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Wednesday, July 22, 2020 | History

2 edition of Mitotic poisons and the cancer problem found in the catalog.

Mitotic poisons and the cancer problem

John Julius Biesele

Mitotic poisons and the cancer problem

by John Julius Biesele

  • 252 Want to read
  • 37 Currently reading

Published by Elsevier Publishing Co. in Amsterdam, London .
Written in English


Edition Notes

Statementby John J. Biesele.
The Physical Object
Pagination214p. :
Number of Pages214
ID Numbers
Open LibraryOL17304001M

  The first part of this investigation, students examine slides of mitosis in an onion root tip and count the number of cells in each phase of the cell cycle. An equation is then used to estimate the percentage of time the cell spends in each phase and . mitotic poisons, are discussed. This is an active area, and the writer has collected and critically presented a sizable mass of data in admirably con-cise and readable form. The substantial bibliography should be of great value to all interested investigators. Ofparticular usefulness to workers in the cancer field, this book should also appeal.

Cancer cells may be more susceptible than normal cells to mitotic catastrophe in response to chemotherapeutic drugs because A. They express unique receptors for these drugs on their surface. B. They may lack key G2/M checkpoint controls. C. They may be resistant to apoptosis. D. A & B. E. None of the above. breakdown, assembly of the mitotic spindle, chromosome condensation, and activation of the spindle assembly check-point [, ]. During metaphase the mitotic chromosomes, which are composed of sister chromatids held together by cohesion, are aligned on the mitotic spindle by stable micro-tubule attachment through their kinetochores. Properly.

The NCI Dictionary of Cancer Terms features 8, terms related to cancer and medicine.. We offer a widget that you can add to your website to let users look up cancer-related terms. Get NCI’s Dictionary of Cancer Terms Widget. Toxicity Tests with Mammalian Cell Cultures 79 culture; in particular, they produce keratin and the cells of the upper layer of the colonies lose their ability to divide and develop a cornified cell envelope. Mouse secondary cultures of Schwann cells are still able to synthesize enzymes typical of myelin-forming cells (White et al., ). (4).


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Mitotic poisons and the cancer problem by John Julius Biesele Download PDF EPUB FB2

Additional Physical Format: Online version: Biesele, John J. (John Julius). Mitotic poisons and the cancer problem. Amsterdam, New York, Elsevier Pub. Co., A spindle poison, also known as a spindle toxin, is a poison that disrupts cell division by affecting the protein threads that connect the centromere regions of chromosomes, known as e poisons effectively cease the production of new cells by interrupting the mitosis phase of cell division at the spindle assembly checkpoint (SAC).

However, as numerous and. Those chemicals can kill or destroye dividing cells or mitotic cells known as mitotic poisons. In other words it is said that those chemical compounds inhibit mitosis is known as mitotic poisons.

It's another name is spindle poison. They can block. Mitotic inhibitors affect cancer cells more than normal cells because cancer cells divide (mitotic cell division) more rapidly therefore are more susceptible to mitotic inhibition.

Different mitotic inhibitors are used to treat particular types of cancers, such as leukemia, lymphoma, breast cancer, lung cancer and other types of cancers. Mitotic Poisons and the Cancer Problem By Dr.

John J. Biesele. viii + (Amsterdam: Elsevier Publishing Company; London: Cleaver-Hume Press, Ltd., ) 37s. : C. Auerbach. Induction of autophagy or inhibition of AMPK or PFKFB3 results in enhanced cell death in mitosis and improves the anti-tumoral efficiency of microtubule poisons in breast cancer cells.

Thus, survival of mitotic-arrested cells is limited by their metabolic requirements, a feature with potential implications in cancer therapies aimed to impair Cited by: A mitotic inhibitor is a drug that inhibits mitosis, or cell drugs disrupt microtubules, which are structures that pull the chromosomes apart when a cell c inhibitors are used in cancer treatment, because cancer cells are able to grow and eventually spread through the body (metastasize) through continuous mitotic division.

Purpose. High proliferation rate is a hallmark of cancer. The mitotic index is a useful and simple method for analysis of cell proliferation.

However, the practical utility of mitotic index as a predictor of prognosis in patients with hepatocellular carcinoma (HCC) Cited by: 4. It effectively functions as a mitotic poison or spindle inhibitor.

Microtubule inhibition therapy by colchicine in severe myocarditis especially caused by epstein-barr and cytomegalovirus co-infection during a two-year period: A novel therapeutic approach.

Mitotic catastrophe is a process of cell death induced by radiation, chemotherapeutic drugs, or hyperthermia. Mitotic catastrophe results from aberrant mitosis, which is followed either by cell death through apoptosis or necrosis or by partial or complete fragmentation of interphase nuclei with eventual cell death or senescence.

Antimitotic substances are tools which enable the cytologist to dissect the interrelated phases of the mitotic cycle. The words “antimitotic substance” can have only a very general significance and include every substance that lessens the number of mitoses in a cell population, whatever the mechanism of this reduction may be.

Mitotic catastrophe, as defined in by the International Nomenclature Committee on Cell Death, is a bona fide intrinsic oncosuppressive mechanism that senses mitotic failure and responds by driving a cell to an irreversible antiproliferative fate of death or senescence.

Thus, failed mitotic catastrophe can promote the unrestrained growth of defective cells, thereby Cited by: There are hundreds of types of cancer; every organ and tissue has possibility of developing cancer, and multiple cell types of the organs and tissues can develop cancer So many regulators, proteins, making all cancers different.

Several different drugs needed to combat them all Different levels of differentiation change diagnosis. Mitotic death is a delayed response of p53 mutant tumours that are resistant to genotoxic damage. Questions surround why this response is so delayed and how its mechanisms serve a survival function.

After uncoupling apoptosis from G1 and S phase arrests and adapting these checkpoints, p53 mutated tumour cells arrive at the G2 compartment where decisions Cited by: The response of cells to anti-mitotic drugs is highly complex.

HCT colon cells expressing GFP-histone H2B were followed by time-lapse imaging for. Microtubule poisons inhibit spindle function, leading to activation of spindle assembly checkpoint (SAC) and mitotic arrest. Cell death occurring in prolonged mitosis is the first target of microtubule poisons in cancer therapies.

However, even in the presence of microtubule poisons, SAC and mitotic arrest are not permanent, and the surviving cells exit the mitosis without cytokinesis Cited by: 8.

In the last decades "anti-mitotic" drugs (i.e: drugs that kill dividing cells) have emerged as a new and very promising strategy for the development of alternative anti-cancer treatments.

The study of the different proteins and cellular structures that can be targeted by drugs to kill cells in mitosis -and therefore kill a tumour on its tracks. The Effect of Nitrogen Mustard on the Life Cycle of Ehrlich Ascites Tumour Cells In Vivo Article (PDF Available) in British Journal of Cancer 18(1) April with 12 Reads.

The mitotic checkpoint was initially recognized 15 years ago in experiments using antimitotic drugs that depolymerize microtubules (Hoyt et al., ; Li and Murray, ).These microtubule poisons cause all kinetochores to become unattached and, therefore, a maximal mitotic checkpoint signal is by: What anti-cancer drugs disrupt the process of the mitotic spindle formation, effect equilibrium between polymerized & depolymerized forms of tubulin & inhibit cell division.

Microtubule inhibitor What anti-cancer drugs use hormones to stop cell functions, or antagonize the action of hormones needed for the cancer cells to survive?.

Abstract. Most hereditary information of cells apparently is carried by DNA. In growing or adult cells, most DNA resides in chromosomes inside the cell nucleus, whereas a smaller fraction (–10%, depending on organism and cell type) is found in Cited by:   Chemotherapy (cancer chemotherapy) is the treatment of cancer with an antineoplastic drug or with a combination of such drugs into a standardized treatment regimen.

Most commonly, chemotherapy acts by killing cells that divide rapidly, one of the main properties of most cancer cells. This means that it also harms cells that divide rapidly under normal. Senescence and mitotic catastrophe (MC) are two distinct crucial non-apoptotic mechanisms, often triggered in cancer cells and tissues in response to anti-cancer drugs.

Chemotherapeuticals and myriad other factors induce cell eradication via these routes. While senescence drives the cells to a state of quiescence, MC drives the cells towards death during .