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M Terada

Publications and source records attributed to M Terada.

At least 19 recordsLinked to original sources
PubMed1992

Establishment of a highly sensitive and specific exon-trapping system.

We have established a highly sensitive and specific exon-trapping system (SETS) with a specific plasmid vector in which an exon in a given DNA segment is identified by its ability to remain as a mature mRNA after splicing. The SETS provides us with the isolation of possible exons rapidly and easily from DNA fragments in chromosomal regions of more than 300 kilobase pairs. Genomic DNA fragments were partially digested and subsequently cloned into plasmid pMHC2, an exon-trapping vector we have constructed. These constructs were transfected into COS-7 cells, and consequent RNA transcripts were spliced in the cells. The resulting mature mRNA was harvested and amplified by using reverse transcription-PCR. Possible exons can be recognized by the sizes of PCR products and cloned into a plasmid vector. The SETS provides a direct means of cloning exons from genomic DNA of more than 300 kilobase pairs within a short period of time. Using this system, we have screened 300-kilobase-pair genomic DNA segments derived from human chromosome 11q13. Human chromosome 11q13 may contain genes responsible for human cancers, because DNA amplification is observed in several malignant tumors. We have successfully identified exon 2 of the HST1 gene and additional transcribed sequences.

Base Sequence↗
PubMed1992

K-sam-related gene, N-sam, encodes fibroblast growth factor receptor and is expressed in T-lymphocytic tumors.

We recently reported the isolation of the K-sam complementary DNA (cDNA), which was amplified preferentially in poorly differentiated types of stomach cancer and codes for one of the heparin-binding growth factor or fibroblast growth factor (FGF) receptor families. The K-sam-related gene, N-sam (NCC-IT-cell-derived sam), was isolated by screening of the cDNA libraries of human immature teratoma cells, NCC-IT. Sequence analysis of the N-sam cDNAs showed that N-sam encodes a human FGF receptor, the FLG protein. N-sam was expressed in lymphocytic leukemia/lymphoma cells, predominantly in the thymic T-cell phenotype. In a T-cell leukemia line, MOLT3, N-sam mRNA expression was markedly enhanced by 12-O-tetradecanoylphorbol-13-acetate treatment and was also up-regulated by basic FGF exposure. These results indicate that N-sam expression is regulated during T-cell ontogeny and modulated by its putative ligand exposure. The results also suggested that interaction between immature T-cell and marrow or thymic interstitial cells might be mediated by N-sam and basic FGF stored in the extracellular matrix of stromal cells.

Base Sequence↗
PubMed1992

Genes preferentially expressed in embryo stomach are predominantly expressed in gastric cancer.

Eight complementary DNA (cDNA) clones highly expressed in fetal rat stomach but not in normal adult rat stomach were isolated after screening 2 x 10(4) independent recombinants from a subtracted cDNA library. The cDNA library was first prepared from RNAs of total stomach at 16 days gestational period, and this cDNA library was subtracted by cDNAs prepared from adult rat total stomach RNA, using a novel PCR-based cDNA subtraction method. Northern blot analysis revealed that as many as six of eight clones thus isolated were overexpressed in at least some of the human or rat gastric cancers. From analysis of partial nucleotide sequence, four cDNA clones were identified as profilin, pro-alpha 1 (1) collagen, nucleolar protein B23.2, and elongation factor 1 alpha subunit. The remaining two clones were derived from novel genes. These novel genes, L-1 and L-2, are developmentally well regulated in the stomach. The present results clearly show that genes expressed preferentially in embryo stomach are most likely to be highly expressed in gastric cancer. The method described here provides us with a rapid method for identification of genes with significantly increased expression in cancer.

Animals↗
PubMed1992

Frequent loss of heterozygosity at the DCC locus in gastric cancer.

We examined 28 cases of surgically resected gastric cancer, excluding the diffuse type, for loss of heterozygosity (LOH) on 12 chromosomal arms using polymorphic DNA markers. LOH on chromosome 18q was detected in 61% (14 of 23) of the cases by the probes OLVIIA8, OLVIIE10, p15-65, SAM 1.1, and OS-4, and a putative common region showing LOH included the locus of the DCC tumor suppressor gene. LOH on chromosome 17p was also frequently found (8 of 19 or 42% of the cases) by the probes p10-3 and pHF12-1, and in 5 of these 6 cases the LOH on chromosome 17p was accompanied by LOH on chromosome 18q. On the other hand, the incidence of LOH was 30% or less using probes pHRnES, pHF12-65, p-c-mybE2.6, NJ3 3.2, pHF12-8, pHINS6.0, p9D11, hp2-alpha, pCMM6, and P1A5 on chromosomes 1q, 5, 6q, 7q, 9, 11p, 13q, 16q, 20, and 22q, respectively. LOH on chromosome 18q was frequent irrespective of the depth of tumor invasion, whereas the incidence of LOH on chromosome 17p was higher in the cases in which the tumor invaded beyond the muscularis propria than in those in which tumor invasion was limited to the submucosa and muscularis propria. These results suggest that LOH on chromosome 18q occurs at an earlier stage than LOH on chromosome 17p and that the inactivation of tumor suppressor genes located on chromosome 17p and 18q (e.g., the p53 and DCC genes) is critically involved in the development of the majority of gastric cancers. While alteration of the p53 gene is observed in various human cancers, that of the DCC gene is considered to occur more selectively in gastrointestinal cancers.

Chromosome Deletion↗
PubMed1992

Detection of novel germ-line p53 mutations in diverse-cancer-prone families identified by selecting patients with childhood adrenocortical carcinoma.

BACKGROUND: Germ-line p53 mutations appear to be inherited among the members of families diagnosed with Li-Fraumeni syndrome (LFS). The mutations detected in those families to date have been clustered in exon 7 of the p53 gene and, typically, have been single-base substitutions resulting in amino acid changes. PURPOSE: Our aim was to define the spectrum of p53 mutations associated with LFS. METHODS: From seven cancer-prone families identified by selecting members with childhood adrenocortical carcinoma as probands, we chose two families, each of which had two members from whom specimens could be obtained for genetic analysis. To detect germ-line p53 gene mutations in these individuals, we performed polymerase chain reaction (PCR)-single-strand conformation polymorphism analysis with Taq polymerase and oligonucleotide primers specific for p53 gene sequences. Genomic DNA extracted from fresh tissue samples and paraffin-embedded tumor samples was amplified, denatured, and electrophoresed on neutral polyacrylamide gels. PCR amplification was also carried out using total RNA from adrenocortical carcinoma samples of the proband in family 1. PCR products were purified, subcloned, and sequenced. RESULTS: We detected novel germ-line p53 mutations in affected members of both cancer-prone families. In the proband of family 1, a single-base deletion was detected at the first nucleotide of codon 307 in exon 8 of the p53 gene, resulting in a premature stop codon in exon 10. In family 2, we detected an A to C transversion at the second nucleotide of codon 286 in exon 8, both in DNA isolated from the adrenocortical tumor of the proband and in DNA isolated from the astrocytoma of the proband's father. This single-base substitution resulted in an amino acid substitution of alanine for glutamic acid. Both of these mutations are located outside the highly conserved region of the p53 gene where mutations in patients with LFS have been reported previously. CONCLUSION: Our results indicate that a wide range of germ-line p53 mutations is inherited in members of diverse-cancer-prone families.

Adrenal Cortex Neoplasms↗
PubMed1992

K-sam gene encodes secreted as well as transmembrane receptor tyrosine kinase.

K-sam was first identified as a gene amplified in the stomach cancer cell line KATO-III. The size of the major transcript of the K-sam gene was 3.5 kilobases in KATO-III cells, and we have previously shown that K-sam encodes a receptor tyrosine kinase that belongs to the heparin-binding growth factor receptor, or fibroblast growth factor receptor, gene family. The K-sam gene expresses multiple sizes of mRNAs in brain tissue, the immature teratoma cell line NCC-IT, and KATO-III. RNA blot analyses with a variety of K-sam probes indicate that there are at least four classes of K-sam mRNAs. Three types of K-sam cDNAs in addition to the previously reported type of K-sam cDNA were isolated, and their nucleotide sequences encode a full-length transmembrane receptor, a secreted receptor with a tyrosine kinase domain, and a secreted receptor without a tyrosine kinase domain.

Base Sequence↗
PubMed1992

p53 mutations in human lung tumors.

Mutation of one p53 allele and loss of the normal p53 allele [loss of heterozygosity (LOH)] occur in many tumors including lung cancers. These alterations apparently contribute to development of cancer by interfering with the tumor suppressor activity of p53. We directly sequenced amplified DNA in the mutational hot spots (exons 4-8) of p53 in DNA samples from 40 lung cancers. Most (31 of 40) samples were preselected for LOH in the region of p53. We detected 23 p53 mutations within these exons in 22 lung cancers; no p53 mutations were found in normal tissue of the patients. One-half of the mutations were G to T transversions on the nontranscribed strand, consistent with mutagenesis by tobacco smoke. Mutations of C to A on the nontranscribed strand, which would result from G to T mutations on the transcribed strand, were detected only in one sample. Three of 23 mutations were nonsense mutations; to date, nonsense mutations of p53 have not been reported in lung cancer. Mutation of this p53-coding region was detected in 20 of 27 small cell lung cancer samples, representing a 70% occurrence. Mutation of the p53 gene is apparently very frequent in small cell lung cancers. When LOH in the p53 region could be determined, complete concordance occurred between a sample having both a p53 mutation and LOH in the region of p53 (18 of 18 samples). Twelve samples of lung cancer had LOH in the region of p53, but the samples had no detectable p53 mutations, suggesting either alterations outside the known mutational hot spots of p53 or alterations of another unidentified tumor suppressor gene in the region of p53.

Amino Acid Sequence↗
PubMed1992

Frequent association of p53 gene mutation in invasive bladder cancer.

Structural alterations of the p53 gene were investigated to elucidate the molecular biological difference between superficial and invasive bladder cancer by polymerase chain reaction single-strand conformation polymorphism analysis. In 25 bladder cancers obtained from 23 patients, p53 gene mutations were investigated in exon regions 4 to 11. Twenty-four were transitional cell carcinomas, and the remaining one was a squamous cell carcinoma. Only one of 13 superficial bladder cancers, including pTis, pTa, and pT1, was found to have p53 gene mutation. However, of 12 invasive bladder cancers with pT2, pT3, and pT4, six primary carcinomas, including a squamous cell carcinoma and one metastatic carcinoma, were found to have p53 gene mutations. The number of cancers examined in Grades 1, 2, and 3 was three, seven, and 15, respectively. p53 gene mutation was not found in any of the ten cancers with Grades 1 and 2, while eight of 15 bladder cancers with Grade 3 were found to have p53 gene mutation. The results indicated that the incidence of p53 gene mutations appeared to be much higher in invasive-type and high-grade bladder cancers than in superficial and low-grade ones. Our results are compatible with the recently published results by Sidransky et al. [Science (Washington DC), 252: 706-709, 1991] showing that p53 gene mutations were frequently found in invasive bladder cancers by sequence analysis on polymerase chain reaction amplified products corresponding to exons 5 to 9. Our results are also compatible with previously reported results by Olumi et al. (Cancer Res., 50: 7081-7083, 1990) showing that the loss of chromosome 17p, revealed by analysis with restriction fragment length polymorphism, was frequent in high-grade bladder cancers. In this study, p53 gene mutations were often found in exon 4 as well as in other exons. Therefore, this region should also be examined for screening of mutations of this gene in bladder cancer. There appeared to be no consistent mutation sites in exons 4 to 11 of the p53 gene and no specific patterns of the mutation in bladder cancer.

Base Sequence↗
PubMed1992

Liver regeneration in recipients and donors after transplantation.

Reduced-size liver grafts from related donors may not be of an optimal size for adequate function in the recipient. Therefore, liver-graft regeneration is clinically important. We evaluated liver regeneration by liver-volume determinations with serial computed tomography scans in four recipients (aged 9 months to 12 years) and their donors (all fathers of the recipients) after living-related liver transplantation. Standard liver volume was calculated from the recipient's body-surface area. In each recipient, the size of the transplanted liver tended to converge to the standard liver volume with time, regardless of whether initial liver-graft volume was smaller or larger than standard liver volume. In addition, transplanted liver in the recipient regenerated much faster than remnant liver in the donor, even though both consisted of the same hepatocytes, which suggests that regeneration is regulated mainly by factors other than the hepatocytes themselves.

Adult↗
PubMed1992

Expression of the heparin-binding growth factor receptor genes in human megakaryocytic leukemia cells.

K-sam/bek, N-sam/flg and FGFR3/sam3 establish gene family of the receptors for heparin-binding growth factors (HBGFs) or FGFs. These mRNAs were detected in human leukemia cells, CMK, K562 and HEL, which have megakaryocytic phenotype or the potency to differentiate into megakaryocytic lineage. In CMK cells N-sam/flg transcript level was enhanced by the culture with 12-O-tetradecanoylphorbol-13-acetate (TPA). cDNA-polymerase chain reaction identified K-sam/bek mRNA in human platelets, suggesting the involvement of HBGFs in megakaryocytopoiesis and functions of platelets.

Base Sequence↗
PubMed1992

Intussusception of an appendiceal mucocele: report of a case.

A 66 year old Japanese female was admitted to our department for the examination and treatment of a mass in the cecum. She had experienced no symptoms or signs other than a positive test result for fecal occult blood. The mass in the cecum was confirmed by barium enema, colonofiberscopy and CT scanning. The presumptive diagnosis was a submucosal tumor of the cecum, however, a laparotomy subsequently revealed intussusception of an appendiceal mass. An ileocaecal resection with an ileocolic anastomosis was therefore performed and the mass was histologically diagnosed as a mucocele of the appendix. This patient is only the 24th case of intussusception of a mucocele of the appendix to be reported in Japan. A review of the available literature on this condition follows the case report.

Aged↗
PubMed1992

In vitro effects of milbemycin oxime: mechanism of action against Angiostrongylus cantonensis and Dirofilaria immitis.

The neuropharmacological mechanisms underlying the action of milbemycin oxime on the motility of Angiostrongylus cantonensis and Dirofilaria immitis were examined in vitro. In A. cantonensis, milbemycin oxime caused inhibitory effects at low concentrations of > or = 10(-9) g/ml, and paralysis was elicited at 10(-8) - 10(-6) g/ml. The paralysis was antagonized by picrotoxin and bicuculline but not by dibenamine. In addition, stimulatory effects were observed when the antibiotic was used at higher concentrations of 3-5 x 10(-6) g/ml, and the action was antagonized by strychnine. Both effects were also observed in the preparation contracted by eserine or pyrantel. When D. immitis was treated with milbemycin oxime at concentrations of 10(-7) and 3-5 x 10(-6) g/ml, only slight inhibitory and stimulatory effects, respectively, were observed. These effects were partially antagonized by picrotoxin and strychnine, respectively. These results suggest that the inhibitory and stimulatory actions of milbemycin oxime are caused through gabergic and cholinergic mechanisms in A. cantonensis and D. immitis.

Angiostrongylus↗
PubMed1992

Localization of HstI transcripts to the apical ectodermal ridge in the mouse embryo.

The HstI gene is a transforming gene, coding for a protein of the fibroblast growth factor family (Sakamoto et al., 1986). Previous RNA hybridization studies with the mouse homolog demonstrated the presence of a 3.0-kb transcript in Day 11 and 14 mouse embryos. Here we detect a 3.0-kb transcript in the limb and body of the dissected Day 11 mouse embryo. PCR amplification using HstI-specific primers also showed comparable results. In order to localize the HstI transcripts during development, corresponding HstI cDNA was isolated, and an HstI-specific region was used as a probe for in situ hybridization analysis. Serial sections of embryos from Day 8 (early-somite stages) through Days 9, 10, 11, and 12 of gestation were examined. With the antisense probe, a signal was detected in the Day 11 and 12 embryo, where it was localized to the apical ectodermal ridge (AER) of the limb bud. This structure is well known for its role in promoting the distal outgrowth of the developing limb bud. Signal was detected in both fore- and hindlimbs during the period of rapid distal growth. This restricted localization suggests a role for HstI in normal embryogenesis, including outgrowth of the limb bud.

Animals↗
PubMed1992

Ordering of human chromosome 3p markers by radiation hybrid mapping.

To construct a panel of radiation hybrids (RHs) for human chromosome 3p mapping, mouse microcell hybrid cells, A9(neo3/t)-5, containing a single copy of human chromosome 3p with pSV2neo plasmid DNA integrated at 3p21-p22 were irradiated and fused to mouse A9 cells. A panel of 96 RHs that retain several sizes and portions of human chromosome 3p segments was used to map 25 DNA markers for chromosome 3p. Eight of them, H28, H29, H32, H33, H35, H38, H48, and H64, were cloned from Alu-primed PCR products using A9(neo3/t)-5 cell DNA as a template. The most likely order of the 24 markers, except for H28, based on the statistical ordering method proposed by Falk, was cen-D3S4-D3S3-D3S30-H29-D3S13-D3S2-+ ++H48-D3F15S2-D3S32-D3S23-CCK-H35-H33- D3S11-D3S12-RARB-THRB(ERBA2-pBH302)- H64-H38-RAF1-D3S18-H32-D3S22-pter. The order and location of these markers were in good agreement with those previously determined by other mapping methods, suggesting that a panel of these 96 RHs is a valuable source for a rapid mapping of human chromosome 3p markers.

Chromosome Mapping↗
PubMed1992

Discordant hepatic uptake of Tc-99m NGA and Tc-99m PMT in a patient with hepatoma.

The authors report discordant hepatic uptake of Tc-99m NGA and Tc-99m PMT in a patient with hepatoma. Tc-99m PMT uptake was delayed and Tc-99m NGA concentrated in another area, thereby demonstrating that the uptake mechanisms for Tc-99m NGA and Tc-99m PMT are different. Tc-99m NGA imaging may be useful in characterizing the focal hepatic lesion of Tc-99m IDA or Tc-99m PMT concentration.

Albumins↗
PubMed1992

Mutations of the p53 tumour suppressor gene in haematologic neoplasms.

Mutations of the p53 tumour suppressor gene have frequently been observed in several types of solid tumours and are believed to be implicated in the development of these tumours. To determine the relevance of p53 mutations in haematologic neoplasms, we performed polymerase chain reaction-single strand conformation polymorphism analysis on the p53 gene in 45 patients with various types of haematologic neoplasms. In exons 5-8 containing highly conserved regions, mobility shifts indicating sequence alterations were detected in four of the 45 patients, and subsequent sequencing was performed. A point mutation resulting in a novel stop codon was detected at codon 213 in one of 23 cases of chronic myelogenous leukaemia (one of five cases of blast crisis). Point mutations causing amino acid substitutions were detected in one of four cases of myelodysplastic syndrome at codon 195, one of three cases of adult T-cell leukaemia at codon 281, and one of eight cases of acute lymphoblastic leukaemia at codon 281, and these missense mutations were accompanied by loss of the wild type allele. Patients harbouring these nonsense and missense mutations were in advanced disease stages. These findings suggest that mutational inactivation of the p53 gene is infrequent but is involved in the tumorigenesis of several types of haematologic neoplasms at least in some cases.

Amino Acid Sequence↗
PubMed1992

Konno procedure for congenital aortic stenosis with a single coronary artery from the left coronary sinus.

A right coronary artery originating from the left coronary sinus and traversing anteriorly is thought to be one of the contraindications for a Konno aortoventriculoplasty in congenital aortic stenosis because this procedure necessitates incision of the right ventricular outflow tract. The case of a 5-year-old girl with congenital aortic stenosis associated with a single coronary artery, successfully treated surgically by the Konno procedure and right coronary artery reimplantation, is reported. Preoperatively there was a pressure gradient between the left ventricle and the ascending aorta of 109 mmHg, which disappeared postoperatively. A postoperative angiography showed a patent right coronary artery.

Abnormalities, Multiple↗