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M Oshimura

Publications and source records attributed to M Oshimura.

264 records · Page 15Linked to original sources
PubMed1976

Non-disjunction of an unusual X chromosome.

Because of multiple abnormalities in her children, a young mother was investigated and shown to have a 47,XXX chromosome constitution. Additional C group chromosomes without visible centromeric constrictions were found in a number of cells from the peripheral blood, and using C and Q banding techniques these chromosomes were identified as X chromosomes. Analysis of the banding karyotypes of 300 cells revealed that the acentric X chromosomes had the ability to replicate and that this replication was associated with non-disjunction leading to aneuploid cells. Even though cultured skin cells did not have acentric or extra chromosomes in addition to the triple-X, examination of buccal mucosa cells for the presence of X-bodies suggested that the phenomenon of non-disjunction was present in the epithelial cells of the patient. In addition to the X without a visible centromeric constriction, either acentric D or E chromosomes were found. The data suggest that a functional defect in the cells per se is responsible for the appearance of the acentric chromosomes.

Adult↗
PubMed1976

Chromosomes and causation of human cancer and leukemia. XXI. Cytogenetically unusual cases of leukemia.

Three male patients with leukemia were found with banding techniques to have unusual cytogenetic pictures in the cells of their marrow, spleen or blood. Case No. 1 (78 yr old) was that of a Ph1-negative CML with a missing Y in the blood (cultured without PHA) and marrow cells. The patient is still alive and responding to therapy. Case No 2 (54 yr old) was considered prior to admission to have either CML or AML, but was shown, in fact, to be in the blastic phase of CML; all the cells in his marrow and spleen were Ph1-positive, but with no evidence of a translocation. Other karyotypic findings (+8, +11, +13, +21) frequently encountered in the blastic phase of CML were present in the cells of this patient. Case No. 3 (50 yr old) with AML was shown to have a Ph1 resulting from a standard translocation, i.e., [t(9;22) (q34;q11)], in a substantial number of the cells in the marrrow and blood (cultured without PHA). The implications of these unusual findings are discussed in relation to the chromosomal pictures usually encountered in these states.

Aged↗
PubMed1975

Chromosomes and causation of human cancer and leukemia. X. Banding patterns in cancerous effusions.

Cells from five cancer effusions (two ovarian carcinomas, two lung cancers, and one carcinoma of the breast) were analyzed by G-, C-, and Q-banding techniques. The following observations were made: 1) The origin of some marker chromosomes could be traced accurately by these banding techniques. 2) Several chromosomes, which appeared normal with conventional staining techniques, were found to be re-arranged ones and, hence, abnormal. 3) Chromosomes No. 1, No. 3 and No. 11 were the most frequently involved in aberrations, whereas No. 12, No. 13, No. 17-20, and No. 22 Were least frequently involved. Only in one case each was the X chromosome or the Y chromosome involved in aberrations. The Y chromosome was found to be missing in all cancer cells of one lung cancer. 4) Each effusion had characteristic markers, invariably present in each cell, whether the cells were near diploid, or polyploid. 5) No common markers were observed in the two ovarian carcinomas studied, whereas the two lung cancers had a few common markers.

Adult↗
PubMed1975

Isochromosome 17 in prostatic cancer.

In a continuing search for karyotypic changes characterizing various human cancers we have examined in detail with Q and G banding techniques the chromosomal constitution of a metastatic cancer of the prostate. The results obtained with these techniques present not only what is to our knowledge the first description of the chromosome constitution in cancer of the prostate but also the first observation of an isochromosome 17 marker in a cancerous state other than a blood disease. Only further studies on the precise identification of individual chromosomes in other cancers will reveal the significance of this marker in human cancer.

Chromosome Aberrations↗
PubMed1975

Meiotic disjunction in t(14;15)6ca heterozygotes and fate of chromosomally unbalanced gametes in embryonic development.

In heterozygous carriers of the mouse reciprocal translocation T(14;15)6Ca, the frequency of nondisjunction involving the minute marker chromosome was 4.4% in the male and 22.2% in the female. The fate of gametes with unbalanced genomes derived from normal as well as abnormal meiotic disjunction in T6 heterozygotes was investigated on the basis of chromosome counts at metaphase II and karyotype analyses in early postimplantation embryos produced by backcrossing with chromosomally normal animals. Results obtained indicate that meiotic, gametic, and zygotic selection attributable to specific types of chromosomal imbalances is minimal, if any, by the late blastocyst stage. All zygotes with unbalanced genomes, except those with 20 normal pairs plus the minute marker, however, die off in the latter half of pregnancy. Therefore, the increased incidence of translocation trisomics among progeny of female as compared with male heterozygotes reflects the higher incidence of nondisjunction in primary oocytes than in spermatocytes.

Animals↗
PubMedDate not supplied

Chromosomal banding of cultured T and B lymphocytes.

Chromosomes of thymus-derived lymphocyte (T-cell) cell lines (CCRF-CEM, CCRF-H-SB-2, MOLT-3, MOLT-4, and RPMI 8402) and the corresponding lines (CCRF-SB and RPMI 8392) with thymus-independent lymphocyte (B-cell) characteristics, were examined with banding techniques. The pairs of cell lines (CCRF-H-SB-2 and CCRF-SB, and RPMI 8402 and RPMI 8392, were confirmed to be of the same origin, respectively, inasmuch as their individual specific variant bands were identical. The MOLT-3 and MOLT-4 cells had common marker chromosomes, indicating that the chromosomal changes in these cells probably occurred in vivo. All of the T-cells had structurally abnormal marker chromosomes, whereas the B-cells were chromsomally normal. The structural changes of the chromosomes suggest that the malignant nature of the present T-cells may be essential for such T-cells to be established in vitro in a standard culture medium.

B-Lymphocytes↗
PubMedDate not supplied

Determination of the chromosomal site for the human radiosensitive ataxia telangiectasia gene by chromosome transfer.

The chromosomal localization of the gene which complements radiation hypersensitivity of AT cells was studied by microcell-mediated chromosome transfer. A 6-thioguanine-resistant derivative of an immortalized AT cell line, AT2KYSVTG, was used as a recipient for microcell-mediated chromosome transfer from 4 strains of mouse A9 cells, 3 of which carried a human X/11 recombinant chromosome containing various regions of chromosome 11, while the other carried an intact X chromosome. HAT-resistant microcell hybrids were isolated and examined for their radiosensitivity and chromosome constitution. The microcell hybrid clones obtained from the transfer of an intact X chromosome or an X/11 chromosome bearing the pter----q13 region of chromosome 11 did not show a difference in radiosensitivity from parental AT cells, while those obtained from the transfer of X/11 chromosomes bearing either the p11----qter or the pter----q23 region of chromosome 11 exhibited a marked radioresistance which was comparable to normal human fibroblasts. A HAT-resistant but radiosensitive variant was further obtained from the microcell fusion with an A9 cell strain carrying an X/11 chromosome bearing the 11p11----qter region, in which a deletion at the 11q23 region was found. The results indicate that the gene which complements a radiosensitive phenotype of AT is located at the q23 region of chromosome 11.

Ataxia Telangiectasia↗
PubMedDate not supplied

Nonrandom loss of chromosome 15 in Syrian hamster tumours induced by v-Ha-ras plus v-myc oncogenes.

Nonrandom chromosome rearrangements, observed in a variety of human and animal tumours, are associated in some cases with enhanced expression or deregulation of cellular oncogenes. Recently, it was shown that normal, diploid rodent cells are neoplastically transformed following transfection with two cooperating oncogenes, for example myc plus ras. However, the number of steps necessary to convert a normal cell into a malignant cell is unknown. If activation of two oncogenes is sufficient for tumorigenicity, tumours derived from diploid cells transformed by the transfected oncogenes may remain diploid or have only random chromosome alterations. We have performed cytogenetic analyses of tumours formed after transfection of Syrian hamster embryo cells with either v-Ha-ras plus v-myc DNAs or polyoma DNA alone. Whereas polyoma-induced, tumour-derived cells were diploid, tumours induced by v-Ha-ras plus v-myc oncogenes were monoclonal and had a nonrandom chromosome change, monosomy of chromosome 15. Thus, an additional change, loss of chromosome 15, is required for or is advantageous for tumorigenicity induced by v-Ha-ras plus v-myc oncogenes. These results suggest that the neoplastic progression of normal, diploid cells requires more than two steps under certain conditions.

Animals↗