Mesothelioma is a very unique cancer because it only has one cause – asbestos. According to most medical experts, nearly all cases of mesothelioma would not exist if the patient was not first exposed to asbestos. But how can asbestos, a naturally occurring mineral that was put into thousands of products, cause mesothelioma?
Asbestos, also known as the “magic mineral,” is heat resistant, anti-corrosive and, because it is composed of fibers, can be woven into textiles. These properties made it attractive to industry but also carcinogenic.
Because asbestos is comprised of microscopic fibers the body’s normal mucosal surfaces in the nose, sinuses, and throat can have difficulty filtering them out. As a result it is thought that after asbestos exposure some fibers can end up in the lungs or stomach and ultimately become lodged in the body’s mesothelial tissue. The mesothelium, which is composed of mesothelial cells, lines the body’s serous cavities and internal organs. The main purpose of these cells is to produce a lubricating fluid that provides a slippery and protective surface to allow intracoelomic movement.
It is still not known precisely how asbestos fibers convert a normal mesothelial cell into a malignant cell. But despite the lack of detail, there is enough information regarding the basic mechanisms behind the process. Mesothelioma might be induced with a direct interaction with the cells by the asbestos fibers or they may be indirectly generating toxic byproducts that can lead to cancer.
Inhaled or ingested asbestos fibers can get lodged in the mesothelium where they can cause inflammation and irritation and this can lead to the production of different body chemical substances known as cytokines. These newly produced cytokines can induce cellular and intercellular changes in the mesothelial cells. The interaction of asbestos fibers and cytokines can lead to malignant transformations in the cells. For example, the inhaled asbestos dust and fibers can reach the lungs and move into their tiny pockets called alveoli. These fibers can remain lodged for years, even for the rest of the person’s life. However it is thought that the amphibole asbestos fibers, which are straighter and longer than chrysotile fibers, remain in the lungs the longest time. The reactivity of these crystalline asbestos fibers to the cells depends on their size, their surface area and their surface chemistry. These fibers tend to move toward the lower portion of the lungs. Mesothelioma often begins in the bottom lobes of the lungs as well as on the surface of the diaphragm.
The asbestos fibers lodged in the lungs can cause lung cancer, asbestosis and mesothelioma. All three diseases develop very gradually and are very serious. The symptoms appear very late, sometimes after 20, 30 or fifty years after asbestos exposure.
Generally, the genes that promote and suppress cellular growth function appropriately and cell division occurs only when needed. Damage to these genes can, however, affect their ability to promote or suppress cell growth. For example, damage due to fibers can lead to various chromosomal abnormalities in patients. If these genes control cell growth or death then uncontrolled cellular replication and immortality may result.
How malignancy of any kind develops, is a very complex process. There are different genetic events involved before resulting making a cell malignant. As more research accumulates regarding the sequence of events that lead to mesothelioma it is hoped that this understanding will lead to both better preventive measures and more effective treatments for mesothelioma.
Disclaimer: The information in this article is for educational and informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this article
March 26, 2013
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