Conclusion

     In conclusion, it is one of my thesis that a bond change in the DNA, or a gene, which changes or fundamentally divides the three groups of Spin, Charge, and Mass in motion, among the future (sense preserving) expression of these as forces causes a division of the genes from naturally being able to be expressed, -or- to repair the original corrupted gene(s). It is as if one gene change causes the switching of the future sense of direction of multiple sets of other genes, changing the chirality and therefore the net gene expression. It would be interesting to correlate simply one thing; the number of genes on average (G,A,T,C) expressed in each of the chromosomes or across all genes of a person, to the incidence of cancers, so as to be able to understand if one set is predominantly affected over the others, and the conversion to all of one sequence or gene as related to the death of cells or their uncontrolled mitosis in the incidences of cancer.

     The problems with the genes as outlined in this paper are of missing or removed genes, and changed or reversed genes. I am speaking very much of expression and interpretation. If we take the groups of spin and charge and mass in motion then we find that these three dissimilar yet fundamental groups in fact must work together both to yield the structure and stability and the interpretation of a temporal direction to the genes in their encoding. When genes change and create this discordancy, they create ambiguity with respect to the reading off of the genes in time, and the next cellular mitosis process, as well as in the interpretation of the genes, and within the error correcting code. As a problem, consider N genes with 2 implying the reversal of a third with respect to all others. In such a case, the direction of all would in a sense begin to be confused by that which interprets the genes, the error correcting code would as well, and yet the error would by chance, be reproduced in future copies.

     Additionally, I would like to say that single occurances of mutations are natural in many senses, as the body changes and develops over time. Consequently, a start or end of a sequence, or a larger sequence, given that these autoregressive types of sequences apparently would have no beginning or end and the fact that a single gene is likely not enough to spark cancer, indicate the concept of regressive sequences are false in some sense, as they are not self starting. They are instead suggestive of a deeper underlying structure to this disease once it has been unfortunately set into motion, by what we should be looking for as an outside cause, but one which becomes internalized. Also there is more to this, as the genes are not entirely self contained, but also exist through future gene expression. I believe that it is not so much single bond changes, but many, occurring in such a way that they dicordantly misorchestrate a folding when the interpretation of the genes or part thereof is reversed in action by way of a retroreflection of their code, as interpreted by the cellular transcription process, when multiple genes are effectively reversed, as any one or all three of their groups in action by separate action or group separation when one or many or two others collectively produce what appears to be a chaotic attractor in the system in interpretation as these reverse together without the other, or do so when part of the genetic sequence is disrupted, and the groups do not work together or to preserve their interpretation or orientation, which is also the tipping point to reversal of one. How these actually become out of balance, and how we judge this is effectively a mystery to me at this point. However, the agent of this action which must be preserved appears to be conservation of their individual laws, and the preservation of the three groups in collective action across many genes. We need not divide them to understand this, nor simply combine them, but understand their mutual interrelationship in the process of the preservation of each individually.

     A cell would not evolve with others, or by itself, if it could not develop new genes. If it had many changes at once, neither would it grow in a way that it could develop slowly enough to acquire new information at a rate for which the growth would not outpace the ability of it to develop, consequently, when cells change with more than two mutuations, unless precisely balanced, they outpace their means, and develop at too fast a pace to be able to truly evolve. These instances likely happen, but the returns are quickly diminishing, because the cells outgrow their ability to match the growth on the level of the cellular process of mitosis and division. If we take the following as a thought puzzle, that we have a cell which divides in two and yet must coexist with others, and that these cells must each remember, or carry on, and preserve their complete evolutionary history within their genetic memories, then the only way for it to preserve the content of these is for them to leave one new gene within the genes in each new successive step of evolution. The follwing aspects of the disease may be taken to be the precursor, the cause, the preexisting preventative measure, and the conclusions to the disease.

     It appears that the problem is that any of multiple genetic problems can cause a disjuncture, but that the body naturally exists so as to re-equilibriate these different types of symmetry once they have become discordant. It is another thesis of this paper that it is not so much specific genetic sequences themselves that cause or encode for cancer, but a common malady of the physical structure of the genes (not working together) in their ability to self equlibriate, balance, and to be of mutually compatible interpretations, not having to do with the code itself as we interpret it on the level of single successfully mated relationships of the bonds only, but instead, the physical structure itself either as a whole, across multiple groups, or even down to the level of the single gene bonds which exist. If one can find a way to allow the body to heal naturally then we need not impose a restriction on the system which changes the genes, but instead potentially acts as the only true mechanism by which it may heal. The notion of a "displaced gene" is useful in this regard, as it is useful to work with the existing terms for a "mutuant gene" and the term I have come up with for genes which naturally evolve from those in the presence of a healthy living cells chromosomes as "naturally occurring, existant, or expressed genes". In this, there would be no definite single or multiple gene sequence for cancer, but instead a physical disease of the body not exclusive from the genes, caused by structural problems, or the replacement of a group in action, on any level, and yet, potentially, one that causes or interacts with an actual nonuniversal genetic sequence. I would also like to suggest that individual genes do not neccessarily work only as particular groups by themselves, but that each may express a particular group or as many together, on the level of their physical expression of these mutual interactions and active or inactive dynamics.

     I would also like to put fourth three other compatible theses; one, that the actual gene repair process is a physical mechanism, independent of specific gene sequences in the sense of its action or their mutually existing identification, and physically instantiated by a commonly evolving condition upon all genes and the gene repair process, stemming from a collective law of physics (as it would be understood), independent of the specific codes of the genes, with potentially certain exceptions, of which my second thesis here is an instance. The second thesis is that the genes that code for the cellular repair process, if disabled or deactivated by a process of physically unnaturally altered genes, likely cause the cell to activate apopeosis and terminate before replication, as a form of self protecting feature. If the net action of this self protection were reversed but the cell lived it would cause cancer. The last, is that finally, this gives reason to believe that the genetic repair process exists on a level which is nonspecific, so that it may repair itself in the sense of the genes that encode for these proteins or macromolecules, and yet it must do so before the repair process is altered as it evolves from the genes. If this is true, it would mean that the repair process must be repaired at the level of the genetic structure, and also that the error repairing mechanism must remain intact for the cell to repair, and also that one must come first. It must be the genes that are repaired first, for if the error correcting mechanism is lost, then the cell cannot truthfully be repaired by itself. In being capable of acting upon the DNA, as well as all other genes in this process, it serves to protect the entire genetic structure as well as itself.

     As a consequence the cells are capable of maintaining the ability to avoid catastrophy in nearly every instance, terminating themselves if naturally left intact and yet unable to ever repair, or if they may run into states for which they would become a cell with a runaway process, or a type of self mutagenesis, at the level of a single larger mutation which is carried on, or a step which would lead to this upon all other cells from a single cell onwards. If this were not true, a single cell would not be characterized as cancerous, since it would not undergo an uncontrolled cellular mitosis. This condition does not neccessarily include those cells which fluctuate largely in their extremal behaviors throughout multiple generations, such as those which vaccilate to a great degree, and go through stages over multiple lineages and are suceptible to future changes beyond a single earlier cellular mutation spreading over a longer timescale, and those less likely either to be prone to this type of capacity or problem. Those cells with this capacity consequently also develop more slowly as diseases, as cells and as a disease, and although potentially of a longer time scale in their development, are consistent with the notion that cells are less protected by this mechanism at the level of a rapidly developing cell or tissue. If this were not true, there would be no cancers occurring by the process of genes crossing between tissues, or reduced from stem cells, or in long term existant tissues. They would not have developed as far as cells, and would not possess a nature to evade these diseases for very long time scales. They are potentially liable to slip into these disease, however they are more likely capable of being self repaired, given their timescales, and a more robust self correcting mechanism.

     From this we learn that individual cells maintain the ability to exist with at least two complete and independent levels of repair, yet each are in fact dependent and interinvolved on the other in their action and practice. With the notion that gene sequences may be prone to physical problems and not ones of interpretation by us as specific codons, and yet may actually interact with the nature of the reality of this disease as a physically existing problem, we find that the arrow is reversed, from pointing at the genes to instead pointing at the physical aspects of the system of a three dimensional nature within time. This also absolutely finalizes a viewpoint that the genes are complete and independent in their design as given, and that there is really no paradox or closed relation surrounding them, in their expression or otherwise. This means that the cellular repair process is truly emergent from the genes, independent of them in action, and dependent on it in its genesis.