Gene mutation’s influence on cancer
Science has proved that many types of cancers are triggered by defective genes, which initiate cell division without due consideration to the molecular messages that usually control the nature and rate of cell division (Audersirk & Byers). The genes tasked with the responsibility of regulating mitotic cell division are often blamed for initiating this process. As such, it could be safely argued that cancers are generally occasioned by the accumulation of mutations in our own genes, a process that leads the genes to decisively alter the behavior of cells, further leading to uncontrolled growth of cells that characterize most cancer cases (CANCERQUEST para. 1).
It is widely believed that certain behavioral and lifestyle risk factors enhance the process of gene mutation and, as such, it is imperative to curtail these factors so as to reduce the risk of getting cancer. According to Emmons et al., behavioral and lifestyle risk factors such as smoking, physical inactivity, lack of proper nutrition, continued exposure to sun, alcohol consumption and depression are thought to contribute towards increased risk of getting cancer (para. 10-17). Lack of adequate information on cancer and failure to go for cancer screening on a constant basis are also thought to contribute. Consequently, we need to make appropriate changes on the above-named risk factors to lessen the chances of being diagnosed with cancer.
A perfect cancer therapy
A theoretically perfect cancer therapy would first and foremost take into consideration the above-mentioned behavioral and lifestyle risk factors. A perfect cancer therapy should also have proper mechanisms of examining DNA sequences of genes charged with the responsibility of cell division to determine if such genes are defective. Specifically, such therapy should have mechanisms and instruments for determining if the p53 gene is defective.
This gene functions to activate genes responsible for inhibiting cell-cycle progression occasioned by DNA damage (Audersirk & Byers). In line with this explanation, a theoretically perfect cancer therapy should also entail having mechanisms in place that have the capability of determining healthy p53 genes in addition to having mechanisms through which the healthy p53 cells are extracted and injected into the tumors to initiate apoptosis (Audersirk & Byers).
Studies about genes becoming mutated
Scientific studies have demonstrated that the likelihood of any gene to under several mutations is exceedingly low. Science has also revealed that “…the transition from a normal healthy cell to a cancer cell is a step-wise progression that requires genetic changes in several different oncogenes and tumor suppressors” (CANCERQUEST para. 2). This process takes time to complete, and thus the reason why cancer is more widespread in older people than in younger generations.
In other words, although the probability of any gene becoming mutated is extremely low, and a series of mutations must take place in the same cell for it to become a cancer cell, older people still stands a bigger chance of developing cancer due to the fact that their cells have had more time to amass the changes that must be present to form cancer cells.
Treatments for cancer: chemotherapy and radiation treatments
It is true that chemotherapy and radiation treatments for cancer may further aggravate the situation for the fact that these therapies are unable to discriminate between cancerous cells and other healthy cells. Indeed, the therapies target any cell that is dividing regardless of the fact that the division may be normal, and this is known to trigger various side effects associated with the therapies such as nausea and hair loss (Audersirk & Byers).
The therapies function under the same principle as apoptosis, a cell suicide program initiated by the p53 gene in the event that the damage caused to the DNA is beyond repair. This process causes the mitotic cell to release itself from other healthy cells and triggers the cell to generate digestive enzymes that severe it’s DNA into small parts. The parts are further broken up into bite-sized components that are then consumed and digested by other body cells (Audersirk & Byers). This makes the cancerous cell to disappear without trace.
Chemotherapy and radiation treatments utilize the same process to eliminate cancer cells by virtue of the fact that the agents used cause weighty DNA damage to both cancerous and healthy cells – enough to initiate the apoptosis process explained above (Audersirk & Byers). It is imperative to remember that many types of cancers are triggered by defective genes. It, therefore, follows that since genes degeneration is ostensibly caused by damage to the DNA, any treatment methodology that occasion’s further damage to the DNA is likely to exacerbate the situation. This explains why increased incidences of new types of cancers might be expected in the future.
The inability of the chemotherapy and radiation therapies to discriminate between healthy and affected cells does not help matters. Furthermore, the artificial process of initiating apoptosis may cause new strains of cancerous cells to develop, further worsening the situation. This is because apoptosis is a normal body’s procedure of getting rid of unwanted cells through the employment of p53 genes; but to cause artificial apoptosis through the employment of agents contained in these therapies which are commonly used to treat various types of cancers might, as a matter of fact, be counterintuitive.
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