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The embryo in recurrent implantation failure
Published in Efstratios M. Kolibianakis, Christos A. Venetis, Recurrent Implantation Failure, 2019
Molecular cytogenetic analysis in embryos from patients with oligoasthenoteratozoospermia (OAT) and RIF that show slow or arrested development in vitro often reveal patterns of polyploidy and postzygotic malsegregation of chromosomes that could be explained by abnormal centrosomal distribution, following cytokinetic failure and defective spindles.11 Delayed division of blastomeres can theoretically result in tetraploidy, either through formation of an abnormal monopolar spindle or failure of both karyokinesis and cytokinesis. The tetraploid blastomere produced by failure of karyokinesis and cytokinesis has two centrosomes that, when duplicated, would produce four. If there is unequal allocation of these centrosomes on the spindle poles, for example, 3:1, then it is possible that unequal numbers of spindle fibers will be present and one-sided divisions will ensue, as most of the chromosomes will be attached and move toward the spindle pole with the greatest number of centrosomes.11 The presence of four centrosomes in an unbalanced arrangement (3:1), three distinct foci at one pole of a spindle and one at the other pole, has been previously reported by Chatzimeletiou et al.9 following cytoskeletal analysis of human preimplantation embryos, but can also occur via mechanisms of centrosome splitting in the presence of impaired DNA integrity and replication.26
Cell division
Published in Frank J. Dye, Human Life Before Birth, 2019
Two types of cell division occur in humans: mitotic cell division and meiotic cell division. Mitosis (or karyokinesis) refers specifically to division of the cell nucleus. Meiosis refers to two consecutive nuclear divisions. In addition, these two types of cell division are fundamentally different in their effect on chromosome number. Mitosis is conservative in that the two resulting daughter cells each have the same number of chromosomes as in the original (mother) cell. Meiosis results in four daughter cells, with each having half the number of chromosomes as in the mother cell. The term cytokinesis is reserved for division of the cytoplasm of the cell.
Cell Biology
Published in C.S. Sureka, C. Armpilia, Radiation Biology for Medical Physicists, 2017
Then, the active cells enter into the last and most important phase of the cell cycle, that is, the M phase. The M phase starts with the nuclear division, corresponding to the separation of daughter chromosomes (termed as karyokinesis) and usually ends with the division of cytoplasm (cytokinesis), in turn forming two separate cells. Depending upon the type of cell, it undergoes either mitotic or meiotic cell division. For examples, somatic cells undergo mitotic cell division but germ cells undergo meiotic cell division.
Therapeutic effects of ephrin B receptor 2 inhibitors screened by molecular docking on cutaneous squamous cell carcinoma
Published in Journal of Dermatological Treatment, 2022
In pathological section of H&E staining, xenograft tumor tissues in the blank control and DMSO groups, tumor cells were aggregated into groups, arranged closely, and pleomorphic, their nuclei were large and deep, with rich cytoplasm and karyokinesis. In tumor sections from the AE and KM groups, the density of tumor cell was decreased, and the cells were disordered and showed apoptosis, the nuclei were condensed or disappeared, and the cytoplasm was concentrated, with degeneration and necrosis evident. In the field of view, homogenization and red staining were observed, suggesting tumor tissue necrosis and inflammatory cell infiltration after treated with AE and KM (Figure 3(C)). In the blank control and DMSO groups, cardiomyocytes and kidney, lung, liver, and spleen tissues were intact in structure and exhibited a normal morphology, the cells were arranged neatly, and the cytoplasm, nuclei, and nucleoli were intact, without distinct changes in morphology. There were no obvious pathological changes in heart, liver, spleen, and lung tissues after AE and KM treatment.
Beneficial and Deleterious Impact of a Nutritional Supplementation for Inhibition of Proliferation of Neuroblastoma in Culture
Published in Nutrition and Cancer, 2019
Brittany Theochares, Rishel Vohnoutka, Edward Boumil, Thomas B. Shea
CucE altered the morphology and inhibited proliferation of neuroblastoma cells in a manner similar to that observed for prostate carcinoma cells (22). Observation of abnormal numbers of nuclei within relatively larger cells is consistent with the possibility that cells entered but could not complete the mitotic phase. In this regard, multiple studies indicate that CucE and other cucurbitacins perturb actin dynamics (15,23–28). One interpretation of our findings is that perturbation of actin dynamics by CucE may have inhibited cytokinesis but not karyokinesis in our neuroblastoma cultures and therefore generated multinucleate cells by so-called “mitotic slippage” (29). Perturbations in the mitotic cycle may also have generated the so-called “monster” cells. The prognostic significance of monster cells in these and in prior studies remains unclear (20,21). Monster cells may represent paraptotic cells (30,31). Interestingly, paraptosis and paraptosis-like cell death have been observed in neurodegeneration, as well as in cancer cells after treatment with natural products or synthetic agents (30).
An overview of potential novel mechanisms of action underlying Tumor Treating Fields-induced cancer cell death and their clinical implications
Published in International Journal of Radiation Biology, 2021
Narasimha Kumar Karanam, Michael D. Story
TTFields are approved for the treatment of GBM and MPM but the fundamental mechanism of TTFields biological action is not known. One could speculate that because of the effect on tubulin due to the dipole moment generated by TTFields on mitotic cells, that the predominantly interphase effects described above could also be generated by altering the properties of key proteins based upon their charge or polarity. This might actually provide for changes in the activity of any number of proteins whose subsequent cascades of signaling are also altered leading to radiation or chemotherapy agent vulnerability and enhanced cell killing. Our current understanding of TTFields’ mechanisms of action suggests that TTFields affect multiple pathways such as cell cycle, karyokinesis, the DNA damage response, DNA replication, and immune response, the identification of which are nearly all from in vitro experiments with little in vivo validation (Figure 3). Moreover, as a physical modality, as described above, TTFields may be comparable toionizing radiation in that they both induce more systemic effects that might render cancer cells more sensitive to different classes of drugs in combination therapy. TTFields’ limited efficacy as a monotherapy in the clinic should be noted in this context (Stupp et al. 2012), however because of the vulnerabilities generated by TTFields exposure, with minimal adverse effects on normal cells or tissues, the potential for the use of TTFields as a neoadjuvant therapy is of paramount importance. Already, ‘concommitant’ application has revealed vulnerabilities that rationally explain the outcomes seen in combination therapies that can likely be enhanced if TTFields were used in advance and during radiation or chemotherapy treatments.