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Cancer is not so much a disease as the natural end state of any multicellular organism. We are all familiar with the basic Darwinian idea that a population of organisms that show hereditary variation in reproductive capacity will evolve by natural selection. Genotypes that reproduce faster or more extensively will come to dominate later generations, only to be supplanted, in turn, by yet more efficient reproducers. The determining factor can be an increased birth rate or a decreased death rate (Strachan, T., & Andrew, R., 2011, page 538). Cellular birth and death are under genetic control, and if somatic mutation creates a variant that proliferates faster, the mutant clone will tend to take over the normal systems of the organism. Cancers are the result of a series of somatic mutations with, in some cases, also an inherited predisposition. Thus cancer can be seen as a natural evolutionary process. Every tumor is individual. There are so many different genes that acquire mutations in one or another tumor, and they interact in such complex ways, that it is not easy to catalogue large quantities of genes and mutations, which leads to difficulty in researching tumors (Strachan, T., & Andrew, R., 2011, page 538 & 539). Cells are under strong selective pressure to evolve into tumor cells. However, although tumors are very successful as organs, as organisms they are hopeless failures. They leave no offspring beyond the life of their host. At the level of the whole organism, there is therefore powerful selection for mechanisms that prevent people from dying from tumors, at least until they have borne and brought up their children. Thus, we are ruled by two opposing sets of selective forces. But selection for tumorigenesis occurs over the short term, whereas selection for resistance occurs over the long term (Strachan, T., & Andrew, R., 2011, page 539). The microevolution from a normal somatic cell to a malignant tumor takes place within the life of an individual and has to start afresh with each new individual. But an organism with a good antitumor mechanism transmits this to its offspring, where it continues to evolve. A billion years of evolution have endowed us with sophisticated interlocking and overlapping mechanisms to protect us against tumors, at least during our reproductive life. Potential tumor cells are either repaired and brought back into line or made to kill themselves (apoptosis). No single mutation can circumvent these defenses and convert a normal cell into a malignant one (Strachan, T., & Andrew, R., 2011, page 539). The early studies of the age-dependence of cancer suggested that on average six or seven successive mutations are needed to convert a normal epithelial cell into an invasive carcinoma. In other words, only if six or seven independent defenses are disabled by mutation can a normal cell be converted into a malignant tumor. The chance that a single cell will undergo six independent mutations is negligible, suggesting that cancer should be vanishingly rare. However, two general mechanisms exist that can allow the progression to happen. Accumulating all these mutations nevertheless takes time, so that cancer is mainly a disease of post-reproductive life, when there is little selective pressure to improve the defenses still further (Strachan, T., & Andrew, R., 2011, page 540). Oncogenes and tumor suppressor genes are the major factors that control the strong cell selective pressure. Oncogenes are genes whose normal activity promotes cell proliferation. Gain-of-function mutations in tumor cells create forms that are excessively or inappropriately active. A single mutant allele may affect the behavior of a cell. The nonmutant versions are properly called proto-oncogenes. Tumor suppressor genes are genes whose products act to limit normal cell proliferation. They are genes to inhibit tumor formation. When tumor suppressor gene products are inhibited, it will lead to cancer cells. Mutant versions in cancer cells have lost their function. Some tumor suppressor gene products prevent inappropriate cell cycle progression, some steer deviant cells into apoptosis, and others keep the genome stable and mutation rates low by ensuring accurate replication. Both alleles of a tumor suppressor gene must be inactivated to change the behavior of a cell. By analogy with a bus, one can picture the oncogenes as the accelerator and the tumor suppressor as the brake. Jamming the accelerator on (a dominant gain of function of an oncogene) or having all the brakes fail (a recessive loss of function of a tumor suppressor gene) will make the bus run out of control. (Strachan, T., & Andrew, R., 2011, page 540).
The New Human Line belongs to the phylum of Strong Chordata. The function of strong promotion of genes in the body can activate the transcription of tumor suppressor genes when they lose their dominant tumor suppression functions. He can also have the DNA go through a -1 or +1 frameshift at a specific site, generate prompt apoptosis in all the deviant cells and thus maintain the accuracy and stability of the genome. The function of suppressing tumor formation of the New Human Line is activated by polarity receptors (please refer to The Energy Control Functions for details). As a new organ unique to the New Human Line, the polarity receptor is responsible for hyperlinking intracellular magnetic moment fields. It can constantly monitor and guard oncogenes through the positive and negative polarity between cellular magnetic moment fields, promptly activate the dominant functions of respective tumor suppressor genes when the dominant functions of oncogenes appear, and carry out modification of the genome through frameshifting. The signal of frameshifting is constituted by the Absolutely Constant Energy Source inside the body. Through a pseudoknot structure and stem-loop structure in the mRNA and the interaction between mRNA and rRNA, the DNA is induced to go through a +1 or -1 sliding and shifting at a defined position, which make the deviant cell experience rapid apoptosis and resume its normal condition.
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