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M Oshimura

Publications and source records attributed to M Oshimura.

At least 235 records · Page 13Linked to original sources
PubMed1984

Cytogenetic and in vitro culture studies on chronic myelomonocytic leukemia.

Six cases of chronic myelomonocytic leukemia were studied with cytogenetic and colony-formation techniques. Chromosome studies on bone marrow cells with the Q-banding method revealed cytogenetic changes in three of the six patients; +5, +8, +21, -13, -X, +1q, and 7q-. Chromosome changes among cases showed no particular correlation with survival or with the tendency to develop the acute phase. In vitro culture studies in the three cases showed that most of the hematopoietic precursors in the patients were considered to be myelomonocytic cells, with a variable number of colonies. Adherent cells from the patient's marrow had inhibitory effects for colony formation; on the other hand, patient serum showed elevated colony-stimulating activity.

Aged↗
PubMed1984

Chronic myelogenous leukemia with a complex Ph1 translocation in an XYY male.

We encountered a 38-year-old Japanese male patient with chronic myelogenous leukemia (CML), whose bone marrow and peripheral blood cells during the chronic and blastic phases contained a complex Ph1 translocation and an extra Y chromosome [i.e., 47,XYY,t(9;22;13)(q34;q11;q14)]. A karyotypic analysis of PHA-stimulated lymphocytes showed the constitutional karyotype to be 47,XYY. Thus, it was considered that CML with a complex Ph1 translocation developed in an XYY male; such a case has not been reported, so far. A B-lymphocyte cell line with the complex Ph1 translocation was established by the procedure of Epstein-Barr virus transformation. The presence of the complex Ph1 translocation in the B-lymphocyte cell line suggests that some of the B lymphocytes in this patient originated from the CML clone.

Adult↗
PubMed1984

Correlation of asbestos-induced cytogenetic effects with cell transformation of Syrian hamster embryo cells in culture.

The cytogenetic effects of chrysotile asbestos on Syrian hamster embryo cells in vitro were investigated at doses which induced morphological and neoplastic transformation but which failed to induce measurable gene mutations in the cells at two genetic loci. Chrysotile asbestos treatment of the cells significantly induced chromosome changes in a dose-dependent manner. Up to 50% of the cells had chromosome abnormalities in number or structure following treatment with asbestos (2.0 micrograms/sq cm) for 48 hr. Numerical chromosome changes were the most pronounced abnormalities although significant increases in metaphases with other chromosome aberrations (breaks, fragments, exchanges, and/or dicentrics) and cells with binuclei or micronuclei were also observed. A linear relationship was observed between the incidences of cells with tetraploid metaphases and binucleated cells, suggesting that binucleation and tetraploidy are related. Cytogenetic effects of other mineral dusts were also tested 48 hr following treatment at a concentration of 2.0 micrograms/sq cm. Crocidolite asbestos was less potent than chrysotile asbestos in its ability to induce cell transformation and cytogenetic damage. Treatment of the cells with thin glass fibers (Code 100) was also able to induce cell transformation and cytogenetic effects, but thick glass fibers (Code 110) were much less potent for both endpoints. Milling of the thin glass fibers decreased the length of the fibers and abolished their ability to induce cell transformation and cytogenetic effects. Nonfibrous alpha-quartz induced neither cell transformation nor cytogenetic effects at the dose of 2.0 micrograms/sq cm. The results indicate that the physical characteristics of the fibers determine their ability to induce cell transformation and their ability to induce chromosome mutations, suggesting a possible mechanistic relationship.

Animals↗
PubMed1983

A summary of cytogenetic studies on 534 cases of chronic myelocytic leukemia in Japan.

Cytogenetic and clinical data on 534 patients with chronic myelocytic leukemia (CML) were collected from 10 institutions in Japan. The results of the analysis of the data were in substantial accord with those of the First International Workshop on Chromosomes in Leukemia and other published data, but certain differences were noted in the frequency of Philadelphia chromosome (Ph1)-negative cases, unusual and complex Ph1 translocations, and additional chromosome changes. Some of the findings are discussed with respect to the origin of unusual and complex Ph1 translocations, the relationship between chromosome abnormalities and survival, and geographic differences in chromosome abnormalities.

Adult↗
PubMed1983

Long-term and dependent growth of human leukemic blast cells with granulocyte-macrophage differentiation in vitro.

A clonal growth of leukemic cells from the bone marrow of a patient with acute myeloid leukemia was observed in vitro for more than 20 months. Cytochemical and electron microscopic studies of the cells growing in vitro demonstrated that they were blast cells, differentiated granulocytes, and macrophages. They showed complete dependence on granulocyte-macrophage colony-stimulating factor for colony formation in agar. In addition to the presence of granulocytic colonies, some showed granulocyte-macrophage characteristics, suggesting that bipotential cells were also involved in long-term growth. Initially, they showed localized proliferation on or around giant fibroblast-like cells. Even after constant growth was established, attempts to transfer these cells were unsuccessful, and their growth was confined to the original flasks. These observations seen to indicate that their growth was not autonomous but dependent on the adherent cells in the flasks. This was also supported by a coculture experiment in which the cells were demonstrated to proliferate for 4 months only in the presence of normal bone marrow particles and bone marrow particle-derived feeder layers. These results suggest that, in some cases, long-term growth of leukemic cells can be induced in vitro by the cocultivation of bone marrow stromal cells.

Adult↗
PubMed1983

Establishment of different clonal strains from a human sarcoma of the stomach: tumorigenic heterogeneity in athymic nude mice.

Twenty five clonal strains have been isolated from a single human sarcoma of the stomach. Two different types of clones have been recognized by their morphology and behavior in vitro. Type I clones were characterized by criss-crossed arrays and multilayers with high terminal density. Type II clones grew in a well-organized monolayer with lower saturation density. Although both types of clones exhibited fibroblastic appearance, type I clones showed a more rounded, refractile shape. The cells of this type showed multiple regions of criss-crossed arrays and multilayers throughout the culture vessels. Saturation density of this type of clone was 2- to 3-fold (1.7 to 2.1 X 10(5) cells/sq cm) higher than that of type II clones. Chromosomal analysis revealed that type I clones were human aneuploid ones with modal chromosome numbers ranging from 51 to 61. With the exception of clones 11 and 19, type I clones were able to produce tumors in athymic nude mice when injected s.c. Type II clones exhibited a more flattened and elongated appearance. The cells grew in a well-organized monolayer resembling fingerprint whorls. They showed lower saturation density (0.7 to 0.9 X 10(5) cells/sq cm). Chromosomal examinations revealed the clones to be human aneuploid ones with modal numbers from 47 to 54. Tumor formation was not observed in nude mice given injections of this type of cell. Both types of clones did not bear antigens cross-reacting with the antiserum against mouse spleen cells but had surface antigens which were affected by the antibody against HL-60 cells and complement. These results suggested that this human sarcoma was heterologous and that cells with widely different tumorigenic potential preexisted in the parental cell population.

Adult↗
PubMed1982

Variant Ph1 translocations in CML and their incidence, including two cases with sequential lymphoid and myeloid crises.

A serial cytogenetic study of 110 cases of chronic myelogenous leukemia (CML) has been performed with G- and/or Q-banding techniques with the following results. (1) Seven out of the 110 cases were karyotypically normal. (2) A variant Ph1 translocation was observed in three cases. In one case, the leukemic cells contained two reciprocal translocations, i.e., a t(3;9) (q21;q34) and a t(17;22)(q21;q11); therefore, a Ph1 chromosome was masked by a translocation of the deleted material from the 17q onto the band q11 of the long arm of a chromosome No. 22. In the second case, a variant Ph1 translocation involved chromosomes No. 9, 20, and 22, resulting in a karyotype interpreted as 46,XX,t(9q+;20q+;22q-); in this rearrangement, one of the segments, i.e., 9q31 or 9q33, seemed to be interstitially deleted and inserted into the interstitial region (q11) of a chromosome No. 20 and the 22q11 leads to qter was translocated onto the 9q. This is the first case in which chromosome No. 20 was involved in a variant Ph1 translocation. In the third case, the karyotype of leukemic cells was interpreted as 46,XX,t(5;9;22)(q13;q34;q11). (3) The frequency of Ph1-negative CML and that of Ph1-positive CML with various types of Ph1 translocation from 15 studies reported as series of 25 or more cases, including the present study, have been tabulated. The incidence of a variant Ph1 translocation was 4.1% (42/1027 cases of Ph1-positive CML); of the 42, 13 were of a simple type and 29 of a complex type. (4) In one case of the present study, a masked Ph1 by a translocation of material onto the short arm of the 22q- was observed in the blastic crisis but not in the chronic phase. From the present study and a review of the published cases, it appears that the incidence of such a "masked" Ph1, which cannot be detected by conventional Giemsa staining, is less than 0.6% in CML cases. (5) The first and the second cases with a variant Ph1 translocation mentioned above developed a myeloid blastic crisis after the induction of remission of a lymphoid blastic crisis. For the present, it is unclear whether the occurrence of such blast cells in the two cases and the cytogenetic findings are coincidental. However, the evidence supports the notion of "lymphoid-myeloid" multipotentiality of certain leukemic cells.

Adult↗
PubMed1982

A summary of cytogenetic, morphologic, and clinical data on t(8q - ;21q+) and t(15q + ;17q-) translocation leukemias in Japan.

Cytogenetic, morphologic, and clinical data of 33 acute nonlymphocytic leukemia (ANLL) patients with t(8q - ;21q+) and 19 patients with acute promyelocytic leukemia (APL) were collected from seven laboratories in Japan. The latter class included 18 patients with t(15q + ;17q-) and one with a normal karyotype. The t(8q - ;21q+) and t(15q + ;17q-) translocations were each shown to be associated with a specific type of ANLL, namely, AML-M2 and APL-M3, respectively. No patient with APL had the M3 variant. The t(8q - ;21q+) translocation seems to be more common as an abnormality in ANLL in Japan as compared to findings in other countries. The high incidence of t(15q + ;17q-) among Japanese patients with APL indicated in this study, however, still awaits confirmation.

Acute Disease↗
PubMed1982

Cytogenetic and hematologic findings in acute myelogenous leukemia, M2 according to the FAB classification.

Chromosome banding studies on leukemic cells from 12 patients with acute myelogenous leukemia (AML), M2 according to the FAB classification, were performed. In 8 cases, chromosome abnormalities were observed; among these 8, 6 were found to exhibit a common chromosome abnormality, i.e., t(8;21)(q22;q22). The present findings strongly support the view that AML with t(8;21) (q22;q22) represents a definite subgroup within the general category of AML; this translocation has not been observed in more than 100 cases of leukemias other than AML M2. When the chromosome findings were collated with the hematologic and clinical data, it was found that the cases with t(8;21)(q22;q22) were not distinguishable from those with karyotypes other than the translocation in M2, in terms of hematologic and clinical findings.

Adult↗
PubMed1982

Factor(s) responsible for the increase in alkaline phosphatase activity of postmitotic granulocytes from normal individuals and patients with chronic myeloid leukemia.

Using postmitotic granulocytes (PMGs) with low neutrophil alkaline phosphatase activity (NAP activity), factor(s) having the capacity to increase their NAP activity were examined in vitro. A high activity of the factor was demonstrated in the cystic fluid of a human squamous cell carcinoma, which is known to produce a large amount of granulocyte-macrophage colony-stimulating factor (GM-CSF). The NAP-stimulating factor increased NAP values both in PMGs from normal bone marrow and PMGs from patients with chronic myeloid leukemia (CML), and NAP values in cells treated with the factor approached or rose above those of normal peripheral granulocytes after 48 hr of culture. The effect of the factor was specific in that the factor caused stimulation only in granulocytic series. These findings may indicate that increases in NAP activity reflect maturation or granulocytes and that low NAP activity of neutrophils derived from patients with CML is due to the immaturity of these cells. The relationship between the factor responsible for the increase in NAP activity and GM-CSF is also discussed.

Alkaline Phosphatase↗
PubMed1981

Chronic myelogenous leukemia with translocations (3q-;9q+) and (17q-;22q+). Possible crucial cytogenetic events in the genesis of CML.

Two reciprocal translocations involving chromosomes 3, 9, 17, and 22 were found in a patient with seemingly Ph1-negative chronic myelogenous leukemia (CML). The two translocations were t(3;9)(q21;q34) and t(17;22)(q21;q11); the breakage in chromosomes 9 and 22 apparently occurred at the same point as in the usual Ph1 translocation, t(9;22)(q34;11). From the present evidence and a review of the literature it appears that the breakage on both chromosomes 9 and 22 at the special regions and the separation of the fragments are present in practically all standard and variant Ph translocations, even those in which the terminal region of the long arm of chromosome 9 and (9q) does not seem to be involved in the rearrangement; however, a translocation between chromosomes 9 and 22 is not an obligatory result of the rearrangement, as seen in the present case. Thus, we postulate that the breakage on both chromosomes 9 and 22 at the special regions and separation of the fragments are the crucial cytogenetic events in the genesis of CML and stress the importance of paying careful attention to the terminal region of 9q, particularly when chromosome 9 does not seem to be involved in the rearrangement.

Adult↗