accuracy in DNA typing of Chlamydia trachomatis antigen between the DNA probe method and PCR method. He also introduced the newly developed LCR method. Dr. Kondo reviewed the methods of DNA diagnosis for malignant lymphoma. Dr. Yaginuma presented the analyzed data of tumor suppressor gene p53 in some gynecological tumors. Dr. Azuma presented a case of chronic granulomatosis with a point mutation on the gp91-phox gene which had been revealed by RT-PCR. Next Dr. Yagihashi introduced the protocol for DNA typing of the HLA class II. Finally, Dr. Tanaka presented the availability of the PCR method for the convalescent screening of bone marrow transplantation. We hope this symposium is fruitful and motivating for all staffs of laboratory medicine and pathology. In closing my remarks, I express our appreciation to all symposists as well as Prof. Hisami Ikeda, president of the 27th general meeting of the Hokkaido branch, the Society of Clinical Pathology, planned this symposium.
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PMID:[Application of gene technology to clinical pathology]. 815 55

Intact nuclei derived from murine metastatic large-cell lymphoma and human chronic myelogenous leukemia cells were digested to discrete subchromatin deoxyribonucleoprotein/ribonucleoprotein precursor complexes by treatment with Msp-I. The resultant complexes were composed of nucleoproteins (NPs) that were isolated and purified by two-dimensional isoelectric focusing/sodium dodecylsulfate polyacrylamide gel electrophoresis (2D-SDS-PAGE), electroelution from the gel, and removal of SDS by extractigel chromatography. Various NPs purified by 2D-SDS-PAGE were examined for the presence of oncogenes and tissue-specific genes using a dot-blot hybridization technique. The RNA polymerase products of NPs were labeled, purified, and subsequently used in a back-hybridization assay to identify transcripts for particular genes. By utilizing a 2D-SDS-PAGE Southwestern technique in parallel with the dot-blot and RNA back-hybridization assays, we assessed whether it is possible to "track" a gene and its associations in particular NPs. In patients with chronic myelogenous leukemia, we screened approximately 1000 NPs for bcl-2 sequences and found them present in a single NP of apparent M(r) approximately 19,000, pI approximately 5.5. In murine RAW117-H10 cells transformed by the abl oncogene, we found by Western analysis that an antigen cross-reacting with abl antigen was localized to a p53 gene-containing NP of apparent M(r) approximately 22,000, pI approximately 7.2. A coincident Southwestern experiment using the same blot showed that the abl gene was bound by the same NP. The techniques described present the basis for "tracking" a particular gene to individual NPs and studying its relationship to other genes, their respective gene products, and its binding properties with particular NPs.
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PMID:Nucleoprotein complexes from metastatic cells containing oncogenes and tissue-specific genes: a novel method to track genes associated with specific nucleoproteins. 816 4

Cells were treated in vitro with oligodeoxyribonucleotide phosphorothioates (ODNs) complementary to sites common to both wild-type and mutant p53 nucleotide sequences. Acute myelogenous leukemia (AML) blasts from peripheral blood were exposed to four different p53 ODNs and showed anti-leukemic effects in suspension culture. This effect continued after removal of the ODN from the medium. Blocking of self-renewal of the leukemic blast stem cells in secondary plating of cells from cloning assays by two of the p53 ODNs was also observed. Control ODNs had no effect on leukemic blasts. Treatment of normal bone marrow cells with the four p53 ODNs did not influence their growth, nor was there any effect by the p53 ODNs on the leukemic cell-line, HL60, that does not express p53. These data suggest that p53 ODNs are selectively toxic to primary myelogenous blasts and may be therapeutically useful in AML.
Leuk Lymphoma 1994 Jan
PMID:Selective cytotoxicity to human leukemic myeloblasts produced by oligodeoxyribonucleotide phosphorothioates complementary to p53 nucleotide sequences. 816 53

While deletion or mutation of the p53 gene is one of the most common molecular alterations detected in a wide variety of tumours, it has been shown to occur in only a relatively small percentage of the leukaemia cases examined. However, it may be that other components of the p53 pathway are involved. Amplification of the MDM2 gene has recently been demonstrated in human sarcomas resulting in an increase in MDM2 protein levels. This protein can bind to p53 preventing the transactivation of p53 responsive genes, thus mimicking mutation or deletion of p53. We have investigated the prevalence of MDM2 amplification in human leukaemias. 101 leukaemia or lymphoma samples and nine cell lines were studied using Southern blotting. In no case was MDM2 amplification present. We conclude that MDM2 amplification is not a common event in human leukaemias.
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PMID:Lack of MDM2 amplification in human leukaemia. 819 38

Anaplastic large-cell lymphoma (ALCL) represents a morphologically distinct type of non-Hodgkin's lymphoma (NHL) characterized phenotypically by the expression of the CD30 antigen, a new member of the nerve growth factor gene family. The lymphoid origin of ALCL has been documented using immunohistochemical and molecular genetic analyses. However, very little is known so far regarding the precise pathogenetic mechanisms involved in its development and progression. Therefore, we investigated bcl-2, p53, and retinoblastoma gene (Rb) expression immunohistochemically; the occurrence of bcl-2, c-myc, and Rb gene rearrangements using Southern blotting; and the presence of ras and p53 gene somatic mutations by single-strand conformation polymorphism assay in a panel of 18 well-characterized ALCLs. In addition, the presence of Epstein-Barr (EBV) and human T-cell lymphotropic virus type I (HTLV-I) genomes were investigated using polymerase chain reaction. We identified abnormal c-myc gene products in 6 of 18 cases (33%) of ALCL. On the other hand, the bcl-2 and Rb genes were not rearranged and K-, N-, and H-ras gene somatic mutations were not found. Significant levels of p53 protein expression were found in more than 60% of ALCLs, but only a single ALCL carried a p53 gene mutation (exon 5). Only 3 ALCL cases, all occurring in human immunodeficiency virus-infected patients, were positive for EBV genomes. On the other hand, contrary to previous findings, no HTLV-I products could be identified. Despite the fact that the c-myc proto-oncogene appears to be frequently altered in ALCL, no pathognomonic abnormality could be identified and therefore additional studies and new strategies should be designed to identify the pathogenetic mechanisms involved in the development of ALCL.
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PMID:Molecular characterization of CD30+ anaplastic large-cell lymphoma: high frequency of c-myc proto-oncogene activation. 820 84

p53 overexpression has been found to be a fairly common feature in high grade lymphomas in the majority of tumoral cells. The results vary from series to series, from 25% to 33% of cases. To assess whether immunohistochemical positivity for p53 correlated with the presence of structural gene abnormalities, DNA from 16 non-Hodgkin's lymphomas with high and low p53 values was amplified and sequenced to determine the existence of point mutations in the highly conserved regions of the p53 gene. In the group of 8 cases containing high levels of protein, 3 cases showed missense point mutations at the codons mapping between exons 5 through 8. Of the 8 cases of tumors containing undetectable or low levels of p53 protein, 1 case presented a nonsense point mutation giving a stop codon. No missense mutations were detected in this group. The finding of p53 mutations in 4 of 16 cases confirms the presence of p53 gene mutations in high grade lymphomas distributed over different histologic groups. These include Burkitt's lymphoma, together with centroblastic, immunoblastic, and large cell lymphoma of mucosa origin. Nevertheless, the absence of mutations in 5 of the 8 cases that overexpressed p53 suggests that the nuclear or cytoplasmic stabilization of p53 protein could also depend on other factors. The absence of detectable levels of p53 protein cannot discount the existence of p53 mutations, as is shown by a case of Burkitt's lymphoma in which a nonsense mutation was detected. The impact of this range of p53 alterations on clinical course and treatment response of the patients deserves to be explored, in an attempt to differentiate the specific consequences of each one.
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PMID:The expression of p53 protein in non-Hodgkin's lymphomas is not always dependent on p53 gene mutations. 821 4

Mutations of p53 gene have been recognized to be the most common genetic changes in human cancers. Recently, p53 gene mutations have been found in some patients with common subtypes of B-cell lymphoma (9/48:18.8%), Burkitt lymphoma (9/27:33.3%) and chronic lymphocytic leukemia (6/40:15%). Evidences to suggest that p53 gene mutations are associated with the disease progression in B-cell lymphoma have emerged. Functions of wild-type p53 and its mutant's probable role in B-cell lymphomagenesis are described in this review.
Leuk Lymphoma 1993 Sep
PMID:Mutations of the p53 gene in B-cell lymphoma. 822 Jan 52

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.
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PMID:Genetic lesions in preleukemia. 824 36

Immunostaining methods were used to detect viral T-antigen and the cellular protein p53 in pathological tissues obtained from transgenic mice carrying JC-SV40 hybrid viral DNAs. A transgenic mouse carrying the SV40 regulatory region and JC virus (JCV) T-antigen-coding sequences exhibited an SV40-characteristic choroid plexus papilloma that expressed JCV T-antigen and p53. JCV-associated pathology was observed in two other mice in which the JCV regulatory signals directed SV40 T-antigen-induced adrenal neuroblastomas and brain neoplastic cells. However, these mice also exhibited an SV40-characteristic osteosarcoma and abdominal lymphoma that contained SV40 T-antigen and p53-positive cells. Contrasting thymic pathology was observed in the two types of mice where the SV40 regulatory region directed a JCV T-antigen-induced thymoma in one mouse, and the JCV regulatory region directed SV40 T-antigen-induced thymic hypoplasia in two other mice.
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PMID:Expression of viral T-antigen in pathological tissues from transgenic mice carrying JC-SV40 chimeric DNAs. 825 Oct 33


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