Conducting a reflective analysis after a section or topic is covered is a successful strategy for mastering academic material. It allows you to summarize the available data and structure them. Thus, it has been found that proto-oncogenes can turn into oncogenes by point mutations, chromosomal insertions, or deletions. At the same time, while suppressor genes are designed to inhibit oncogenesis, mutations in them can, on the contrary, lead to the amplification of harmful mutations. Loss of function of suppressor genes resulting from mutations becomes the cause of cancer development: the cell divides abnormally, increasing the cell mass of the tissue. In the same way, numerical statistics for oncogenes and suppressor genes were passed in class. I must admit that, in general, these are the numbers that I expected: a large number of suppressor genes are necessary to suppress oncogenes. At the same time, the survival rate for both categories is equal, which suggests that they are mutually related. It has also been shown that the maintenance gene can catalyze cancer development. It is worth noting that this is not a straightforward process: mutations in the maintenance system entail profound changes in defense mechanisms. The more significant number of oncogenes and suppressor genes responsible for cell survival determines the evolutionary driving forces that make cells remain viable even in the face of mutation. Zero oncogenes have been found in the support system, confirming the deleterious nature of such oncogenes. Finally, the dominance of suppressor genes over oncogenes in fate cells also has an explanation. Since differentiation is accompanied by mutations, the cell must protect itself in case of an unforeseen increase in oncogenicity.
Three key ideas have been assimilated by me within this topic. The first one concerns the diversity of sources of cancer cell development. In fact, it is a mistake to believe that cancer is initiated by only one factor: on the contrary, a combination of biological, physical, infectious, and even chemical causes can trigger cancer development. Secondly, I have learned that there is a complex mechanism of cancer cell formation involving proto-oncogenes, which, when amplified, can be modified to oncogenes. To suppress them, suppressor genes are activated, among which p53 is the best known. Finally, I have learned the relationship between age and the likelihood of developing cancer. As life expectancy increases, the number of mutations increases, and thus the likelihood of cancer increases. I found it amazing that science knows precisely what the frequency of mutations is: 1 error in a billion bases is deficient. In addition, I was struck by the information that the mutated gene is dominant. The question I still have involves the refinement of numerical statistics. If human DNA includes 3 billion base pairs — a total of six per DNA molecule — does this mean that only three harmful mutations are possible in a single cell?