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Endopolyploidy in irradiated p53‐deficient tumour cell lines: Persistence of cell division activity in giant cells expressing Aurora‐B kinase
It is described here that catalytically active Aurora‐B kinase is expressed in the nuclei of many endopolyploid cells in interphase, as well as being present at the centromeres, mitotic spindle and cleavage furrow during their attempted mitotes. Expand
[Genome multiplication mechanisms in the development of albumen gland polyploid cells of Succinea lauta (Gastropoda:Pulmonata). V. Polyploidizing mitosis and endomitosis].
Endomitosis can be defined as a real phase of the cell cycle and is in agreement with dynamics and speed of DNA and RNA synthesis during cell polyploidization and differentiation. Expand
Polyploid tumour cells elicit paradiploid progeny through depolyploidizing divisions and regulated autophagic degradation
‘neotic’ ETC resulting from genotoxically damaged p53 function‐deficient tumour cells develop through a heteronuclear system differentiating the polyploid genome into rejuvenated ‘viable’ subcells and subnuclei, which become degraded and eliminated by autophagy. Expand
The gametogenesis and sexual cycle of the bivalve Corbicula japonica Prime (1864) in the mouth of the Kievka River (Sea of Japan)
It was shown that the reproductive cycle in C. japonica is determined by the water temperature, that gametogenesis starts at the boundary between April and May, that spawning occurs from mid-July to mid-September, and that gonads are in a stage of relative sexual inactivity in the autumn and winter. Expand
Endopolyploidy as a morphogenetic factor of development
  • A. P. Anisimov
  • Biology, Medicine
  • Cell biology international
  • 1 December 2005
Endopolyploidy is an adaptive morphogenetic factor, but its concrete role may differ in different tissues and organisms depending on cell specialization and histogenetic particularities. Expand
Proliferation and growth of intestinal epithelium in Ascaris suum (Nematoda) during postnatal ontogeny. Communication III. Mitotic anomalies and changes in ploidy and nucleus size.
The previously established sixfold increase in the mean volume of intestinal cells during postnatal ontogeny of the ascarid is due to their transition to the new ploidy level and additional "paragenomic" growth of the polypoid cells. Expand
Tumor cell embryonality and the ploidy number 32n: Is it a developmental checkpoint?
It is interesting therefore that p53-deficient tumor cells also polyploidise by restitution cycles up to 32n and although the reversion of cycling 4n is dominating, 32n is the point from which they are still capable of reduction in ploidy “de-polyploidizing,” in contrast, more rare tumor cells of higher ploids are never seen reverting. Expand