Details of a Researcher - TOKINO Takashi

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ASSIGNMENT OF 54 COSMID CLONES TO 5 REGIONS OF CHROMOSOME-10

SE MOLE, MS JACKSON, T TOKINO, Y NAKAMURA, BAJ PONDER

GENOMICS ( ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS ) 15 ( 2 ) 457 - 458 1993.02

Article, review, commentary, editorial, etc. (scientific journal)

IDENTIFICATION AND CHARACTERIZATION OF A CDNA, WHICH IS HIGHLY HOMOLOGOUS TO THE RIBONUCLEOPROTEIN GENE, FROM A LOCUS (D10S102) CLOSELY LINKED TO MEN2 (MULTIPLE ENDOCRINE NEOPLASIA TYPE-2)

S TAKIGUCHI, T TOKINO, T IMAI, A TANIGAMI, K KOYAMA, Y NAKAMURA

CYTOGENETICS AND CELL GENETICS ( KARGER ) 64 ( 2 ) 128 - 130 1993

We previously reported a nearly 1-Mb contig of cosmid and YAC clones at D10S102, a locus that is tightly linked to the gene responsible for multiple endocrine neoplasia type 2 (MEN2A). Subclones of 159 genomic EcoRI fragments in the contig were tested on ''zoo blot'' to detect DNA sequences conserved in various species. Nine fragments found to contain conserved sequences were used as probes for screening cDNA libraries. One of these probes, y300-pL50, recognized a cDNA from a human fetal brain library. The cDNA encoded a protein consisting of 270 amino acids, whose predicted sequence has a high degree of homology to heterogeneous nuclear ribonuclear protein. This expressed sequence may be a candidate for the gene responsible for MEN2A.

Mapping of human chromosome 3 and its application to human diseases

K. Yamakawa, Y. Nakamura, E. Takahashi

Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme 38 ( 3 ) 215 - 227 1993

Book review, literature introduction, etc.

PubMed

IDENTIFICATION OF 57 CONVENTIONAL RFLP AND 6 VNTR SYSTEMS WITH 32 DNA CLONES ON CHROMOSOME-11P15

K TAKITA, A TANIGAMI, T TOKINO, C JONES, Y NAKAMURA

GENOMICS ( ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS ) 13 ( 4 ) 1296 - 1299 1992.08

DOI PubMed CiNii

A HIGH-RESOLUTION CYTOGENETIC MAP OF 168-COSMID DNA MARKERS FOR HUMAN CHROMOSOME-11

TA HORI, E TAKAHASHI, A TANIGAMI, T TOKINO, Y NAKAMURA

GENOMICS ( ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS ) 13 ( 1 ) 129 - 133 1992.05

DOI PubMed CiNii

INHERITED P53 GENE-MUTATIONS IN BREAST-CANCER

D SIDRANSKY, T TOKINO, K HELZLSOUER, B ZEHNBAUER, G RAUSCH, B SHELTON, L PRESTIGIACOMO, B VOGELSTEIN, N DAVIDSON

CANCER RESEARCH ( AMER ASSOC CANCER RESEARCH ) 52 ( 10 ) 2984 - 2986 1992.05

Article, review, commentary, editorial, etc. (scientific journal)

Recent evidence has implicated germ-line mutations of the p53 gene as the cause of cancer susceptibility in the Li-Fraumeni syndrome, associated with the development of breast cancer and other neoplasms. Furthermore, somatic mutations of the p53 gene have been detected in a high percentage of non-familial breast cancers. We therefore sought to identify potential carriers of p53 gene mutations in a cohort of patients with early onset breast cancer. We examined 126 consecutive patients who developed breast cancer at or before the age of 40 for mutations of p53 within conserved regions of the gene. One patient with an inherited germ-line mutation of the p53 gene was identified but the functional significance of this mutation was not clear. It thus appears that only a small percentage of patients with breast cancer under the age of 40 carry germ-line mutations of the p53 gene, an observation which has implications for potential screening and risk assessment in such patients.

DETAILED ANALYSIS OF AN AMPLIFIED REGION AT CHROMOSOME-11Q13 IN MALIGNANT-TUMORS

A TANIGAMI, Takashi Tokino, K TAKITA, M UEDA, F KASUMI, Y NAKAMURA

GENOMICS ( ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS ) 13 ( 1 ) 21 - 24 1992.05

DOI PubMed CiNii

IDENTIFICATION OF RAS ONCOGENE MUTATIONS IN THE STOOL OF PATIENTS WITH CURABLE COLORECTAL TUMORS

D SIDRANSKY, Takashi Tokino, HAMILTON, SR, KW KINZLER, B LEVIN, P FROST, B VOGELSTEIN

SCIENCE ( AMER ASSOC ADVANCEMENT SCIENCE ) 256 ( 5053 ) 102 - 105 1992.04

Colorectal (CR) tumors are usually curable if detected before metastasis. Because genetic alterations are associated with the development of these tumors, mutant genes may be found in the stool of individuals with CR neoplasms. The stools of nine patients whose tumors contained mutations of K-ras were analyzed. In eight of the nine cases, the ras mutations were detectable in DNA purified from the stool. These patients included those with benign and malignant neoplasms from proximal and distal colonic epithelium. Thus, colorectal tumors can be detected by a noninvasive method based on the molecular pathogenesis of the disease.

DOI PubMed CiNii

ASSOCIATION BETWEEN CHROMOSOME-11Q13 AMPLIFICATION AND PROGNOSIS OF PATIENTS WITH ESOPHAGEAL CARCINOMAS

M MORI, Takashi Tokino, A YANAGISAWA, M KANAMORI, Y KATO, Y NAKAMURA

EUROPEAN JOURNAL OF CANCER ( PERGAMON-ELSEVIER SCIENCE LTD ) 28A ( 4-5 ) 755 - 757 1992.04

Ninety pairs of normal and tumour tissue DNAs were isolated from paraffin-embedded blocks of advanced oesophageal carcinoma cases and examined for gene amplification at chromosome 11q13 by dot-blot hybridisation using the int-2 gene as a probe. 22 of 90 carcinomas (24%) showed more than two times amplification. Although no significant correlation was observed between gene amplification and histological type or metastasis to lymph node, a tendency for deeper invasion to be associated with more frequent amplification was observed. In relation to prognosis, patients with amplification had a lower survival rate than those without amplification. This tendency was evident both in the group with well differentiated type carcinoma and in the group which had no metastasis to lymph node. Thus, gene amplification of the int-2 locus may be a useful prognostic factor.

PREDICTIVE TESTING FOR MULTIPLE ENDOCRINE NEOPLASIA TYPE-1 USING DNA POLYMORPHISMS

C LARSSON, J SHEPHERD, Y NAKAMURA, C BLOMBERG, G WEBER, B WERELIUS, N HAYWARD, B TEH, T TOKINO, B SEIZINGER, B SKOGSEID, K OBERG, M NORDENSKJOLD

JOURNAL OF CLINICAL INVESTIGATION ( ROCKEFELLER UNIV PRESS ) 89 ( 4 ) 1344 - 1349 1992.04

Mulitple endocrine neoplasia type 1 (MEN1) is an autosomal dominantly inherited predisposition to neoplastic lesions of the parathyroids, pancreas, and the pituitary. We have previously located the predisposing genetic defect to the long arm of chromosome 11 by genetic linkage. In this study, 124 members of six MEN1 families, including 59 affected individuals, were genotyped for restriction fragment length polymorphisms with different DNA probes, and the genetic linkage between these marker systems and MEN1 was determined. 13 marker systems (17 DNA probes) were found to be linked to MEN1. These markers are located within a region on chromosome 11 spanning 14% meiotic recombinations, with the MEN1 locus in the middle. Four of the marker systems are on the centromeric side of MEN1, and four on the telomeric side, based on meiotic crossovers. The remaining five DNA probes are closely linked to MEN1, with no crossovers in our set of families. The 13 marker systems can be used for an accurate and reliable premorbid test for MEN1. In most clinical situations it is possible to identify a haplotype of this part of chromosome 11 with the mutant MEN1 allele in the middle. The calculated predictive accuracy is > 99.5% if three such marker systems are informative. Therefore, genetic linkage testing can be used for informed genetic counseling in MEN1 families, and to avoid unnecessary biochemical screening programs.

THE 11Q23 BREAKPOINT IN ACUTE-LEUKEMIA WITH T(11-19)(Q23-P13) IS DISTAL TO THOSE OF T(4-11), T(6-11) AND T(9-11)

D CHERIF, H DERSARKISSIAN, J DERRE, T TOKINO, Y NAKAMURA, R BERGER

GENES CHROMOSOMES & CANCER ( WILEY-LISS ) 4 ( 2 ) 107 - 112 1992.03

Thirteen cosmid probes were mapped on the long arm of chromosome 11 between 11q22 and 11q24 by nonradioactive in situ hybridization. Starting with these localizations and those of other probes mapped to 11q23, four acute leukemias with translocations involving 11q23 were studied with the same method. The translocation breakpoints of the t(4;11)(q21;q23), t(6;11)(q27;q23), t(9;11)(p21-p22;q23), and t(11;19)(q23;p13) were confirmed to be distal to CD3D. The probe cC111-304 was proximal to the t(11;19) breakpoint while distal to the breakpoints of the other rearrangements. In view of the diversity of chromosomal abnormalities involving band 11q23, our finding extends the molecular heterogeneity of the breakpoint localization in leukemias with rearrangements involving 11q23.

DOI PubMed CiNii

31 NEW RFLP SYSTEMS DETECTED BY 24 DNA MARKERS ON HUMAN CHROMOSOME-10

T TOKINO, S TAKIGUCHI, A TANIGAMI, T BRAGG, C JONES, Y NAKAMURA

GENOMICS ( ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS ) 12 ( 2 ) 401 - 402 1992.02

Article, review, commentary, editorial, etc. (scientific journal)

DOI PubMed CiNii

PHYSICAL MAPPING OF A 950-KB REGION SURROUNDING A LOCUS (D10S102) TIGHTLY LINKED TO THE MEN2A GENE

T TOKINO, T IMAI, A TANIGAMI, S TAKIGUCHI, Y NAKAMURA

GENOMICS ( ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS ) 12 ( 2 ) 394 - 400 1992.02

DOI PubMed CiNii

MAPPING OF 262 DNA MARKERS INTO 24 INTERVALS ON HUMAN CHROMOSOME-11

A TANIGAMI, Takashi Tokino, S TAKIGUCHI, M MORI, T GLASER, JW PARK, C JONES, Y NAKAMURA

AMERICAN JOURNAL OF HUMAN GENETICS ( UNIV CHICAGO PRESS ) 50 ( 1 ) 56 - 64 1992.01

We have extended our mapping effort on human chromosome 11 to encompass a total of 262 DNA markers, which have been mapped into 24 intervals on chromosome 11; 123 of the markers reveal RFLPs. These clones are scattered throughout the chromosome, although some clustering occurs in R-positive bands (p15.1, p11.2, q13, and q23.3). Fifty-two of the markers were found to contain DNA sequences conserved in Chinese hamster, and some of these 52 also cross-hybridized with DNA from other mammals and/or chicken. As the length of chromosome 11 is estimated at nearly 130 cM, the average distance between RFLP markers is roughly 1 cM. The large panel of DNA markers on our map should contribute to investigations of hereditary diseases on this chromosome, and it will also provide reagents for constructing either fine-scale linkage and physical maps or contig maps of cosmids or yeast artificial chromosomes.

ISOLATION AND MAPPING OF 68 RFLP MARKERS ON HUMAN CHROMOSOME-6

S SAITO, K OKUI, Takashi Tokino, M OSHIMURA, Y NAKAMURA

AMERICAN JOURNAL OF HUMAN GENETICS ( UNIV CHICAGO PRESS ) 50 ( 1 ) 65 - 70 1992.01

We have isolated 68 new RFLP markers on human chromosome 6. Of these, 64 were localized on chromosomal bands by the fluorescent in-situ hybridization (FISH) method, 25 on the short arm and 39 on the long arm. Their distribution was uneven; the markers were localized predominantly in regions of R-positive banding. Eleven markers defined VNTR loci. This expanded collection of DNA markers will contribute to high-resolution linkage mapping of genes causing inherited disorders and will provide useful reagents for isolation of putative tumor-suppressor genes on chromosome 6 that appear to be involved in malignancies. Furthermore, the new markers will be guideposts for detailed linkage and physical maps of this chromosome.

CHROMOSOMAL SITES FOR HEPATITIS-B VIRUS INTEGRATION IN HUMAN HEPATOCELLULAR-CARCINOMA

T TOKINO, K MATSUBARA

JOURNAL OF VIROLOGY ( AMER SOC MICROBIOLOGY ) 65 ( 12 ) 6761 - 6764 1991.12

The discovery that hepatitis B'virus (HBV) integrates into host chromosomes raises the question of whether such viral DNA integration correlates directly with the activation of specific oncogenes or the inactivation of anti-oncogenes. To obtain insight into this problem, we randomly collected HBV integrant samples from different human hepatocellular carcinomas and identified the site of chromosomal integration by using in situ hybridization and/or linkage analysis with the flanking cellular DNAs as probes. Our findings did not specifically identify particular HBV DNA integration sites in chromosomes, although chromosomes 11 and 17 seemed to have more than the average number of integrants.

CHROMOSOME DELETIONS ASSOCIATED WITH HEPATITIS-B VIRUS INTEGRATION

T TOKINO, H TAMURA, N HORI, K MATSUBARA

VIROLOGY ( ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS ) 185 ( 2 ) 879 - 882 1991.12

Article, review, commentary, editorial, etc. (scientific journal)

DOI PubMed CiNii

CLINICAL EPIDEMIOLOGY AND EVALUATION OF GENE AMPLIFICATION AT CHROMOSOME LLQ13 IN THE 90 CASES OF ESOPHAGEAL CARCINOMAS

M KANAMORI, M MORI, T TOKINO, A YANAGISAWA, Y KATO, Y NAKAMURA

AMERICAN JOURNAL OF HUMAN GENETICS ( UNIV CHICAGO PRESS ) 49 ( 4 ) 121 - 121 1991.10

Research paper, summary (international conference)

ISOLATION AND MAPPING OF 62 NEW RFLP MARKERS ON HUMAN CHROMOSOME-11

T TOKINO, E TAKAHASHI, M MORI, A TANIGAMI, T GLASER, JW PARK, C JONES, TA HORI, Y NAKAMURA

AMERICAN JOURNAL OF HUMAN GENETICS ( UNIV CHICAGO PRESS ) 48 ( 2 ) 258 - 268 1991.02

To obtain new RFLP markers on human chromosome 11 for a high-resolution map, we constructed a cosmid library from a Chinese hamster X human somatic hybrid cell line that retains only human chromosome 11 in a Chinese hamster genomic background. A total of 3,500 cosmids were isolated by colony hybridization with labeled human genomic DNA. DNA was prepared from 130 of these cosmid clones and examined for RFLP. In 62 of them, polymorphism was detected with one or more enzymes; four RFLPs were VNTR systems. All polymorphic clones were assigned to one of 22 intervals obtained by mapping on a deletion panel of 15 somatic hybrid cell lines containing parts of chromosome 11; 11 clones were finely mapped by in situ hybridization. Although RFLP markers were scattered on the whole chromosome, they were found predominantly in the regions of R-banding. These DNA markers will contribute to fine mapping of genes causing inherited disorders and tumor-suppressor genes that reside on chromosome 11. Furthermore, as one-third of the cosmid clones revealed a band or bands in Chinese hamster DNA, indicating sequence conservation, this subset of clones may be useful for isolating biologically important genes on chromosome 11.

ALLELOTYPE STUDY OF PRIMARY HEPATOCELLULAR-CARCINOMA

M FUJIMORI, T TOKINO, O HINO, T KITAGAWA, T IMAMURA, E OKAMOTO, M MITSUNOBU, T ISHIKAWA, H NAKAGAMA, H HARADA, M YAGURA, K MATSUBARA, Y NAKAMURA

CANCER RESEARCH ( AMER ASSOC CANCER RESEARCH ) 51 ( 1 ) 89 - 93 1991.01

Accumulation of mutations in oncogenes and tumor suppressor genes transforms a normal cell to a malignant cell by allowing it to escape from normal control of growth. In order to learn (a) how many tumor suppressor genes are involved in the tumor progression of hepatocellular carcinoma (b) whether there is any association among allelic losses of chromosomes, or (c) whether integration of hepatitis B virus into host DNA influences any particular chromosomal losses, we have examined loss of heterozygosity with 44 restriction fragment length polymorphism markers in 46 cases of hepatocellular carcinoma. The markers represented all chromosomal arms except 5p, 8p, 9p, 18p, and acrocentric chromosomes. Allelic losses in tumors indicated that five tumor suppressor genes, located on chromosomes 5q, 10q, 11p, 16q, and 17p, may be involved in this cancer. However, no significant associations were observed among the various allelic losses or between the integration of hepatitis B virus and chromosomal losses. Furthermore, a deletion map for chromosome 16q indicated the localization of a tumor suppressor gene between q22 and q24 and that for chromosome 17p suggested the existence of a second tumor suppressor gene in addition to the p53 gene.

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