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Реферат: Mitosis In Cancerous Cells Essay Research Paper

Название: Mitosis In Cancerous Cells Essay Research Paper
Раздел: Топики по английскому языку
Тип: реферат Добавлен 08:01:48 15 ноября 2010 Похожие работы
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Mitosis In Cancerous Cells Essay, Research Paper

Mitosis in cancerous cells

Mitosis, the process in which a cell undergoes nuclear division, is one of the four subdivisions of the cell cycle responsible for cell growth and reproduction. The first step in mitosis is prophase. In prophase the chromatin, diffuse in interphase, condenses into chromosomes. Each chromosome duplicates and has become two sister chromatids. At the end of prophase, the nuclear envelope breaks down into vesicles. The following step in mitosis is metaphase. During metaphase the chromosomes align at the equator of the cell and are held in place by microtubules attached to the spindle and part of the centromere. Next is anaphase, in which the centromeres divide. The sister chromatids separate and move toward opposite poles. The last phase of mitosis is telophase. Here the daughter chromosomes arrive at the poles and the microtubules disappear. The cytoplasm divides, cell membrane closes inward making two daughter cells.

This is a very complex process which needs to be completed perfectly, in order for the cell to divide and replicate normally. Very often a cell loses its regulation, and begins replicating out of control, that is it becomes cancerous.

Abnormal cell growth is often known as cancer. During which, cancer cells do not respond normally to the body’s control mechanisms. They often divide excessively, invade other tissues and, if unchecked, can kill the whole organism. Researchers studying cancer cells in culture have found that they do not respond to the normal signals that stop growth such as contact inhibition. They continue to grow until nutrients in the growth medium are exhausted. Other differences exist between normal and cancer cells. These indicate abnormalities in the cell cycle of cancer cells. Cancer cells that stop dividing do so at random points in the cycle, instead of the restriction point in G1 also known as Gap 1 in the cell cycle.

Cancer cells in culture continue to divide indefinitely as long as nutrients are available. Normal cells in culture divide only about 20 to 50 times before they stop. It is clear that genetic changes are responsible for these abnormalities. However, the exact reasons the cells stop in the middle of the cell cycle are not known.

Once the control mechanisms in normal cells are known, then these questions about cancer cell development may soon be answered. Scientists are making great discoveries in understanding cancer. And are believed to within the decade, have a much better view of the cancerous state.

Sometimes normal cell genes that inhibit uncontrolled mitosis do not function correctly (for example if mutated) or are absent as a result of an inherited genetic disease. At other times, the reverse situation occurs in which a gene or genes that activate cell replication become overly active, or mutate so as to become constantly active. Abnormal oncogene activation has even been documented to occur by means of viral transmission of oncogenes, or viral infection with concomitant activation of endogenous oncogenes. For example, the Rous sarcoma virus has been shown to cause mammary gland (breast) cancer in mice. Epstein-Barr virus has long been known to cause a cancer called Burkitt’s lymphoma.

It may be that viruses may prove to cause a number of cancers that we have yet to understand. And yet viruses may themselves prove to be a major weapon in the fight against cancer, as laboratory genetically engineered viruses are designed that invade cancerous cells and fix or kill the cancer cell at the level of the genome.

Chemical carcinogens function to convert normal cells to cancerous cells by inducing mutations in genes that are critical for regulation of cell replication. A simple screening test for chemicals to check whether they are likely to be carcinogenic to many life forms is the Ames test, developed at Ames University in Iowa, USA. The test involves the exposure of special strains of a bacterium to the suspected carcinogen. If the suspected carcinogen induces nutritional mutations in the bacteria, it is deemed wise not to allow higher life forms to be exposed to the suspected carcinogen.

The use of bacterial (prokaryotic) cells for testing suspected carcinogens is advantageous because the cells replicate so rapidly (every 5-30 minutes). This allows the exposure of the bacterial cell DNA (genes) to the suspected carcinogen during DNA replication. The use of bacteria also allows researchers to see the effects, if any, of the suspected carcinogen on extremely large numbers of cell progeny and cell generations.

Chemical carcinogens are categorized as direct carcinogens, procarcinogens, and promoter carcinogens. Direct carcinogens cause fibroblasts (connective tissue cells) grown in culture and subjected to the chemical to become cancerous. Examples of direct carcinogens include many toxic and complex organic chemicals used in industry. Procarcinogens are not carcinogenic when applied to cells, but become carcinogenic when metabolized by cells. Their metabolic intermediates are carcinogenic. Examples of procarcinogens include nitrates and nitrites such as are found in pepperoni and other foods, and tar created from inhaled tobacco products. Promoter carcinogens, like procarcinogens, are not directly carcinogenic, but rather amplify the carcinogenic effect of other carcinogens. In a sense, promoters act synergistically with other carcinogens. Examples of promoter carcinogens include many chemicals in tobacco smoke and drinking alcohol (ethanol).

Carcinogens stimulate conversion of cells to cancer cells. Some substances may act directly as carcinogens, some may act synergistically with other agents to become carcinogenic, and some substances may be metabolized to become carcinogenic.]

Whatever the mechanisms, cells have a genetic internal ‘clock’ of a sort that determines how many times a cell divides over its lifetime. The more complicated a cell is, the less often it replicates, and the more complicated, the more it will replicate. This is why nerve cells do not replicate in adults. Muscle cells also rarely if ever replicate in an adult. Less complicated cells like those that protect body (epithelial cells) replicate about every twenty-four hours. Blood cells formed in the bone marrow also replicate very rapidly.

When cancer cells are treated through the use of chemotherapy and nuclear medicine (radiation) therapy, the rapidly dividing cancer cells are greatly affected by these therapies. This is because dividing cells are very active metabolically and their DNA (genes) are more sensitive to chemicals or radiation that might damage the DNA as it is being replicated.

The problem is, non-cancerous cells that also replicate rapidly like cancer cells are also sensitive to chemotherapy and radiation. Cells such as epithelial cells and bone marrow blood cells. This explains why chemotherapy and radiation therapy causes patients to suffer from abnormal blood counts and to have problems holding down food (vomiting a lot). Their bone marrow precursor blood cells, and also their epithelial cells lining their gut, are severely affected by the cancer treatment (designed to affect cancer cells that are also in high states of metabolism and that also have their genes exposed frequently as their chromosomes are frequently in existence.]

[SIDEBAR: The ability to identify cells that are undergoing mitosis is very important in the field of pathology, where tissue biopsies are often checked for cancer or pre-cancerous conditions. Looking at a biopsy, the pathologists looks for the ratio of dividing cells to non-dividing cells. This ratio is called the mitotic index.

Different tissues have different mitotic index values. For example, the mitotic index of adult brain or muscle tissue should be zero, whereas the mitotic index value of cervical tissue (part of the female uterus) might be 1:10. Suppose a biopsy specimen of muscle tissue revealed by light microscopy that about 1 in 10 muscle cells were undergoing mitosis (see photograph). Would you suspect a neoplastic condition (cancer or pre-cancer condition)?]

Normal cells of tissues and organs exhibit a common growth control phenomenon known as contact inhibition. When normal cells replicate, they cease dividing when they encounter neighboring cells. Contact inhibition of cells in tissues generally leads to monolayer tissue growths in culture.

[SIDE_BAR: Cancer cells do not exhibit contact inhibition and continue to replicate in spite of contacting neighboring cells. It is this feature of cancer cells that makes them so damaging to an organism. Without contact inhibition, cancer cells grow, and grow, and grow, damaging the organism by a multitude of mechanisms. Cancer cells use precious nutrients, but do not perform useful, normal physiological function for the organism. Cancer cells sometimes grow into nearby organs, disrupting normal anatomy and physiological function, or perhaps impinging on nerve tracts and causing subsequent sensory or motor deficits.]

[Key Point: Cancer cells do not stop growing when they contact neighboring cells. They do not exhibit contact inhibition. Normal cells do, and form tissue culture monolayers as a result.]

[SIDEBAR: Uncontrolled replication of cells leads to tumors, that is cell overgrowths,, whether benign or cancerous. Benign tumors are simply excessive cell growths that will not cause any significant harm. Malignant tumors, that is cancer, are cell growths where the cells are replicating without any inhibition of cell growth, and they will cause death to the organism if allowed to continue growing. Here are the naming conventions used for the more common tumors.

Resource Page

1. Randall Oelerich. Cell Replication/Cell Division 1998-1999. December 2, 1999.

2. National Health Museum. Mitosis: Labeled Diagram . 1999. December 6, 1999.

3. The Reproduction of Cells December 7, 1999

4. Cell . Funk & Wagnalls New Encyclopedia: Vol. 5. 1992. Publisher Funk & Wagnalls

Corp. :New York

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