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At least 235 records · Page 13Linked to original sources
PubMed1995

An improved method of mouse liver micronucleus analysis: an application to age-related genetic alteration and polyploidy study.

The performance of a micronucleus test in liver cells in vivo requires two laborious procedures: stimulation of hepatocytes to division and dissociation of liver tissue into a single-cell suspension. We propose the method of inhalation treatment of mice with carbon tetrachloride to induce cell proliferation and alkaline dissociation of previously fixed tissue. The micronucleus incidence and ploidy classes in terms of cytophotometric DNA content were determined in liver of mice of three age groups (around 2.5, 5.0 and 7.0 months old) after CCl4 treatment or partial hepatectomy. The data obtained show that both methods give the same results. The fraction of micronucleated hepatocytes was 0.69% at the age of 2.5 months; it increased to 8.5% and then to 13.5% at 5.0 and 7.0 months respectively. Simultaneously, the ploidy classes changed both with the aging of the animal and after induced liver regeneration. The percentage distribution of micronucleated cells by ploidy class showed that cells carrying micronuclei were the higher ploidies rather than the population in general. Since polyploid cells contain multiple molecular targets for genetic damage, the micronucleation index per genome unit was estimated. Then the real rate of accumulation of both intrinsic endogenous (and probably the exogenously induced) preclastogenic genetic alterations in hepatocytes during the adulthood of mice was evaluated to be 0.03% per diploid genome per day. This seems to be the first description of the phenomenon of liver cell aging in terms of micronuclear aberrations.

Administration, Inhalation↗
PubMed1986

Chromosomal changes in a documented case of malignant histiocytosis: significance of polyploidy.

A case of malignant histiocytosis was studied by cytology, cytochemistry, electron microscopy, and cytogenetics. It was shown that the malignant cells expressed a fully differentiated histiocytic pattern with high macrophagic activity. This correlated with the presence of polyploid metaphases. The significance of polyploid cells in the definition of malignant histiocytosis is discussed.

Aged↗
PubMed1996

Induction of polyploidy in adenovirus E1-transformed cells by the mitotic inhibitor colcemid.

Adenovirus-transformed cells were tested for their ability to synthesize DNA in the presence of cell cycle inhibitory drugs. We show that transformed cells are completely resistant to the mitotic inhibitor colcemid, partly resistant to lovastatin, mimosine, aphidicolin and genistein but not to hydroxyurea or thymidine. When treated with colcemid, AdE1-transformed cells continue to synthesize DNA but do not divide and, therefore, become highly polyploid. This effect is dependent on the presence of both E1A and E1B.

Adenovirus E1 Proteins↗
PubMed1990

Flow cytometric studies of the survival of cytochalasin-induced polyploidy in Chinese hamster ovary cells.

A method has been developed to estimate the post-irradiation survival of cytochalasin B-induced polyploidization of adherent Chinese hamster ovary cell using the flow cytometer. After exposure to radiation, surviving cells are allowed to become polyploid in the presence of cytochalasin, and are detached using trypsin, fixed by the addition of glutaraldehyde and stained using mithramycin. DNA content distributions are polymodal, and the absolute number of cells per culture in any given ploidy class is estimated by reference to a non-fluorescent bead internal standard, detected using forward scatter. Post-irradiation survival is defined as the ability to reach a given DNA content, and is reduced exponentially with dose. A bioassay to determine optimum cytochalasin concentrations can be derived from the relative size of the 2C (G0/G1) peak in the DNA content distribution. At culture densities greater than about 8 x 10(4) cell/cm2 the relative number of cells reaching at least 16C is reduced, but this inhibition is partially reversible by an increase in the medium glucose concentration, but not by the use of cytochalasin D or dihydro B.

Animals↗
PubMed2025

Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.

Polyploid Giant Cancer Cells (PGCCs) occur across multiple cancer types and are associated with therapy resistance, genome instability, disease progression, and metastasis. PGCCs can grow through endocycles, a variant cell cycle of alternating Growth (G) and DNA Synthesis (S) phases without cell division. Unlike programmed endocycles that occur during normal tissue development, PGCCs switch from mitotic cycles to unscheduled endocycles in response to stress. PGCCs can subsequently return to error-prone divisions which generate aneuploid daughter cells that contribute to disease progression. However, the regulation of PGCC cell cycles and contributions to cancer are still being defined. Filling this knowledge gap will lead to the development of improved cancer therapies. In this study, we used a molecular-genetic system in the model organism Drosophila melanogaster to examine how oncogenes interact with unscheduled endocycles in vivo. We found that several oncogenes promote bypass of an endocycle arrest, resulting in increased polyploid cell size and DNA content. The extent of this increased growth was dependent on the type of oncogenic mutation. When these polyploid cells returned to division, RasG12V promoted continued divisions of polyploid daughter cells with elevated genome instability. RasG12V expression during transient endocycles and subsequent divisions also induced expression of a matrix metalloprotease and a Wnt pathway ligand. Importantly, RasG12V with transient endocycles enhanced the growth of large, neoplastic tumors. These findings indicate that oncogenic mutations can synergize with transient, unscheduled endocycles to promote tumorigenesis with important broader implications for cancer prognosis and therapies.

Animals↗
PubMed1998

Age-associated mosaicism and polyploidy in Down's syndrome.

Age-related increases in the frequencies of cells with chromosome 21 loss and of polyploid cells were documented in short-term peripheral blood lymphocyte cultures from 54 patients with Down's syndrome (DS), ages 0 to 48 years. The polyploid data, together with previous work from this laboratory with non-DS subjects, suggest that this may be a useful indicator of aging in lymphocytes.

Adolescent↗
PubMedDate not supplied

The initiation and control of trophoblastic growth in the mouse: binucleation and polyploidy.

Initially diploid, pure trophectodermal derivatives were dissociated and grown in culture. Over the 72-hour time course in vitro, uninucleate, binucleate and a small number of multinucleate cells appeared. Moreover, the pattern of binucleation found in these trophoblast cultures resembled that seen during the development of the mouse liver. Thus, the binucleates displayed a progressive increase in nuclear DNA content and the increased DNA values ranged from 2c to 32c. Furthermore, the proportion of uninucleate and binucleate cells changed systematically with growth in vitro and the final binucleate cell population became, on average, 10 to 15 per cent of the total. These results, together with those of other studies, suggest that mouse trophoblast can initially become giant through a binucleate phase.

Animals↗
PubMed2003

Vanadate, an inhibitor of tyrosine phosphatases, induced premature anaphase in oocytes and aneuploidy and polyploidy in mouse bone marrow cells.

Protein tyrosine phosphatases are needed for activating maturation promoting factor, meiotic spindle assembly and spindle checkpoint inactivation. The protein phosphatase inhibitor vanadate was used to upset the kinase-phosphatase equilibrium during oocyte maturation (OM) and the metaphase anaphase transition (MAT) prior to cytogenetic analyses of mouse oocytes and bone marrow cells. ICR females received pregnant mare serum gonadotrophin (PMSG) and 48h later received human chorionic gonadotrophin (hCG). Vanadate doses of 0, 5, 15, and 25mg/kg were administered intraperitoneally immediately after hCG and ovulated oocytes and bone marrow cells were processed for cytogenetic analyses 18h after hCG. Data were analyzed by Chi-square and Fisher's exact tests. Vanadate induced different cytogenetic abnormalities in oocytes and in bone marrow cells. The frequencies of oocytes exhibiting premature anaphase (spontaneous activation) in vanadate exposed mice were significantly (P<0.01) elevated over controls; whereas, in bone marrow cells, the levels of tetraploidy, hyperploidy and premature centromere separation were significantly (P<0.01) increased by vanadate treatment. These results suggest that alteration of the kinase-phosphatase equilibrium during OM and the MAT leads to cytogenetic abnormalities that differ between oocytes and bone marrow cells.

Anaphase↗