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Biomedical subjects

M Terada

Publications and source records attributed to M Terada.

At least 523 records · Page 29Linked to original sources
PubMed1986

A novel transforming gene, hst, from human stomach cancers and a non-cancerous portion of stomach mucosa.

DNAs from 21 human stomach cancers, 16 metastatic stomach cancers to lymph nodes, and 21 non-cancerous mucosae of the stomach from a total number of 26 patients with stomach cancer were assayed for their transforming activity to NIH3T3 cells. Three samples of DNA were positive in transfection assay; one was from a primary stomach cancer of one patient (No. 361), the second was from a non-cancerous portion of stomach mucosa of the same patient (No. 363) and the third was from a lymph node metastasis of stomach cancer from another patient (No. 51). A portion of the transforming gene was cloned and a cDNA clone for this gene was isolated. The reading frame essential for the transforming activity was identified. From the results of sequence analysis of cDNA and Southern blot analysis, this transforming gene did not have homology with any oncogene reported previously. We applied the term, hst (human stomach cancer), to this novel transforming gene. This hst gene was not only responsible for acquisition of transforming activity of No. 361 DNA, but also for that of No. 363 and No. 51 DNAs; all the transformants induced by Nos. 361, 363, and 51 DNAs contained hst gene.

Cell Transformation, Neoplastic↗
PubMed1986

Histologic demonstration of antigens reactive with anti-p21 ras monoclonal antibody (RAP-5) in human stomach cancers.

The immunohistochemical reactivity of RAP-5, a monoclonal antibody (MoAb) raised against a synthetic peptide corresponding to positions 10-17 of the ras gene product from T24 bladder carcinoma, was studied in 96 surgically resected stomach cancers of humans. The cytoplasm of cancer cells in 65 cases (68%) was positively stained with MoAb RAP-5, although the staining was heterogeneous among cancer cells. There was no definite correlation between depth of tumor invasion and reactivity to MoAb RAP-5. Cancer cells of poorly differentiated tumors showed a tendency to react less frequently and less intensely to MoAb RAP-5. In nontumorous gastric mucosa, parietal cells and some portions of intestinal metaplasia were stained with MoAb RAP-5. These findings suggest an increased expression of the ras gene product (p21) in about two-thirds of gastric adenocarcinomas and in some nonneoplastic gastric epithelial cells.

Antibodies, Monoclonal↗
PubMed1986

Detection of mutant diphtheria toxin-resistant Chinese hamster lung cells in situ by autoradiography.

An autoradiographic method was developed to detect diphtheria toxin-resistant (DTr) Chinese hamster lung cells in situ. With this method, a dose-dependent increase in the number of DTr cells was observed after exposure of the cells to increasing concentrations of ethyl methanesulfonate (EMS). Segregation of EMS-induced DTr cells in a sector of single colonies was clearly demonstrated. It was also found by this method that the number of DTr cells induced by a fixed concentration of EMS was not determined by the number of cell divisions during the expression time but by the period after exposure of the cells to EMS.

Animals↗
PubMed1985

Activated c-raf gene in a rat hepatocellular carcinoma induced by 2-amino-3-methylimidazo[4,5-f]quinoline.

A rat hepatocellular carcinoma, IQ7, induced by 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) gave two transformants of NIH 3T3 cells on DNA mediated gene transfer. One of these transformants was examined further and secondary and tertiary transformants were obtained. The secondary transformant was tumorigenic in nude mice. The activated oncogene in this primary transformant was identified as rat c-raf by Southern blot analysis.

Animals↗
PubMed1985

Amplified DNA sequences in cancers.

Amplification of genes other than known oncogenes was analyzed using an in-gel DNA renaturation method, in which a mixture of restriction fragments of radioactively labelled tracer DNA and unlabelled driver DNA was electrophoresed and amplified DNA fragments were visualized after two cycles of denaturation and renaturation in the gel. Different DNA fragments were found to be amplified more than 400 fold in NB1, a neuroblastoma cell line, in Y79, a retinoblastoma cell line and in H69, a small cell lung carcinoma cell line, in addition to 120 to 160-fold amplification of N-myc gene in these three cell lines.

Cell Line↗
PubMed1985

Determination of methamphetamine and its metabolites in rat tissues by gas chromatography with a nitrogen-phosphorus detector.

A method for the determination of methamphetamine and its metabolites in tissues of the rat receiving methamphetamine was developed using gas chromatography with nitrogen-phosphorus detection. The extraction procedure, volatility of various derivatives, the acylation procedure, mass spectra of various derivatives and the recovery of methamphetamine and its metabolites in rat tissues are reported. The detection limits of pentafluorobenzoyl derivatives of methamphetamine and amphetamine, and heptafluorobutyryl derivatives of p-hydroxymethamphetamine and p-hydroxyamphetamine, were ca. 0.1 and 0.15 ng, respectively. This method could be used to determine concentrations as low as 10-15 ng/g of methamphetamine and its metabolites; recoveries from the rat brain, liver and serum were 94-106, 103-115 and 94-96%, respectively.

Amphetamine↗
PubMed1985

Activation of K-ras and oncogenes other than ras family in rat fibrosarcomas induced by 1,8-dinitropyrene.

Oncogenes of fibrosarcomas of rats, induced by subcutaneous injection of 1,8-dinitropyrene (1,8-DNP), were examined by NIH 3T3 cell transfection assay and Southern blot analysis. Transformants containing rat specific repetitive sequences were obtained with DNAs of 4 fibrosarcomas, 1,8-DNP1, 1,8-DNP2, 1,8-DNP3 and 1,8-DNP7. A transformant, 1,8-DNP2-2, induced by DNA of a fibrosarcoma, 1,8-DNP2, and 7 secondary transformants derived from it contained rat K-ras sequences. Another transformant, 1,8-DNP2-1, induced by the same sarcoma did not have a ras family oncogene. This indicates that the sarcoma, 1,8-DNP2, has at least 2 transforming genes. The transforming genes of 6 other transformants derived from 3 sarcomas did not contain ras family or neu transforming genes.

Animals↗
PubMed1985

Molecular cloning of an activated human oncogene, homologous to v-raf, from primary stomach cancer.

Transfection with high molecular weight DNA from a primary stomach cancer induced foci of transformed NIH 3T3 cells, and the transformed cells were tumorigenic in nude mice. By screening with a human Alu-family probe, we isolated the human DNA sequence from the secondary transformant cells. This transforming sequence encompasses about 60 kilobase pairs and is unrelated to known human transforming genes. Examination of homologies between this sequence and retroviral oncogenes revealed that the human transforming sequence is closely related to the v-raf oncogene of murine transforming retrovirus 3611-MSV.

Animals↗
PubMed1985

Monoclonal antibodies to human protein C: effects on the biological activity of activated protein C and the thrombin-catalyzed activation of protein C1.

Thirteen monoclonal antibodies designated as MFC-1 to MFC-13 were obtained from hybridoma cells cloned after the fusion of mouse myeloma cells with spleen cells of mice immunized with purified human protein C. Studies were made to determine where the antibodies bound to the molecule of protein C and whether they affected the biological actions of protein C. By using the immunoblotting technique, six of these antibodies were shown to bind to the light chain of protein C, and five to the heavy chain of protein C and also activated protein C. The remaining two antibodies bound to neither the light chain nor the heavy chain, though both antibodies bound to the intact protein C. Antibodies specific for the light chain did not bind to the gamma-carboxyglutamic acid-domain. Two of the antibodies specific for the heavy chain (MFC-13 and -1) inhibited the amidolytic activity of activated protein C. The MFC-13 also inhibited the activity of bovine activated protein C, but not that of human Factor IXa, Factor Xa, or thrombin. In addition to these two antibodies, another one for the heavy chain (MFC-10) and two antibodies for the light chain (MFC-9 and -11) inhibited the inactivation of Factor Va by human activated protein C. One of the antibodies which inhibited the enzyme activity (MFC-1) blocked the inhibition of activated protein C by protein C inhibitor. Another one for the heavy chain (MFC-5) inhibited the activation of protein C by thrombin regardless of the presence or absence of thrombomodulin. Based on these results, we have established the positions of some monoclonal antibody-binding sites on the protein C molecule.

Animals↗
PubMed1985

Activation of c-Ki-ras gene in human pancreatic cancer.

DNA isolated from a lymph node with metastasis from pancreatic adenocarcinoma in a Japanese male patient transformed NIH3T3 cells upon transfection by the calcium-phosphate precipitation technique. Analysis of DNA from the transformant revealed the presence of an activated human c-Ki-ras gene, which is considered to be responsible for the transformation of the NIH3T3 cells.

Adenocarcinoma↗