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Biomedical subjects

M Oshimura

Publications and source records attributed to M Oshimura.

At least 253 records · Page 14Linked to original sources
PubMed1981

A 14q+ chromosome in a malignant lymphoma in a patient with Down's syndrome.

A 17-year-old Japanese boy with Down's syndrome developed leukemic lymphosarcoma; histology of a lymph node biopsy revealed a malignant lymphoma, of the poorly differentiated lymphocytic (ML-PDL) or possibly lymphoblastic type (ML-LB). The Giemsa-banding technique for chromosome analysis revealed the karyotype of the lymphoma cells to be 47, XY, + 21, 14q+. A chromosome study of PHA-stimulated lymphocytes showed a 21-trisomic pattern, i.e., 47, XY, + 21. The 14q+ marker was a product of a translocation in which the long arm of chromosome No. 8 (probable break at band q11) was translocated to the long arm of a No. 14 at band q32, which is a region usually affected in various types of lymphomas. Two normal No.8 chromosomes were present. Thus, the lymphoma cells were partially trisomic for chromosome No. 8.

Adolescent↗
PubMed1981

Two cases of acute myelogenous leukemia with high terminal deoxynucleotidyl transferase activity responding to vincristine-prednisolone treatment with complete remission.

Increased TdT activity was demonstrated in 2 cases of AML. One of them had Ph1 positive chromosome due to a standard translocation of t(9:22). Treatment with cytosine arabinoside, daunorubicin, 6-mercaptopurine and prednisolone was ineffective or only partially effective. Switching to the vincristine and prednisolone therapy resulted in a complete remission in both cases.

Adult↗
PubMed1978

Murine myeloid leukemia: colony formation in vitro.

Normal and myeloid leukemic spleen cells from RF mice were cultured in vitro in plasma clots. In situ histochemical staining and karyotypic analysis of the colonies formed in the clot revealed that the colonies produced by leukemic and normal progenitors were indistinguishable morphologically and cytochemically. Colonies of leukemic origin were identified by in situ karyotypic analysis, a method not previously utilized in studies of hematopoietic proliferation in semi-solid matrices.

Animals↗
PubMed1977

N-band polymorphism of human acrocentric chromosomes and its relevance to satellite association.

With the aid of Q- and N-banding techniques we investigated the relationship between the length of satellite stalks, the appearance of N-bands and the frequency of satellite association of individual acrocentric chromosomes in the cells of seven individuals, including one male with a satellited and small Y-chromosomes. The appearance of N-bands, seemed to be a constant and characteristic property of individual acrocentric chromosomes, independent of the status of concentration of the chromosomes at metaphase. The homolog with longer satellite stalks had larger N-bands and participated in satellite association at a higher frequency than the one with shorter stalks. It appeared that N-bands were present along the whole length of the satellite stalk, the size of which could possibly reflect the amount of rDNA present in the nucleolar organizers in human chromosomes.

Chromosomes↗
PubMed1977

Chromosomes and causation of human cancer and leukemia. XXIII. Near-haploidy in acute leukemia.

A case of acute lymphoblastic leukemia (ALL) with a near-haploid (27 chromosomes) leukemic cell population in the marrow has been described and the findings compared to those of the only other such case in the literature. In both cases the cells with 27 chromosomes, except for one chromosomal group, had karyotypic findings which were identical. Cells with 54 chromosomes, karyotypically exact duplicates of the cells with 27 chromosomes, were also encountered; on morphological basis it appeared that the marrow contained large and small lymphoblasts, possibly matching the metaphases with 54 and 27 chromosomes, respectively. The genesis of the cells with 27 chromosomes was uncertain and several postulates are discussed, as well as the relation of the findings to the cytogenetic observations encountered in ALL and their possible role in human leukemogenesis.

Bone Marrow↗
PubMed1977

Chromosomes and causation of human cancer and leukemia. XXV. Significance of the Ph1 (including unusual translocations) in various acute leukemias.

The following rare Ph1-positive chromosome constitutions, based on the cytogenetic findings in three cases with acute leukemia, are presented. 1) A hypodiploid karyotype, primarily 43, -X, -7, -8,9p+ and a Ph1, in a patient with acute lymphoblastic leukemia (ALL) in relapse, followed by a complete remission and a normal chromosomal picture and then by the appearance of cells with a 46,XX,Ph1 karyotype. The Ph1 was due to a standard translocation between chromosomes no. 9 and no. 22. 2) The first demonstration of an unusual Ph1-translocation between chromosomes no. 19 and no. 22 in a condition other than chronic myelocytic leukemia (CML), i.e., acute myeloblastic leukemia (AML). 3) The presence of a Ph1 in acute erythroleukemia (EL) due to a translocation between chromosomes no. 4 and no. 22, this apparently being the first description of such a translocation in any disease. The cytogenetic findings, particularly those in the Ph1-positive case of ALL, were evaluated in relation to the cytologic and immunologic features, clinical courses and implications, and the interrelationship between the three conditions (AML, blastic phase of CML and ALL), which have to be considered in cases of Ph1-positive acute leukemia.

Adult↗
PubMed1977

Chromosomes and causation of human cancer and leukemia. XXVI. Binding studies in acute lymphoblastic leukemia (ALL).

Chromosomes were studied in the bone marrow cells of 101 patients with acute lymphoblastic leukemia (ALL) hospitalized at or attending the clinics of Roswell Park Memorial Institute (RPMI) between January, 1968, and December, 1976. Aneuploidy was observed in about 50% (54/101) of the cases. Two cases were hypodiploid and the remaining were either pseudo or hyperdiploid. The frequency of abnormalities and the chromosomal numbers were similar to those of 106 cases studied in our laboratory prior to 1968. Of 50 recently unselected cases of ALL in whom Q- and G-banded karyotypes were attempted, 31 were successfully analyzed with these techniques. The banding patterns revealed 16 cases to have chromosome abnormalities and four of these to have a similar abnormality, i.e., partial deletion of the long arm of chromosome no. 6: two cases had a 6q- with additional abnormalities and two had 6q- as the sole karyotypic abnormality. The breakpoint in chromosome no. 6 seemed to involve a segment from q21 to q25. An isochromosome of the long arm of no. 7, i(7q), was observed in two cases, two additional no. 21 chromosomes were observed in five cases and, except for the Y, all other chromosomes participated in the karyotypic changes encountered in the 16 cases in which banding analyses were performed. Banding analysis has afforded the first reliable approach towards ascertaining karyotypic evolution in ALL, which was achieved in eight cases of the present study. The chromosomes contributing to this karyotypic evolution were distributed widely. Thus, all chromosomes except the Y participated in numerical and/or structural karyotypic changes. Even though nonrandom chromosome changes may occur early in ALL, the pristine prototypic picture of the karyotypes in ALL is often obfuscated by successive chromosomal changes and hyperdiploidy by the time the karyotypes are analyzed in this condition. Further cytogenetic studies are required, with special attention to karyotypic evolution, in order to uncover the significance of chromosomal changes in early and late ALL.

Adolescent↗
PubMed1977

Establishment and characterization of leukemic T-cell lines, B-cell lines, and null-cell line: a progress report on surface antigen study of fresh lymphatic leukemias in man.

Permanent human hematopoietic cell lines representing T-cell, B-cell and non T/non B (null-cell) leukemia have been established. Comparative analyses were made for their phenotype characteristics. A number of characteristics common within the 7 T-cell lines studied or distinct from other leukemia-type lines were described. Usefulness, validity and limitation of these findings are discussed in connection to the attempt at classification of ALL, CLL and blastic phase of CML. The great majority of CLL were SmIg+-B-cell leukemia and a single case of T-cell CLL was documented. Except 10% as T-cell ALL and a single case of B-cell ALL, the majority of ALL were found to be the non T/non B ALL. Nevertheless, little evidence was suggested from the present study in favor for a notion that the T-cell ALL and the non T/non B ALL are two distinct diseases.

Antigens, Neoplasm↗
PubMed1977

Chromosomes and causation of human cancer and leukemia. XX. Banding patterns of primary tumors.

Banding techniques were used in the study of the chromosomes of primary tumors from 16 patients with various types of cancer. The initial analysis with conventional Giemsa staining revealed chromosome abnormalities in 13 of the 16 tumors. Eleven of these 13 tumors and 2 of the 3 with normal karyotypes were reexamined with Q-, G-, and C-banding techniques: The 2 tumors were conventionally stained normal karyotypes were found to have no abnormalities. Nine of the tumors wre characterized by numerical changes only and 4 by both numerical and structural abnormalities. In 11 tumors, excessive chromosomes, identified with banding techniques, were usually found in the following groups (number of tumors involved is shown in parentheses): No. 5 (5), No. 8 (6), No. 11 (5), no. 13 (5), and No. 21 (5). The primary tumors examined had hyperdiploid modes; only 4 of these tumors contained marker chromosomes, as opposed to the high frequency of markers in metastatic cancer cells and the presence, usually, of high polidy (near-triploidy or near-tetraploidy). The data suggested that the karyotypic changes in primary cancers consist primarily of numerical changes (hyperploidy), rather infrequent appearance of marker chromosomes, and, when present, only 1 or 2 markers.

Adolescent↗
PubMed1977

Cytogenetic and immunoglobulin markers of human leukemic B-cell lines.

This study describes the establishment of two permanent leukemic B-cell lines (BALM-1 and -2) originating from the blood cells of a patient with a B-cell type of acute lymphoblastic leukemia. The cells of BALM-1 and -2 exhibited cell surface markers compatible with B-cell origin. The identity between the leukemic cells in vivo and those of the BALM lines was established on the basis of the karyotypic picture, including marker chromosomes 14q+ and t(12;17;?) and cell surface immunoglobulins (K, delta, and mu chain determinants).

Antigens, Neoplasm↗
PubMed1976

Chromosomes and causation of human cancer and leukemia. XVII. Banding studies in acute myeloblastic leukemia (AML).

Chromosomes were studied in the bone marrow and/or blood cells from 38 patients with acute myeloblastic leukemia (AML). The initial analysis with conventional Giemsa staining revealed that 16 of the 38 patients with AML studied had chromosomal abnormalities. The cells of these 38 patients (16 with abnormal karyotypes and 22 with normal karyotypes) were re-examined with Q- and G-banding techniques. Twenty-two patients with conventionally stained normal karyotypes did not show any abnormalities, even with banding techniques. Three cases had a common translocation between the long arm of No. 8 and No. 21, i.e., [t(8;21)(q22;q22)], the so-called prototypic karyotype. Two cases had a 45, XX,-21 karyotype; and three cases had trisomy of the long arm of chromosome No. 1. The banding patterns revealed that in two of the three latter cases, the presence of the trisomy of the long arm of No. 1 apparently occurred late in the disease. Therefore, it is possible that the trisomy of the long arm of No. 1 might bear a relationship to selective growth advantage of the leukemic cells in some cases with AML. The presence of extra No. 8 and No. 9 chromosomes and deletion of the long arm of No. 7, frequently reported in several leukemic disorders, were also found in the present cases, but with other chromosomal abnormalities. Chromosomes No. 6,No. 15,No. 19,No. 20, and X were not involved in any structural and/or numerical changes. The present data suggest that some chromosomal changes are nonrandom in AML and that further chromosomal studies may lead to a division of AML patients into subgroups on the basis of their karyotypes.

Adult↗
PubMed1976

The chromosomes and causation of human cancer and leukemia. XIX. Common markers in various tumors.

Most human cancers are associated with abnormal (marker) chromosomes. In past and present studies banding analysis have uncovered a much larger number of markers in cancer cells than was seen with standard (Giemsa) staining. Furthermore, common markers of identical morphology and origin were found in tumors of related or unrelated tissues or organs, suggesting that in all probability such markers, although present in cancers of diverse nature, may indicate a common etiology, either related to the causation of the cancers, to the progression of the tumors, or to the predilection of certain chromosomes to undergo morphologic changes leading to marker formation. Even though some markers were common to different tumors, the bulk of the markers in the cancers studied could not be identified with certainty and their nature varied from tumor to tumor.

Aged↗
PubMed1976

Trisomy of the long arm of chromosome No. 1 in human leukemia.

We encountered a karyotypic abnormality, i.e. a trisomy of part of or the whole long arm of chromosome No. 1, in 4 patients with leukemia; 3 with acute myeloblastic, leukemia (AML) and 1 with chronic myelocytic leukemia (CML) in the blastic phase. Q- and G-banding techniques revealed that in two patients with AML and in the one with CML, this karyotypic abnormality was not an initial one and was apparently associated with clinical progression of the disease. This chromosome change is a common karyotypic abnormality in blood disorders, especially in AML, and possibly bears a relationship to selective growth advantages of the leukemia cells.

Chromosomes, Human, 1-3↗