Mitosis is a process of cellular division. What happens though when Mitosis (process of cellular division) goes wrong? You can get a disease from Mitosis going wrong, some very bad ones too. A widely known disease caused by cellular division going wrong is Cancer and Tumors.
(1)Disrupted passage through mitosis often leads to chromosome missegregation and the production of aneuploidy progeny. Aneuploidy has long been seen as a frequent characteristic of cancer cells. Also Aneuploidy has been seen as a frequent characteristic of tumorigenesis.
Mitotic spindle assembly are drugs that are frequently used to treat various types of human tumors. These lead to chronic mitotic arrest if they are sustained from the activation of mitotic checkpoint. 100 years ago a man named, Theodore Boveri, was studying sea urchin embryos that contained aberrant numbers of spindle poles. …show more content…
He discovered that the progeny produced contained abnormal numbers of chromosomes. That condition was known as aneuploidy. In that time aneuploidy was already known to be a common characteristic of tumors. Boveri having discovered this proposed that aneuploidy progeny produced from a disrupted mitosis became the progenitor cells of tumors. However the original hypothesis remains untested so it is assumed that there is a link between mitosis, aneuploidy, and cancer.
(2)Although mitosis has potential to cause tumorigenesis, mitosis has served as a successful antitumor target. Drugs that arrest cells in mitosis, they are known as antimitotic, have become the common treatment for various kinds of human tumors. An Antimitotic can be used to treat breast cancer, ovarian cancer, and also non-small-cell lung cancer. (3)However the mechanism that would link long-term mitotic arrest to cell death has remained completely and utterly unexplored. Some of the first evidence of a clinically relevant linkage between mitotic arrest, the mitotic checkpoint whose action is responsible for that arrest, and cell death are written in various papers. One such paper is the Tao and colleagues paper. (4)Mitotic checkpoint inactivation is a lethal thing. A weakened checkpoint always generates chromosomal instability. For a long time is has been recognized that missegregation of large numbers of chromosomes results in rapid cell death. It is self-evident that a minimum number of genes and/or chromosomes must be required for viability. Cells, this includes human cancer cells that exhibit chromosomal instability, in which the mitotic is completely inactivated by siRNA (small interfering RNA). (5)Tumors are associated with having a weakened mitotic checkpoint. A frequent occurrence in human tumor and cell lines is the inability to sustain mitotic check point signaling. It is judged by a reduced mitotic after long-term drug-mediated spindle disruption. The message gathered from this is that many tumors and tumor cell lines, including the ones that are chromosomally unstable, have a weakened checkpoint signal that is sufficient for maintaining a viable population of cells. Yet also allowing them to missegregate small numbers of chromosomes per division. This then results in aneuploidy and also chromosomal instability. Chronic activation of the mitotic checkpoint is a common chemotherapeutic strategy. Now that you know a little about how mitosis is connected to diseases mainly cancer and tumors in this paper we are going to hear about how meiosis is connected to pharmaceuticals or drugs. (1)Meiosis is a type of cell divison that reduces the number of chromosomes in the parent cell by half thus producing then four gamete cells. This process is essential to produce egg and sperm cells for a process called sexual reproduction. But what happens when a drug might try and interfere with meiosis and try to break it up? Will meiosis be affected in a positive way or a negative way? Will meiosis be affected at all? Lets find out shall we. (2)Drugs like chlorpromazine, fluphenazine, trifluoperazine, procaine, dibucaine, theophylline, propranolol, vinblastine, vincristine, and W7 have all been shown to prevent formation of the ternary activated complex calmodulin. Several soluble or membrane proteins, inhibit meiosis reinitiation in starfish oocytes when applied from outside. Inhibition occurs only if drugs are present in the medium during the hormone dependent period. Inhibition can be overcome by raising external concentration of 1-MeAde. (3)In contrast, direct intracellular microinjection of these drugs, even at concentrations far exceeding I50 for external application. To
(1)Disrupted passage through mitosis often leads to chromosome missegregation and the production of aneuploidy progeny. Aneuploidy has long been seen as a frequent characteristic of cancer cells. Also Aneuploidy has been seen as a frequent characteristic of tumorigenesis.
Mitotic spindle assembly are drugs that are frequently used to treat various types of human tumors. These lead to chronic mitotic arrest if they are sustained from the activation of mitotic checkpoint. 100 years ago a man named, Theodore Boveri, was studying sea urchin embryos that contained aberrant numbers of spindle poles. …show more content…
He discovered that the progeny produced contained abnormal numbers of chromosomes. That condition was known as aneuploidy. In that time aneuploidy was already known to be a common characteristic of tumors. Boveri having discovered this proposed that aneuploidy progeny produced from a disrupted mitosis became the progenitor cells of tumors. However the original hypothesis remains untested so it is assumed that there is a link between mitosis, aneuploidy, and cancer.
(2)Although mitosis has potential to cause tumorigenesis, mitosis has served as a successful antitumor target. Drugs that arrest cells in mitosis, they are known as antimitotic, have become the common treatment for various kinds of human tumors. An Antimitotic can be used to treat breast cancer, ovarian cancer, and also non-small-cell lung cancer. (3)However the mechanism that would link long-term mitotic arrest to cell death has remained completely and utterly unexplored. Some of the first evidence of a clinically relevant linkage between mitotic arrest, the mitotic checkpoint whose action is responsible for that arrest, and cell death are written in various papers. One such paper is the Tao and colleagues paper. (4)Mitotic checkpoint inactivation is a lethal thing. A weakened checkpoint always generates chromosomal instability. For a long time is has been recognized that missegregation of large numbers of chromosomes results in rapid cell death. It is self-evident that a minimum number of genes and/or chromosomes must be required for viability. Cells, this includes human cancer cells that exhibit chromosomal instability, in which the mitotic is completely inactivated by siRNA (small interfering RNA). (5)Tumors are associated with having a weakened mitotic checkpoint. A frequent occurrence in human tumor and cell lines is the inability to sustain mitotic check point signaling. It is judged by a reduced mitotic after long-term drug-mediated spindle disruption. The message gathered from this is that many tumors and tumor cell lines, including the ones that are chromosomally unstable, have a weakened checkpoint signal that is sufficient for maintaining a viable population of cells. Yet also allowing them to missegregate small numbers of chromosomes per division. This then results in aneuploidy and also chromosomal instability. Chronic activation of the mitotic checkpoint is a common chemotherapeutic strategy. Now that you know a little about how mitosis is connected to diseases mainly cancer and tumors in this paper we are going to hear about how meiosis is connected to pharmaceuticals or drugs. (1)Meiosis is a type of cell divison that reduces the number of chromosomes in the parent cell by half thus producing then four gamete cells. This process is essential to produce egg and sperm cells for a process called sexual reproduction. But what happens when a drug might try and interfere with meiosis and try to break it up? Will meiosis be affected in a positive way or a negative way? Will meiosis be affected at all? Lets find out shall we. (2)Drugs like chlorpromazine, fluphenazine, trifluoperazine, procaine, dibucaine, theophylline, propranolol, vinblastine, vincristine, and W7 have all been shown to prevent formation of the ternary activated complex calmodulin. Several soluble or membrane proteins, inhibit meiosis reinitiation in starfish oocytes when applied from outside. Inhibition occurs only if drugs are present in the medium during the hormone dependent period. Inhibition can be overcome by raising external concentration of 1-MeAde. (3)In contrast, direct intracellular microinjection of these drugs, even at concentrations far exceeding I50 for external application. To