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M C Yoshida

Publications and source records attributed to M C Yoshida.

At least 163 records · Page 9Linked to original sources
PubMed1982

Induction of supermelanin synthesis and morphological changes in interspecific reconstituted cells and its reversal by tumor promoter.

Chloramphenicol-resistant (CAPr) reconstituted cells and cybrids were isolated by fusion of karyoplasts (or intact cells) of mouse amelanotic melanoma B16 cells with cytoplasts of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) -deficient, CAPr rat myoblastic cells, L6TG.CAPr, and double selection in HAT medium containing CAP. Reconstituted cells or cybrids exhibited unique cellular arrangement, and about one third of the isolated clones expressed high tyrosinase activity and marked melanin synthesis, although the parental mouse cells expressed low tyrosinase activity and the parental rat cells did not express tyrosinase activity. These phenotypic changes have been stable for more than a year. The phenotypic reversions of these clonal cells were induced by treatment with a tumor promoter. There were changes in the morphology of the treated cells to that of the mouse B16 cells and extinction of tyrosinase activity and melanin synthesis in pigmented clonal cells. These phenotypic changes and reversions induced by a promoter were repeatedly reversible.

Animals↗
PubMed1982

Chromosome and cell surface marker studies in 1-propyl-1-nitrosourea-induced thymic lymphomas of the rat.

Immunological cell surface markers were studied in seven transplantable 1-propyl-1-nitrosourea-induced thymic lymphoma lines in F344 rats by reactivity to anti-Thy-1.1, anti-rat Ig (anti-Ig), and anti-rat T-cell (anti-T) sera, and by the capacity to form rosettes with guinea pig red blood cells. All the tumor lines were estimated to be sensitive to anti-Thy-1.1 but insensitive to anti-Ig serum in the presence of complement. The differences in reactivity to anti-T serum and rosette-forming capacity (RFC) allowed classification of the lines into three types. In type I, three lines were highly sensitive to anti-T serum but low in RFC, indicating that these lymphomas probably originated from relatively mature intrathymic T cells. In type II, two lines were moderately sensitive to anti-T serum and relatively high in RFC, indicating that these lymphomas derived from intrathymic T cells. In type III lymphomas, the remaining two lines were not only insensitive to anti-T serum but also low in RFC, suggesting that these lymphomas might have arisen from immature precursors of T and/or B cells. The chromosome study revealed that type I lymphomas were diploid, with slight numerical and structural variations. Type II lymphomas were pseudodiploid or hypotetraploid, with considerable variation in the number and morphology of chromosomes. Type III lymphomas had a diploid or hyperdiploid constitution, with a moderate degree of karyotypic variation. Neither consistent nor common karyotypic alterations among the seven lines were found, although the karyotypic instability seemed to be related to the immunological types of the lymphoma lines, possibly reflecting the differentiation process of the target cells involved in the malignant transformation.

Animals↗
PubMed1982

Suppression of tumorigenicity in interspecific reconstituted cells and cybrids.

The effect of cytoplasms on the expression of tumorigenicity was examined in interspecific reconstituted cells and cytoplasmic hybrids (cybrids) formed by fusions between karyoplasts (or intact cells) from highly tumorigenic mouse melanoma B16 cells and cytoplasts from non-tumorigenic, hypoxanthine-guanine phosphoribosyl-transferase (HGPRT)-deficient and chloramphenicol (CAP)-resistant rat myoblastic cells, L6TG X CAPr. The reconstituted clones and cybrid clones isolated in the double selection medium, HAT and CAP, acquired CAP-resistance, and each showed unique morphology and cellular arrangement. Tumorigenicity was suppressed in all the reconstituted clones and cybrid clones examined at an early stage after their isolation, but re-appeared in some clones after prolonged cultivation of the cells.

Animals↗
PubMed1981

Karyotypic changes in serial transfers of leukemic cells of AKR mouse.

Four spontaneous AKR leukemias (T67, T68, T70, and T74) with a modal chromosome number of 40 were transplanted serially to syngeneic mice in order to assess the significance of trisomy 15 and other karyotypic changes in the development of leukemia. In T67 and T70, the chromosomally normal cell disappeared completely or decreased considerably in frequency at the first passage in vivo. The karyotype of the modal cells changed continuously in T67 during transplantation, conserving trisomy 17, while the pseudodiploid cells with trisomy 15 and monosomy X were stable from the first to the seventh transplant generations of T70. In contrast to these results, the primary cell population of T68 and T74 with modal cells having a normal karyotype remained essentially unchanged throughout 7 or 15 transplant generations, despite the occurrence of aneuploidy, which included trisomy 15 or trisomy 17 in low frequencies. It is thus evident that the diploid cell is compatible with being leukemic and that neither trisomy 15 nor trisomy 17 is necessary for the initiation and progression of AKR leukemia, although the former was detected in three of four primary leukemias used for this experiment and in all four during transplantation.

Aneuploidy↗
PubMed1979

Chromosome markers in 12 inbred strains of the Norway rat, Rattus norvegicus.

Morphological details of metaphase chromosomes were compared among 12 inbred strains of rats (Rattus norvegicus) by means of conventional Giemsa staining and by a sequential Q- and C-banding method. Inter-strain variations were found in seven pairs, as identified on the basis of size differences in the short arms and/or satellites of chromosomes 3 and 12 and the X chromosome and in the centromeric C-bands of chromosomes 4, 5, 7, and 9. All pairs were homomorphic in the inbred strains, while F1 hybrids between two inbred strains showed certain heteromorphic pairs expected from the parents. These chromosome markers appear to be useful for characterization of inbred strains as well as for various genetic studies, including linkage analyses.

Animals↗
PubMed1978

Specificity of the deletion of chromosome No. 15 in mouse plasmacytoma: brief communication.

Q-banding studies in two independent hyperdiploid mouse plasmacytomas, 63-1 and the NP-38-ABCD subline of MSPC-1, revealed that deletion of a No. 15 chromosome was common. The deletion of No. 15 appeared to result from a translocation between No. 12 and 15 in the NP-38-ABCD, as in most plasmacytomas. In 63-1, however, No. 10 was probably a recipient chromosome of the missing segment from the deleted No. 15, and both chromosomes No. 12 remained intact. These karyotypic features suggest that the deleted No. 15 is a tumor-specific marker chromosome in mouse plasmacytoma and that an abnormality of No. 12 is not essential for development of the tumor. The constitution of chromosomes in the two plasmacytomas remained remarkably stable in their homogeneous modal population.

Animals↗
PubMed1977

Karyological characterization of a human lymphoblastoid cell line resistant to 6-thioguanine.

A mutant human lymphoblastoid cell line, Raji-TG, resistant to 10micron g 6-thioguanine (TG)/ml was produced from wild-type cells after exposure to ethylmethane sulfonate. The Raji-TG cells showed their failure to incorporate 3H-hypoxanthine, only 2% as much hypoxanthine guanine phosphoribosyl transferase (HPRT) activity as wild-type cells, and no revertant in HAT selective medium containing bypoxanthine, aminopterin, and thymidine. Raji-TG cells, which were maintained routinely in regular medium lacking TG for as long as 2 years, still retained resistance to the drug and inability to grow in HAT medium. A fusion of Raji-TG cells and mouse cells resistant to 5-bromodeoxyuridine and lacking thymidine kinase formed hybrids, and the resulting hybrid colonies proliferated in HAT medium. These observations strongly supported the hypothesis that Raji-TG line cells might be originated from a mutational event with deficiency of HPRT. Both parental and the mutant have a modal chromosome number of 49 with a remarkably stable karyotype. Excess chromosome materials are found in chromosomes 1, 5, 7, 14, and 16. Chromosome 8 is completely missing, but is represented by two respective isochromosomes of the short and long arms of No. 8. Five different marker chromosomes could be distinguished, and most of their origin has been determined. Isolation of Raji-TG X mouse hybrid clones which contained one of each marker chromosome is of considerable value in mapping human genes on regions within particular chromosomes.

Animals↗
PubMed1976

Confirmation of the human thymidine kinase locus, 17q21 leads to 17qter, by means of a man-mouse somatic cell hybrid, D98/AH-2 X LMTK-Cl-lD.

A large metacentric marker chromosome, m20, in a line of human D98/AH-2 cells was identified by Q bands as being a translocation (1;17)(p36;q21). This was confirmed by means of somatic cell hybridization between D98/AH-2 and thymidine kinase (TK) deficient mouse cells. The hybrid clones by HAT selective system retained m20, indicating the presence of TK locus on this chromosome. The results also provide evidence that TK gene is located on the distal region of the breakpoint in 17q21 but not on 17q21 leads to 17pter.

Animals↗
PubMed1976

Karyotypes of vasoformative sarcomas arising from BALB/3T3 cells attached to polycarbonate plates.

Four vasoformative sarcoma in vivo tumor lines arising from the s.c. implantation of 3 X 10(4) BALB/3T3 cells attached to a 1- X 5- X 10-mm polycarbonate platelet were shown to be quite similar in chromosome constitution to the parental 3T3 line. All tumors contained the same marker chromosomes that were present in the parent BALB/3T3 cells. The findings conclusively showed that the tumors had derived from BALB/3T3 cells and not from host cells or from the in vivo fusion of the inoculated 3T3 cells with host cells. Each tumor line had a unique karyotype that was markedly more homogeneous than that of the parental BALB/3T3 cells, strongly suggesting that each tumor represented a separate clone. An M1 marker chromosome was consistently present in each of the four tumor lines but was present in only about 50% of the parent BALB/3T3 cells; it therefore appeared to be a distinct and stable feature of the tumors.

Animals↗