Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have demonstrated that synthetic oligonucleotide representing glucocorticoid responsive element (GRE I) of MMTV inserted into the enhancerless early promoter of SV40 in p delta SVE-CAT expression vector, enhances transient expression of chloramphenicol acetyltransferase gene in HeLa and hepatoma cells cultivated in the presence of dexamethasone. The following changes in the structure of the core sequences (GTTACAAACTGTTCT) of the synthesized GRE eliminated its enhancing ability: i, changes in the left end of the core sequences from GTTACAAAATGTTCT to TCTTCAAACTGTTCT or to TACTCAAACTGTTCT; ii, the increase of gap between TGTTCT and the inverted repeat of this sequence. The above changes did not eliminate specific binding of glucocorticoid receptor to the synthetic oligonucleotides studied.
Acta Biochim Pol 1991
PMID:Introduction of the glucocorticoid binding sequences into the expression vector p delta SVE-CAT and its effect on the CAT gene expression in mammalian cells. 179 99

The results of induction chemotherapy were analysed in cases of advanced ovarian carcinoma grade III (FIGO) during second-look operation. In 108 cases after the first operation with varying degree of radical removal of the tumour chemotherapy was given by the PAC schedule (cisplatin, adriablastin, cyclophosphamide) achieving in 90 cases 9 treatment courses. The results were evaluated using WHO clinical criteria. The best therapeutic results were noted in patients after radical operations or with aggressive cytoreduction of tumour mass. The clinical assessment of chemotherapy was corrected during the second-look operation which led to reduction of the percent of cured cases.
Ginekol Pol
PMID:[Results of a 2-year study of multiple drug induction chemotherapy in patients with advanced ovarian carcinoma FIGO grade III]. 270 2

Ten women with primary ovarian carcinoma in clinical progression grade III degree according to FIGO received intraperitoneal chemotherapy. They all had surgical treatment and 9 of them received after operation intravenous cytostatics PAC or PC. Cisplatin 100-220 mg/m2 was given intraperitoneally through a Tenckhoff catheter for long-term dialysis. Before beginning of intraperitoneal chemotherapy in 6 cases the malignant lesions were under 2 cm in diameter, and in 4 cases the size of these lesions was exceeding 2 cm with far advanced disease. In patients with malignant lesions under 2 cm CR was obtained in 4 cases, SD in 1 case and PR in 1 case. In the group with malignant lesions exceeding 2 cm the results of intraperitoneal treatment were: SD in 2 cases and PD in 2 cases. Intraperitoneal chemotherapy is an effective method in ovarian carcinoma when intravenous chemotherapy is ineffective. This is another method which provides a chance of prolongation of the life of the patients.
Ginekol Pol
PMID:[Clinical aspects of intraperitoneal chemotherapy in patients with ovarian carcinoma]. 270 1

The occurring frequency of 14 most common chemotherapy and anti-nausea drug side-effects was examined. The studies were performed on 29 women with ovarian cancer treated by total number of 125 chemotherapy courses (schedule PAC and Acy) and additionally, in order to eliminate nausea caused by the chemotherapy, by anti-nausea drugs (Zofran, Solu-Medrol, Droperidol, Metoclopramide + Fenactil, Torecan). Zofran caused the fewest number of side-effects, solu-medrol inhibited nausea and vomiting significantly, however it caused many side-effects such as flush on a face, restlessness, incitement and headaches. Torecan did not prevent patients from vomiting. The greatest number of side-effects was observed after droperidol and metoclopramide + fenactil treatment.
Ginekol Pol 1993 Sep
PMID:[Side effects of drug treatment for ovarian cancer after administration of antiemetic drugs]. 814 54

Although patients with thromboembolic disease frequently have family histories of thrombosis, well-defined defects such as inherited deficiencies of anticoagulant proteins are found only in minority of cases. Herein, we present a family study of 42 years old woman with recurrent deep vein thrombosis which occurred first time four years ago during pregnancy, in subclavian vein, in relation to cardiac stimulator implantation because of atrio-ventricular III(0) block. Her laboratory investigation demonstrated normal APTT time, prothrombin time, platelet number, antithrombin III and protein C activity. Plasma antiphospholipid antibodies contents was within the normal range. The result of activated protein C(APC) resistance test was abnormal (R=1.64). Family study revealed similar degree of APC-resistance defect in her DVT symptomatic mother and two healthy young daughters (R=1.73 and 1.54 respectively). Additionally, a slightly reduced total protein S plasma concentration was found in the patient and her two children. The influence of a slightly reduced protein S level on the results of APC-resistance was excluded by evaluation of normalized activated protein C sensitivity ratio (nAPC-SR) as described de Ronde and Bertina.
Pol Arch Med Wewn 1995 Dec
PMID:[Thrombophilia in a family with resistance to activated protein C and protein S deficiency]. 861 15

The presence of point mutation G-->A of nucleotide 1691 of Factor V gene (Leiden mutation) is responsible for the resistance of factor Va to activated protein C (APC-resistance) and is associated with an increased risk for thrombosis. Herein, we reported on a case of 20 year male with a two years history of recurrent, extensive deep vein thrombosis. His family history showed grand-mother from mother side, who died from thromboembolic disease many years ago. His laboratory investigation reveals abnormal results of APC-resistance test (R = 1.80) and normalized APC-resistance test sensitivity ratio (0.57). Moreover, on the basis of a sequence specific primer polymerase chain reaction (SSP-PCR) a heterozygous from (G/A at 1691 position) of Leiden mutation was found. Family study showed two between 8 others asymptomatic persons with abnormal results of APC-resistance test and heterozygous genotype.
Pol Arch Med Wewn 1996 May
PMID:[Point mutation G-->A nucleotide 1691 factor V gene as a cause of developing thrombotic complications in a family with plasma resistance to activated protein C]. 884 15

Suppression of the fibrinolytic activity plays an important role in the prevention of hemorrhage during pregnancy and labor. A hypofibrinolytic and hypercoagulable state may be established in the placenta during pregnancy. However, little infraction is present in the normal placenta. This evidence shows that placenta maintains the fibrinolytic activity in spite of hypercoagulable state. As there is a high amount of APC in the placenta, APC is thought to be involved in fibrinolysis of placenta. Thus, we studied the role of APC on fibrinolysis in placenta. (1) uPA activity of cell membrane reappears after incubation with uPA/PAI-1 complex and a large amount of APC by flow cytometry, (2) APC was made PAI-1/APC complex after incubation of uPA/PAI-1 complex with APC. Our results suggest that APC is the important substance for fibrinolysis in the placenta by decreasing of PAI activity.
Pol J Pharmacol
PMID:Relationship of urokinase type plasminogen activator, plasminogen activator inhibitor type 1 and activated protein C in fibrinolysis of human placenta. 911 54

To make use of antigonadotropin and antiproliferating action of the synthetic analogs of GnRH there was applied this decapeptide in 33 patients with ovarian cancer who were treated traditionally by chemotherapeutics PAC and radiotherapy. The monitoring of treatment was supported on the clinical opinion of the whole and locally state of health, the USG examinations of pelvic and diaphragm, the measure of level of CA-125 and second-look operations. There were got statistically characteristic rise of remissions and stabilizations of neoplastic process.
Ginekol Pol 1996 Oct
PMID:[GnRH analogs for treatment of ovarian cancer]. 928 30

Dendritic cells (DC) are potent APC that may be involved in the pathogenesis of HIV-1 infection. We studied the APC function of DC from HIV-1-infected subjects that were derived from monocyte-depleted PBMC by culture in human IL-4 and human granulocyte-macrophage CSF. The cultured cells from the HIV-1-infected subjects had similar morphology and phenotype of mature DC (CD80 = 41 +/- 8%, CD86 = 77 +/- 5%, CD40 = 87 +/- 6%, CD1a = 1 +/- 1%) to DC cultured from seronegative subjects. The yield of these DC was lower than from HIV-1-seronegative subjects (4 +/- 0% vs 11 +/- 2%, p < 0.01), and the lower DC yields correlated with lower numbers of blood CD4+ T cells (r = 0.60, p < 0.01) and higher plasma viral load (r = -0.49, p < 0.01). DC from HIV-1-infected subjects were infected with recombinant vaccinia virus vectors expressing Gag, Pol, and Env and were able to stimulate equal or higher levels of MHC class I-restricted, anti-HIV-1 memory CTL (CTLm) than were similarly treated, autologous B lymphocyte cell lines. DC pulsed with peptides representing HIV-1 CTL epitopes stimulated higher levels of anti-HIV-1 CTLm responses than did DC infected with the vaccinia virus-HIV-1 constructs. Allogeneic, MHC class I-matched DC also stimulated anti-HIV-1 CTLm activity in cells from HIV-1-infected subjects. DC from early and late stages of HIV-1 infection had a similar ability to activate CTLm specific for targets expressing either HIV-1 genes via vaccinia virus vectors or HIV-1 immunodominant synthetic peptides. However, DC from either early or late stages of HIV-1 infection could not overcome the defect in anti-HIV-1 CTLm response in advanced infection.
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PMID:Cultured blood dendritic cells retain HIV-1 antigen-presenting capacity for memory CTL during progressive HIV-1 infection. 936 24

Information about the mechanisms that generate mutations in eukaryotes is likely to be useful for understanding human health concerns, such as genotoxicity and cancer. Eukaryotic mutagenesis is largely the outcome of attacks by endogenous and environmental agents. Except for DNA repair, cell cycle checkpoints and DNA damage avoidance, cells have also evolved DNA damage tolerance mechanism, by which lesion-targeted mutation might occur in the genome during replication by specific DNA polymerases to bypass the lesions (translesion DNA synthesis, TLS), or mutation on undamaged DNA templates (untargeted mutation) might be induced. DNA polymerase zeta (pol zeta), which was found firstly in budding yeast Saccharomyces cerevisiae and consists of catalytic subunit scRev3 and stimulating subunit scRev7, has received more attention in recent years. Pol zeta is a member of DNA polymerase eta subfamily, which belongs to DNA polymerase B family, and exists in almost all eukaryotes. Human homolog of the scRev3 gene is located in chromosome region 6q21, and the mouse equivalent maps to chromosome 10, distal to the c-myb gene and close to the Macs gene. Alternative splicing, upstream out-of frame ATG can be found in yeast scRev3, mouse and human homologs. Furthermore, the sequence from 253-323 immediate upstream of the AUG initiator codon has the potential to form a stem-loop hairpin secondary structure in REV3 mRNA, suggesting that human REV3 protein may be expressed at low levels in human cells under normal growth conditions. The functional domain analysis showed that yeast Rev3-980 tyrosine in conserved region II is at the polymerase active site. Human REV3 amino acid residues 1 776-2 195 provide a REV7 binding domain, and REV7 amino acid residues 1-211 provide a bind domain for REV1, REV3 and REV7 itself. More interestingly, REV7 interacts with hMAD2 and therefore might function in the cell cycle control by affecting the activation of APC (anaphase promoting complex). Currently it has been known that pol zeta is involved in most spontaneous mutation, lesion-targeted mutation via TLS, chemical carcinogen induced untargeted mutation and somatic hypermutation of antibody genes in mammalian. In TLS pathway, pol zeta acts as a "mismatch extender" with combination of other DNA polymerases, such as pol iota. Unlike in yeast, it was found that pol zeta also functioned in mouse embryonic development more recently. It was hypothesized that the roles of pol zeta in TLS and cell cycle control might contribute to mouse embryonic lethality.
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PMID:DNA polymerase zeta: new insight into eukaryotic mutagenesis and mammalian embryonic development. 1280 Feb 16


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