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