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For a long period, it has become clear that cancer frequently impinges on citizens who are above 50 years. Although the youthful populace also gets afflicted with such illnesses, the majority of populace suffering such ailments as cancer is the old populace (Hobson, 2009). Through the following observation, researchers have started to investigate the affiliation between biological procedures that direct disease and aging processes. Researchers have to this point been able to determine the connection between the two.
Researchers have substantiated two ways of viewing the correlation between cancer and age. According to the findings provided, are that the forces that cause damage to human genes may be similar to the forces that compel both cancer and aging (Hobson, 2009). Therefore, this suggests that the processes guard against cancer, the genome and permanence. However, the second reason seems to be a bit complex concerning the correlation among the two. Naturally occurring tumor suppressor molecules prevent the cells from reproducing or regenerating sporadically.
The tumor suppressor cell provokes the fatality of the cells through a procedure regarded as apoptosis or it can shut down the cell’s ability to replicate. These two progressions produced by the suppressor molecules serve to protect the people during their reproductive periods. Therefore, as the populace gets older, the molecules abilities to guard the body through the two methods reduce. For this reason, the body becomes vulnerable to cancer attacks justifying the statement that the cancer cases are more extensive in the old people.
For the young generation, the susceptibility is markedly reduced through the action of the suppressor molecules. The older people experience corporal changes that augment the probability of disease and disability and which interfere with the body’s ability to withstand cancer threats. Cancer occurs mainly because of any transformations or alterations on the oncogenes, tumor suppressor molecules and microRNA genetic material (Croce, 2008, 502). These modifications are usually somatic procedures, even though origin transmutation can dispose an individual to genetic or ancestral cancer.
In cancer, a single alteration may not be sufficient to initiate cancer instead, cancer development is a multistep progression with alterations occurring in oncogenes (Croce, 2008, 502). Oncogenes are proteins that predetermine for the control of cell propagation, apoptosis or even the two processes. These genes are activated by structural transformations that originate from mutations or amplification (Croce, 2008, 503). Chromosomal reorganization, transmutations and gene extension, help in activation of oncogenes presenting an enlargement benefit or amplified continued existence of cells bearing such variations.
In cases where, the oncogenes are activated by mutations, the preset protein is altered structurally in ways that allow for its transforming action. Myc is a replication regulator and its genes are usually translocated from the original chromosome to another chromosome. Chromosomal translocations help in joining the cellular oncogene together with immunoglobin that are believed to be vital, in the initiation of the oncogenic progressions in the developments of certain cell types. The translocation can be considered essential in essence, that it helps in the study of the means, heredity and biological outcomes of the translocations.
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