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Mosaicism in Preimplantation Embryos
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Maurizio Poli, Antonio Capalbo
Defective mitotic events appear to be mainly caused by faulty cell cycle control, centrosome and mitotic spindle functional deficiency, and inefficiency in the chromosome cohesion apparatus (9). Although ovarian stimulation regimens were also suggested to impact the incidence of mitotic errors (10), this hypothesis has yet to be validated through more comprehensive, sensitive, and up-to-date technologies and properly designed studies.
Antitubulin Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Microtubules are polymers of tubulin that are integral components of the mitotic spindle and are involved in microtubule assembly (through polymerization) and disassembly (through depolymerization), processes that are in dynamic equilibrium. The Vinca alkaloids and eribulin work by interfering with microtubule assembly, whereas the taxanes and epothilones exert their effect by stabilizing microtubules (Figure 4.1). Recently discovered experimental agents with related mechanisms of action are described in Section 4.6.
Mosaicism Mechanisms in Preimplantation Embryos
Published in Darren K. Griffin, Gary L. Harton, Preimplantation Genetic Testing, 2020
Maurizio Poli, Antonio Capalbo
Causative factors for defective mitotic events include relaxed control of the cell cycle, aberrations of the centrosome and mitotic spindle, and defects in chromosome cohesion [6]. In addition, it has been suggested that ovarian stimulation regimens and IVF culture conditions may also promote the occurrence of mitotic errors [10]. However, these results were generated using fluorescent in situ hybridization (FISH), and more comprehensive, sensitive, and up-to-date technologies, in carefully designed studies, would be required to validate these findings.
MOS mutation causes female infertility with large polar body oocytes
Published in Gynecological Endocrinology, 2022
Guangzhong Jiao, Huayu Lian, Jinhao Xing, Lili Chen, Zhaoli Du, Xiaoyan Liu
Proper oocyte maturation is essential for subsequent fertilization and early embryonic development, which is necessary for successful reproduction [1]. We can evaluate the morphology of human oocytes with the help of assisted reproductive technology [2]. Maturation of oocytes requires two meiosis. During meiosis, bipolar meiotic spindles form and homologous chromosomes are arranged through microtubule-organizing centers (MTOCs) [3–5]. After the spindle is assembled, with the extrusion of the first polar body, the oocyte extrudes half of its genetic material and then goes directly into the metaphase II (MII); the oocyte arrests at MII until fertilization [6, 7]. Unlike the symmetric cell division that occurs in mitosis, mammalian oocyte meiosis is characterized by asymmetric division, producing a highly polarized and large metaphase II-arrested oocyte and a small polar body [8]. The failure of asymmetric oocyte division results in the production of large polar bodies in oocytes, usually due to low oocyte quality or aging after ovulation [9]. In mice, some studies have identified abnormal gene expression leading to a meiotic spindle dysfunction phenotype; however, the genetic etiology of human oocytes remains largely unknown.
Complete Hydatidiform Mole and Co-Existing Live Fetus after Intracytoplasmic Sperm Injection: A Case Report and Literature Review
Published in Fetal and Pediatric Pathology, 2021
Verda Alpay, Didem Kaymak, Hakan Erenel, Ismail Cepni, Riza Madazli
Complete mole occurs after fertilization of an enucleated egg by two spermatozoa or a haploid spermatozoon that than duplicates [1]. During ICSI procedure one sperm cell is injected to the ovum, so fertilization of an enucleated egg by two sperm cells is excluded. The induced superovulation may be one of the causes of an enucleated egg during ICSI [7]. Other explanations of the loss of maternal chromosomal material may be the disruption of the meiotic spindle because of oocyte handling or due to fragmentation or degeneration of the oocyte [7, 20]. Hamanoue et al. [14] reported that two pronuclei and two polar bodies were confirmed in the pretransferred embryos during ICSI procedure. We have also observed two pronuclei and two polar bodies in the embryos before transfer demonstrating proper fertilization has occurred. Therefore, observation of pronuclear and embryonic development under stereomicroscopy does not exclude the complete hydatidiform mole. It is impossible to identify molar gestation by microscopic examination of the pretransferred embryo in ART procedures [7].
Targeted drug therapy in non-small cell lung cancer: Clinical significance and possible solutions-Part I
Published in Expert Opinion on Drug Delivery, 2021
Archana Upadhya, Khushwant S. Yadav, Ambikanandan Misra
The taxanes (paclitaxel and docetaxel) inhibit depolymerization of microtubules thus changing microtubule dynamics and eventually causing cell death by blocking cellular mitosis [115]. The factors for resistance to taxane-based therapy are increased expression of class III tubulin [116] and its mutations, up-regulation of histone deacetylase 6 (HDAC 6) and impairment of the mitotic spindle checkpoint [111]. The function of the mitotic spindle checkpoint is to block the segregation of abnormal chromosomes. In lung cancer cells, the mitotic spindle checkpoint is dysregulated [79,111]. The taxanes bind specifically to class I β tubulin isoform which differs in critical binding residues from the class III β isoform [117]. Class III β – tubulin is one of the β isoforms that heterodimerize with α subunits to form microtubules essential for cell division [117] and its high expression correlates with poor survival in NSCLC [118]. Histone acetylation and deacetylation regulate transcription of DNA segments. Histone acetylases (HATs) promote transcription while histone deacetylases (HDACs) inhibit transcription by making DNA inaccessible. Histone deacetylase six interacts with histone and non-histone substrates. Non – histone interactors are α-tubulin, contractin and heat shock protein 90 (Hsp90) which when modified by HDAC6 can promote cell proliferation, metastasis, invasion, and mitosis [119].