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Biomedical subjects

B J McGee

Publications and source records attributed to B J McGee.

At least 19 recordsLinked to original sources

Extent and rate of chromosome segregation in two intraspecific mouse cell hybrids: A9 x diploid foetal erythrocyte and A9 x B82.

Patterns of chromosome segregation were studied in 2 different intraspecific mouse cell hybrids: (1) A9 x B82, formed by fusing 2 cell lines of heteroploid fibroblasts, and (2) UWE, originating from the fusion of A9 cells with euploid foetal erythrocytes. Detailed analyses of Giemsa (G)-banded chromosomes and chromosome arms of both parental and hybrid cells were made for each hybrid type, in order to determine the specificity of the losses and to assess the influence of ploidy and cell differentiation. Unlike the A9 x B82 hybrids, which revealed a significant chromosome loss under selective tissue culture pressures only after 9 months, the UWE hybrids showed a sharp reduction in the total chromosome number during the initial 2 months under similar pressures. However, with no additional cloning, UWE remained karyotypically stable after that time. This rapid chromosomal segregation in UWE hybrids may be caused by properties of the parental foetal erythrocytes. In UWE cells, the majority of the chromosome arms were retained or duplicated. Less than a quarter of the total number of chromosome arms were segregated or lost, and these were all chromosome arms with abnormal mouse G-banding patterns, present only in the heteroploid A9 parental cells. In two of the four A9 x B82 hybrid lines, there was marked segregation of chromosome arms whose banding patterns were identical to those of wild type mouse telocentric chromosomes. For both types of intraspecific cell hybrids, two thirds or more of the chromosome arms had banding patterns which were the same as those of the wild type genome.

Animals↗

Karyotypic analyses of parental and hybrid intraspecific mouse cells, A9/B82, by giemsa- and centromeric-banding.

Hybrids between A9 (HGPRT-) and B82 (TK-), mouse heteroploid fibroblast lines, were obtained through continuous cultivation and clonal selection; such hybrids showed marked segregation and by conventional stains displayed chromosome numbers and distribution similar to that of either parental type. Detailed analyses by Giemsa (G)- and centromeric-banding of these parental lines, and of 4 of the reduced hybrids, maintained in culture for up to 5 years, revealed the following points: (1) The distribution of the majority of individual chromosomal classes was similar for 3 of the hybrid cell lines. (2) Over two-thirds of the chromosomal arms in both the parental lines and hybrid lines were identical to normal mouse telocentric chromosomes. (3) For 2 of the hybrid lines, segregation was particularly marked with respect to those chromosomal arms whose G-banding patterns were identical to the wild-type genome; this indicated that segregation had occurred at the expense of redundant chromosomal material introduced by cell fusion. These banded studies demonstrated that segregation chiefly accounted for the sharp reduction in chromosome numbers while recombination accounted for the chromosome heterogeneity of the hybrid cells as compared to the parental genomes.

Animals↗

Transformation of mouse cells by fusion with chronic granulocytic leukemia cells: possible role of human chromosome.

In vitro properties of somatic cell hybrids between non-malignant B82 mouse fibroblasts and human chronic granulocytic leukemia spleen cells include lack of cell density-dependent growth inhibition and growth in soft agar. These phenotypic expressions of cell transformation appear linked to the retention by the cells of chromosome 7 from the human leukemic genome.

Animals↗

Chromosome 11 long arm partial deletion: a new syndrome.

Deletion of the distal end of the long arm of a chromosome 11 (11q-) was demonstrated by G-bands in a malformed 4.3-year-old girl. Comparison of her phenotype with those of the four previously reported cases of 11q-, three with a proven and one a presumed similar deletion, suggests that this defect results in a clinical picture most noticeable for the association of variable mental retardation, marked speech deficit, trigonocephaly, and pronounced growth failure.

Abnormalities, Multiple↗

Chromosome band analysis in 19 cases of chronic myeloid leukemia: 9 chronic, 10 blastic, two with Ph1 (22q-) translocation on 17 short arm.

The results of Giemsa band analyses of the marrow cells of 19 cases of CML in the chronic or blast phase are reported. All but one of the 14 Ph1 positive cases showed the 9q+pattern, the exceptional one being 16p+. All 10 blast cases showed additional rearrangements, which are described. In two of the cases, one blastic, one chronic, which were -22, Ph1 negative, the 22q- member was identified as a translocation on the short arm of one 17 which was dicentric.

Chromosome Aberrations↗

Trisomy 8 Syndrome.

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Abnormalities, Multiple↗

17 long arm isochromosome. A common anomaly in malignat blood disorders.

A cytogenetic anomaly consisting in the replacement of a 17 by its long arm isochromosome was identified as the only alteration in the marrow cells of two patients with acute granulocytic leukemia. In one case, the specific nature of the abnormal chromosome was established by newly available techniques. Since its identification in 1965, this structural anomaly, which implies 17 long arm duplication and short arm deletion, has been observed, as a sole or as an associated finding, in the malignant cells of a spectrum of blood disorders, including acute granulocytic leukemias, the blast crisis of chronic myeloid leukemia and lymphoreticular proliferative disorders. Attention is called to this particular rearrangement for its clinical as well as fundamental implications, as its presence in blood forming cells unfailingly hearalds a fast, fatal course of evolution.

Aged↗

XYY and crime.

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Adult↗