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N Kanda

Publications and source records attributed to N Kanda.

At least 73 records · Page 4Linked to original sources
PubMed1991

Structure, chromosome location, and expression of the human smooth muscle (enteric type) gamma-actin gene: evolution of six human actin genes.

Recombinant phages that carry the human smooth muscle (enteric type) gamma-actin gene were isolated from human genomic DNA libraries. The amino acid sequence deduced from the nucleotide sequence matches those of cDNAs but differs from the protein sequence previously reported at one amino acid position, codon 359. The gene containing one 5' untranslated exon and eight coding exons extends for 27 kb on human chromosome 2. The intron between codons 84 and 85 (site 3) is unique to the two smooth muscle actin genes. In the 5' flanking region, there are several CArG boxes and E boxes, which are regulatory elements in some muscle-specific genes. Hybridization with the 3' untranslated region, which is specific for the human smooth muscle gamma-actin gene, suggests the single gene in the human genome and specific expressions in enteric and aortic tissues. From characterized molecular structures of the six human actin isoform genes, we propose a hypothesis of evolutionary pathway of the actin gene family. A presumed ancestral actin gene had introns at least sites 1, 2, and 4 through 8. Cytoplasmic actin genes may have directly evolved from it through loss of introns at sites 5 and 6. However, through duplication of the ancestral actin gene with substitutions of many amino acids, a prototype of muscle actin genes had been created. Subsequently, striated muscle actin and smooth muscle actin genes may have evolved from this prototype by loss of an intron at site 4 and acquisition of a new intron at site 3, respectively.

Actins↗
PubMed1990

Assignment of the vascular smooth muscle actin gene ACTSA to human chromosome 10.

Human vascular smooth muscle actin gene (ACTSA) was cloned and its unique sequence was used as the hybridization probe for Southern blot analysis of DNAs from 18 rodent-human somatic cell hybrids; the gene was assigned to human chromosome 10. Regional mapping by in situ hybridization showed that the gene is located on the long arm (q22-q24) of the chromosome. Thus, the gene is on a different chromosome from the other four actin genes so far examined.

Actins↗
PubMed1990

c-myb gene analysis in T-cell malignancies with del(6q).

Three T-cell malignancies with del(6q) were analyzed for karyotypes and alteration of the oncogene c-myb that is assigned to 6q22-q24. Patients were diagnosed as having non-Hodgkin T-cell lymphoblastic lymphoma, adult T-cell leukemia, and acute T-cell lymphoblastic leukemia, and the deletions of chromosome 6 were del(6)(q21q25), del(6)(q21q23), and del(6)(q21) or del(6)(q21q27), respectively. Tumor cell DNAs were obtained from cultured pleural fluid or from fresh peripheral blood and marrow samples and were analyzed by Southern blot hybridization, using c-myb oncogene probes. Rearrangements, deletions, or amplifications were absent in these tumor DNAs, thereby indicating that the del(6q) breakpoint in these T-cell malignancies was located outside of the c-myb gene. Northern blot analysis revealed the elevated expression of c-myb in the non-Hodgkin lymphoma patient, in accord with lineage characteristics.

Adolescent↗
PubMed1990

Current urinary mass screening for catecholamine metabolites at 6 months of age may be detecting only a small portion of high-risk neuroblastomas: a chromosome and N-myc amplification study.

We studied 96 infants and children with untreated neuroblastomas. Chromosomes of tumor cells were analyzed in 68, and N-myc copy numbers were determined in 67 patients. Patients found by a mass screening program for 6-month-old infants (group A1, 39 patients) or those less than 12 months of age found clinically (group A2, 13 patients) were rarely in the disseminated stage (A1, three of 39; A2 one of 13); their tumors usually had near-triploid (3n) or hypertetraploid (greater than 4n) karyotypes (A1, 28 of 37; A2, nine of 11), and never had N-myc amplification (A1, zero of 34; A2, zero of 11). In contrast, children 12 months or over (group B, 27 patients) were usually in the disseminated stage (19 of 27) (P less than .0001); their tumors usually had near-diploid (2n) or near-tetraploid (4n) karyotypes (16 of 20) (P = .0027), and often had N-myc amplification (nine of 22) (P less than .0001). Of the 40 clinically found patients (A2 and B), six had undergone the screening with a negative result at the age of 6 months. Two of the six patients had N-myc amplification in the tumors. Most tumors found by the screening showed known characteristics predicting a good prognosis, and the majority of tumors showing characteristics predicting a poor prognosis were found in patients aged between 12 and 36 months. Our chromosome and N-myc amplification studies suggest that a low-risk tumor does not usually evolve to a high-risk tumor. Thus, the current mass screening program may be detecting only a small portion of highly malignant neuroblastomas at the earliest stage. Infants should be screened twice, at 6 months as well as at 12 months of age, for the early detection of high-risk neuroblastomas.

Age Factors↗
PubMed1990

Detection of preleukemic state of adult T-cell leukemia (pre-ATL) in HTLV-1 carriers.

The prevalence of the preleukemic state of adult T-cell leukemia (pre-ATL) was studied in Nagasaki prefecture, one of the endemic human T-lymphotropic virus type 1 (HTLV-1) areas in Japan. Pre-ATL cases have the monoclonal proliferation of abnormal lymphocytes, without signs of malignant proliferation or clinical signs and symptoms related to leukemia. HTLV-1 carriers who have monoclonal integration of HTLV-1 proviral DNA may be at high risk of developing ATL. Abnormal lymphocytes with either bilobular or large and chromatin-rich nuclei were found in 63/356 (17.7%) of HTLV-1 carriers among inhabitants. We analyzed DNA of peripheral lymphocytes from 108 carries with abnormal lymphocytes by Southern blot technique. Monoclonal integration of HTLV-1 has been detected in 12 cases (11.1%). These results lead to the conclusion that the prevalence rate of pre-ATL among all HTLV-1 carriers is about 2%. Pre-ATL is presumed to be the clinical stage which precedes ATL, although the possibility remains that the HTLV-1 carrier may develop symptoms of ATL directly, without going through the pre-ATL stage.

Adult↗
PubMed1989

Cytogenetic findings and prognosis in neuroblastoma with emphasis on marker chromosome 1.

The relationship between cytogenetic findings and prognosis in 51 pediatric patients with neuroblastoma is described. Patients were classified into the following four groups based on karyotypic findings: (1) near diploidy, 42 to 47 chromosomes (n = 11); (2) hyperdiploidy, 50 to 56 chromosomes (n = 4); (3) near triploidy, 60 to 77 chromosomes (n = 33); and (4) hypotetraploidy, 80 to 83 chromosomes (n = 3). Patients with near diploid or hypotetraploid karyotypes also had several structural abnormalities including marker chromosome 1, with or without double minutes (DM) or homogeneously staining regions (HSR). Most of these patients were 1 year of age or older and had advanced tumors. The patients who were in the hyperdiploid or near triploid category had few structural abnormalities; all of them, except one, were younger than 1 year of age, had localized tumors, and are long-term, disease-free survivors. Kaplan-Meier analysis of survival rates disclosed a significant difference favoring the latter group (P less than 0.001). N-myc gene amplification was found in five patients of the former group but in no patients of the latter group. The presence or absence of DM or HSR in the former group had no statistically demonstrable effect on survival. However, the presence of marker chromosome 1 appears to indicate a poor prognosis. Five patients with Stage IV-S disease had near triploid abnormalities similar to findings in patients with localized tumors. We propose that localized and Stage IV-S neuroblastomas can be classified as one disease category, and that patients with near diploid or hypotetraploid karyotypes are clinically distinct from those having hyperdiploid or near triploid karyotypes. We consider that chromosomal pattern is a more influential prognostic factor than age, disease stage, or N-myc gene amplification.

Child↗
PubMed1989

Human cardiac myosin heavy chain gene mapped within chromosome region 14q11.2----q13.

Our previous report demonstrated that two human cardiac alpha- and beta-myosin heavy-chains (MHCs) which correspond to MYH6 and MYH7 respectively, according to Human Gene Mapping nomenclature, were mapped to human chromosome 14 and that human cardiac and skeletal MHC genes do not cosegregate. For further analysis, the regional mapping method was used. DNA from 4 human deletion and 3 human duplication cell lines were prepared for southern blotting, hybridized with human cardiac alpha- and beta-MHC DNA probes, and the hybridization intensity relative to 46,XX or 46,XY DNA was estimated. The results showed that two human cardiac MHC genes segregated with the 14cen----q13 region of the long arm of human chromosome 14. In situ hybridization of 3H-labeled human cardiac alpha-MHC probe to normal human metaphase chromosome independently confirmed this result.

Base Sequence↗
PubMed1989

Cytoplasmic localization of human repetitive DNA revealed by in situ hybridization.

Previously, we showed that a human repetitive DNA sequence (Sau3A family) belonging to a satellite DNA is unstable and constantly excised from the chromosomes (R. Kiyama, H. Matsui, and M. Oishi, 1986, Proc. Natl. Acad. Sci. USA 83, 4665). The unusual property of the repetitive DNA, along with another repetitive DNA (Alu sequence), was further investigated by in situ hybridization in several different human cells including HeLa, bone marrow, and peripheral blood cells. We found that the excised repetitive DNA sequences are localized not only in nuclei, but also in cytoplasm. These results have confirmed the instability of these DNA sequences in the chromosomes and further suggest that the alpha satellite DNA and the Alu sequence which were excised from the chromosomes are released from nuclei to cytoplasm.

Bone Marrow↗
PubMed1988

Molecular cloning and chromosomal localization of a gene coding for human cardiac myosin heavy-chain.

A human cardiac myosin heavy-chain (MHC) gene, cloned in a charon 4A phage, was isolated using two rat cardiac pCMHC DNA clones (pCMHC26: alpha-MHC type; and pCMHC5: beta-MHC type) as probes and shown to correspond to cardiac myosin heavy-chain of the alpha-type. The 4.3-KB cardiac genomic DNA clone was used as a probe in the Southern analysis of human genomic DNA from human-Chinese hamster or human-mouse somatic cell hybrids. The results show that the human cardiac MHC gene is assigned to chromosome 14 and the human cardiac and skeletal MHC genes do not cosegregate as do the mouse cardiac and skeletal MHC genes.

Chromosome Mapping↗
PubMed1988

Chromosomal localization of Sau3A repetitive DNA revealed by in situ hybridization.

The Sau3A DNA family consists of unique alphoid human repetitive DNA which is prone to be excised from the chromosomes and exhibits restriction fragment length polymorphism. We studied the chromosomal localization of the DNA by in situ hybridization using cultured normal human lymphocytes. Under standard hybridization conditions, the sequence hybridized with the centromeric regions of chromosomes 1, 2, 4, 11, 15, 17, 18, 19 and X, but under high stringency hybridization conditions, it hybridized with the centromeric regions of chromosomes 1, 17 and X, and particularly chromosome 11. Based on these results, we discuss the evolutionary relationship among the sequences of the Sau3A DNA family.

Biological Evolution↗
PubMed1988

Clinical significance of gene amplification studied in human neuroblastoma xenografts: relationship with tumor growth rate, chemotherapeutic sensitivities and levels of neuron-specific enolase.

Tumor doubling time, sensitivity to chemotherapeutic agents and concentrations of neuron-specific enolase were studied in nine human neuroblastoma xenografts, in which amplifications of N-myc, clones 8 and G21 were known; N-myc was amplified in eight, clone 8 in five and clone G21 in four of these nine xenografts. Tumor doubling time was longest in one xenograft, TNB10, which lacks the amplification of either N-myc or clone 8 or G21, and shortest in TNB1 in which all three DNA sequences are amplified with a DNA rearrangement in clone 8. No correlations were found between genomic amplification of N-myc, clones 8 and G21 and effectiveness of five chemotherapeutic drugs tested, except for cis-platinum. cis-Platinum was found to be effective on all but the one xenograft, TNB10, with the longest tumor doubling time. Concentration of neuron-specific enolase in tumor extract was lowest in TNB1 and correlated with the length of the tumor doubling time.

Animals↗