What keeps cancer cells alive?
Interestingly, cause and effect relationships in cancer are difficult to prove e.g. whether shortened telomeres initiate or prevent cancer. Correlative evidence might appear to show that telomere uncapping and resultant DNA damage signals may suppress cancer cell cycle checkpoints, because the damage cannot be repaired in the absence of telomerase. However, when alterations in specific cell cycle regulatory pathways, e.g. inactivation of p53, cells can continue to divide still having critically shortened telomeres, while expressing DNA damage pathways. This is a bypass of senescence (M1) with cells continuing to divide. When many telomeres are shortened to the extent that end - end chromosome fusions occur, this produces chromosome - breakage - fusion - bridge cycles known as M2 or crisis. Crisis stage M2 leads to extensive chromosomal alterations, the hallmark of cancer. It is hypothesized that transpositional states based in quantum entropic conditions lead to transitions from altered cell cycle checkpoints encouraging cells to grow to meet increased energy exigencies. Terminally shortened telomeres may not prevent cell divisions in a rarity of human cells that can bypass this stage. This type of rare cell manifests the hallmarks of telomere stability with reactivation of telomerase. The fundamental mechanisms underpinning a bypass of senescence M1 and continuance to the crisis point (M2) may be based in quantum phenomena which ultimately determine such biochemical changes. Actively dividing cancer cells could then survive and continue to replicate. Further hypothesized is the idea that an electromagnetic physiologic immune response provides the encouragement for certain cells to divide and grow while avoiding crisis stages, in spite of having terminally shortened telomeres. This explanation is proposed for contrasting normal mitosis versus neoplasia.
It is further hypothesized that MRT may stimulate up regulation of telomerase when telomere length diminishes too greatly in specific tissues, and functionality is decreased. Telomerase is projected to be a defensive mechanism of the body, because telomerase increases telomere length. In cancer, when telomeres become too shortened, telomerase is up-regulated to increase telomere length, but in crisis stages, M1 -M2, quantum state entropy is too great for the defensive mechanism to overcome. Thus, telomerase produces increased lengths of telomeres in actively dividing cancer cells, therein keeping the cancer cells dividing and surviving; and as actively mitotic cells increase energies from fissions/ fusions of subatomic particles, the cancer cells increase energy, as the chain reaction proceeds. In simple terms, the cancer cells have superseded the normal cells while using the natural defense mechanisms of normal cells to survive and multiply. The degree of chaos/quantum entropy from fissions/fusions overcomes the natural defense mechanisms based in telomerase production.
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