Human Chromosomes

Therman, Eeva; Susman, Millard

doi:10.1007/978-1-4684-0529-3

Cited by 69 publications

(32 citation statements)

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“…60,61 MNCs are relatively common in changed cell growth of neoplasia as compared to absence in normal cell growth except in senescence. 30,[62][63][64] The escape of karyoplasts from such MNCs with production of mitotic offspring cells is not a novel process. [65][66][67] But, when cell-produced proteases was inhibited, tumors/malignant cells did not develop.…”

Section: Endopolyploidy and Tumorigenesismentioning

confidence: 99%

“…Presently, pictorial examples are an only way of counter-acting point (2) especially, for recognition of endopolyploidy in cancer cells which often have over-contracted chromosomes. 30 Other relevant observations to the present study are: (1) association between senescence and heterochromatization (h-chromatization) of telomeres, centromeres and interstitial chromosomal regions 6,31 which causes clumping of chromosomes from chromatin-stickiness with consequent mal-segregations and breakage in mitosis, 16,30 (2) polyploidy and multinucleation are features of senescent flat cells 28,[32][33][34] and (3) karyoplasts budded-off from surfaces of multinucleated cells (MNCs) and formed small cells with/without mitotic activity. [35][36][37] This latter phenomenon of nuclear budding-offs surrounded by a complete cell membrane, is a constitutive process in human red-blood cell maturation.…”

Section: Introductionmentioning

confidence: 99%

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Genetic stability of senescence reverted cells: Genome reduction division of polyploidy cells, aneuploidy and neoplasia

Walen

2008

Cell Cycle

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Cell senescence from exhausted cell expansions to cells with short, dysfunctional telomeres is considered to be a non-replicative, irreversible state with possibility in tumor therapy. This leads to questions of senescence-stability which in genomic-probe, manipulated senescent flat cells resulted in reversions to mitotic cells. Additionally, rarer mitoses were present spontaneously in months, old, live flat cell cultures. These latter senescence-escaped cells were analyzed by cytogenetics to determine their origin from either stable G 0 /G 1 diploid and/or from unstable endopolyploid cells. Endo-polyploidization in senescence is associated with re-replication of genomically damaged G 2 /M cells. One source for genomic damage is senescence-specific occurrence of heterochromatization. It causes gluing of chromosomes together with consequent malsegregations in mitosis which was a feature of the present reverted cells. In addition endo-polyploidy cycled with the characteristic presence of diplochromosomes (i.e., pairs of sister chromosomes) undergoing two consecutive bipolar divisions into genome reduced cells. Both diploid and tetraploid, aneuploid cells were also present as reverted cells. For in vitro cell senescence reversion to mitotic cells is therefore, concluded to be associated with occurrence of genomic instability. These results are discussed with reference to a meiotic-like somatic cell division of cycling endopolyploidy and as a possible mechanism of aneuploidization in tumor development. The extracellular matrix is evaluated in regard to a role as a protective shield against nuclear budding-offs (karyoplasts) from the flat cells to form mitotically-capable reverted cells.

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Section: Endopolyploidy and Tumorigenesismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genetic stability of senescence reverted cells: Genome reduction division of polyploidy cells, aneuploidy and neoplasia

Walen

2008

Cell Cycle

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“…Autosomal trisomy in humans is known of the 13th, 18th, and 21st chromosomes. Individuals with trisomy of these chromosomes can be born, although they will experience developmental disorders, whereas trisomy of the other chromosomes causes fetal miscarriage or death (Therman and Susman, 1993). This may be because the number of genes on these additional chromosomes from viable trisomes is smaller than that of the other chromosomes, and thus gene expression in these trisomy individuals is not so severely disturbed as to prevent birth.…”

Section: Introductionmentioning

confidence: 99%

Gene Expression and Distribution of Swi6 in Partial Aneuploids of the Fission Yeast Schizosaccharomyces pombe

Chikashige

Tsutsumi

Okamasa

et al. 2007

Cell Struct. Funct.

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ABSTRACT. Imbalances of gene expression in aneuploids, which contain an abnormal number of chromosomes, cause a variety of growth and developmental defects. Aneuploid cells of the fission yeast Schizosaccharomyces pombe are inviable, or very unstable, during mitotic growth. However, S. pombe haploid cells bearing minichromosomes derived from the chromosome 3 can grow stably as a partial aneuploid. To address biological consequences of aneuploidy, we examined the gene expression profiles of partial aneuploid strains using DNA microarray analysis. The expression of genes in disomic or trisomic cells was found to increase approximately in proportion to their copy number. We also found that some genes in the monosomic regions of partial aneuploid strains increased their expression level despite there being no change in copy number. This change in gene expression can be attributed to increased expression of the genes in the disomic or trisomic regions. However, even in an aneuploid strain that bears a minichromosome containing no protein coding genes, genes located within about 50 kb of the telomere showed similar increases in expression, indicating that these changes are not a secondary effect of the increased gene dosage. Examining the distribution of the heterochromoatin protein Swi6 using DNA microarray analysis, we found that binding of Swi6 within ~50 kb from the telomere occurred less in partial aneuploid strains compared to euploid strains. These results suggest that additional chromosomes in aneuploids could lead to imbalances in gene expression through changes in distribution of heterochromatin as well as in gene dosage.

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“…The advent of various banding techniques on chromosomes led to further extensive and very reliable identification of loci and chromosomal segments being translocated to other chromosomes. The chromosomal aberrations (deletions, duplications, translocations inversions and heteroploidy: aneuploidy and polyploidy) were identified and when in higher frequency were tagged to be associated with neoplastic transformations [4][5][6][7][8][9]. Some additional aberrations like acrocentric associations sometimes leading to Robertsonian translocations, premature centromeric divisions (PCD) were added by various research workers to be associated with some or the other disease including malignancy.…”

Section: Introductionmentioning

confidence: 99%

Gross Chromosomal Aberrations are Early Alarms for Malignancy: A Re-Emphasis

Goswami¹

2017

Hereditary Genet

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A few chromatin dots of variable sizes were encountered in squashes of brain tumour tissues viz. medulloblastoma, ependymoma and tuberculoma along with hyper and hypoploid chromosome counts way back in 1973. Similar chromosomal features were again observed in metaphases of persons exposed to methylisocyanate gas in Bhopal during midnight of 2nd to 3rd December, 1984. Follow-up studies continued during 1984-1999 and comparative assessments on chromosomal damages were attempted by SCE (sister chromatid exchanges) as well as by scoring more than a dozen types of chromosomal aberrations on 678 individuals by C and G-banding and Feulgen's and Aceto-orcein staining procedures on cultured-lymphocytes, details of which, have been published earlier. This short paper reemphasizes the importance of certain chromatin dots (named as Marker dots) which were seen emanating from chromosomes. These marker dots appeared reliable early indicators of neoplastic transformations. During follow-up studies on various malignancies we had recorded presence of these marker dots in almost all of them. This computation of slides involved careful scrutiny of more than 40,000 metaphases from patients of various malignancies, pathological disorders and newly discovered chromosome syndromes (e.g. Crossed Renal Ectopia with pelvic lipomatosis; Hemihypertrophy with melanosis of Ito, etc.). Intriguingly, only selective chromosomes are involved (chromosomes 1, 2, 3, 5, 6, 8, 9, 11, 12, 13, 16, 17 and Y) in emanating marker dots. Obviously, it appears that the molecular attenuation of chromatin structures movable from chromosomes is related with triggering neoplastic transformations. Specific attention was paid on appearance of "marker dots" which were observed in seemingly normal persons but later, after a gap of 2 to 6 years, some of them exhibited signs of malignancy. Such observations were possible only on those persons who could be re investigated after a gap of 2 or 3 years. Gross chromosomal aberrations such as PCD (premature centromeric divisions) acrocentric associations, hyperploid cells, translocations and deletions with marker dots appear to be precursors to firm installation of chromosomal mutagenesis in cultured lymphocytes. Obviously, search for marker dots and these aberrations in metaphases of person(s) belonging to a cancer-patient family can be of vital importance to warn for early diagnosis and prognostic approach. Marker dots simply "alarm" to inform firm installation of chromosomal mutagenesis which encompasses various chromosomal aberrations. In turn, due to many other intragenic factors, cells are transformed to malignant cells in certain individuals.

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Human Chromosomes

Cited by 69 publications

References 0 publications

Genetic stability of senescence reverted cells: Genome reduction division of polyploidy cells, aneuploidy and neoplasia

Genetic stability of senescence reverted cells: Genome reduction division of polyploidy cells, aneuploidy and neoplasia

Gene Expression and Distribution of Swi6 in Partial Aneuploids of the Fission Yeast Schizosaccharomyces pombe

Gross Chromosomal Aberrations are Early Alarms for Malignancy: A Re-Emphasis

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