Oliver Thewalt

    Oliver Thewalt

    Theoretical Physics | Quantum Biology | Dark Matter Research Cluster

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    Cancer Research by Quantum Biology - An Introduction based on contemporary microbiology

    Working Hypothesis:

    There is no cancer as such, the approach to treat cancer as a disease is not very helpful: what is missing in western science it to understand that there are mind and environment (also radiation and toxic substances) induced "quasi inflammatory" metastatic states on quantum level ..... ~Quantum Biology



    Quote by DuJuan Ross as comment to this article: Cancer may be an Ancient ‘Safe Mode’ Mechanism that Evolved to Protect Us

     

    "It's MUTATION, Evolution of biology does not function without mutation. Therefore,for the continued fitness of entire species to profit from evolution,some mechanism has to weed out alleles in danger of becoming obsolete. Tragic from a human familial standpoint. But vital in the aegis of whole orders."

     

    Cancer Cells - Course of cellular evolution

    Unquote

     

     I agree to the thesis by DuJuan Ross, that cancer is not a disease as such.

     

     

    1. Is cancer a metabolic rebellion against host aging? In the quest for immortality, tumor cells try to save themselves by boosting mitochondrial metabolism

    2. DuJuan Ross

    Quote:"

     

    >The mutiny-preventive stopgaps and checkpoints serving the integrity of a human cell that must be faithfully photocopied betw. 100 and 120 TRILLION times commands an ineffably crucial task.Rare as nuclear laminopathies occur in live births,still,the photocopyng hardware can and does get missensed sometimes, yes,even after 8,000,001 successful births. Aberrant cells w/ misshapen, herniated nuclei can only replicate non-stop morphologic pathogenesis throughout a body. Defective nuclear mechanics, due to breached scaffolds and faulty membranous anchoring of filament, sets off a chain reaction of senescence-events that range from susceptibility to heat shock, to cardiomyopathy, then to early demise.

    .......In Nature, ants and bees commit suicide for the good of their colonies. Likewise, a fundamental feature of organic Life, is the apoptosis of certain cells whose usefulness to the soma ostends to be superfluous at some point. In the early history of cancer treatment, researchers operated under a significant misapprehension: instead of looking for agents that kill dividing cells, they should have been looking for agents that coaxed cell suicide...!

    ....Now that research is on the right path,results in curing some cancers may improve. Chemotherapy has not been wholly ineffective,mind you!.But its effectiveness was only by accident (It does manage to alleviate short-term agony in some victims of malignancies).

     

    .........Mutation in nature is random,but selection is not. Both are needed for a species to continue to thrive, gene-wise.Mutation in a most important gene in chromosome 17 is the defining feature of a lethal cancer. In some 55% of all human cancers, TP53 is defective. That figure rises to 92% in lung cancers. People born with a defective version of TP53 out of the 2 inherited autosomally, have a 95% chance of getting cancer.

     

    ......Now, oncogenes are genes that encourage a cell to grow. For normative expression purposes, it's vital that these genes are switched OFF most of the time.If they become jammed ON, the result can be disastrous. As serum sodium in a cell is the polar opposite cation of a potassium ion, tumor suppressors, coded by TP53, are the opposite of oncogenes.

    Whereas oncogenes cause cancer if jammed ON, tumor suppressor genes cause cancer if they are jammed OFF.


    ----The job gets done by various means, the most prominent way being to arrest a cell at a certain point in the cycle of its division and growth, then 'release it from arrest at a certain checkpoint in the proteomic sytem if all its papers are in order', so to speak. To progress beyond THAT much, ergo, a tumor must contain a cell that has both a jammed-on oncogene and a jammed-off tumor suppressor gene.

    Unlikely event, thankfully, but that's not the omega of the affair! To avoid scrutiny and grow uncontrollably, a tumor must now evade an even more stringent checkpoint, manned by a gene that looks for abnormal behavior in a cell membrane and issues a cue to different genes to dismantle that cell from the inside, i.e. commit suicide. This is what TP53 does by coding for the protein p53.

     

    .........One of the primary jamming-on oncogenes --- one that works in concert to promote Farnesyltransferase inhibition so as to normalize nuclei afflicted with progerin -cumulus---- is called RAS. It has 3 variants: H, K and N, each with specific proofreading roles. As oncogenes go, early-on in mammalian evolution, there may only have been one called MYC. Both division and death are triggered by this gene.


    Problem with a lone oncogene type is that external forces, mainly viral, co-evolve too clever at duping it with false survival signals. Cells, thus, that were earmaked for suicide kept on multiplying monstrously, as is the pattern....

    ..... So, like a government initiative to establish correective checks and balances, a three-branch motif allowed for two more co-equal oncogenes to tether together. The others were BCL-2 and RAS, controlling each other's rampancy and gullibility to false signals from viruses.

    RAS, in the aegis of nuclear morphology,signals an enzyme called GGTase1 (geranygeranyl transferase) to buffer the efficacy of zinc mettalloprotease STE-24 and the actual CaaX motif by adding a 20-carbon isoprenoid feature to the tetrapeptide box domain. Mainly, this is to ensure continuous membrane-friendliness of associated protein residues by causing stronger hydrophobicity needed for them to link up.

    ...........Viruses, however, are notorious for learning from their past insufficiencies! Human papillomavirus,which causes cervical cancer, for example,boasts 2 genes whose job it is to switch off TP53 from making the guardian protein p53. It has also 'learned' to cancel orders for other tumor suppressors that usually come thru in reconnaissance roles.

     

    ------Diseases attributed to the mutancy of LMNB-1 and LMNB-2 are only about 3. It works in much the same way as the A laminopathies do,but minus prelamin degradation and fewer prenylated protein truncations distorting its CaaX motif. LMNB-1 is vital for gene transcription and mitosis, and its irregularities are on chromosome 5q23.3 and 5q31.1 where myelodysplasias in the form of Pelger-Huet Anomaly (PHA) is the result of a mislocalized lamin B receptor site.


    Cerebellar dysgenesis eventually happens when the myelin sheathing erodes and avails the CNS to unbearable cumulative stress.. More common is the defect,point mutational, due to lamin B-2 disappearance at pos. 13.3 on chromosome 19's short arm. This is where lipdystrophy in the guise of Barraquer-Simons Syndrome causes complete loss of adipose fat in limbs and neck.

    More severe still, is adult-onset autosomal dominant leukodystrophy, which attacks the CNS in progressive stages after teen years (ADLD). Myelin-loss of the cerebellum at this magnitude may be attributable to the gross overexpression of a B lamin.

     

    There are still many gaps in understanding the pathogenesis of laminopathic diseases. Investigation will improve with the sophistication of an already - superlative toolkit, I believe."

    Unquote DuJuan Ross

     

     

     Cancer cell vs normal cell

    Additional Source:

    Prelamin A causes progeria through cell-extrinsic mechanisms and prevents cancer invasion

     

       

    Oliver Thewalt 15.10.2014

    My question to DuJuan Ross in this context was:

     

    Why don't those cells commit suicide? (Why is apoptosis no more happening sometimes? ("programmed" cell death))

     

    His answer:

     

    Quote: (DuJuan Ross)"

     

    Only a choice number of cells are designated for apoptosis. Apoptosis is as fundamental to organic life as metabolism and cell division. Oncogenes have a small window of regulatory time for catalyzing cell growth. Tumor suppressors use the topoisomerase p-53 to police cells so that oncogenes don't overgrow. But, sometimes p-53 gets tricked and oncogenes keep growing, disobeying commands to kill themselves. This leads to rogue tissue growth."
    Unquote

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    Research Article about Quantum Biology and Cancer Research


    Papers that will be discussed:

    Two-compartment tumor metabolism: autophagy
    in the tumor microenvironment and oxidative
    mitochondrial metabolism (OXPHOS) in cancer
    cells.

     

    Cytotoxic killer t cell attacking a cancer-cell

     

    http://www.tandfonline.com/doi/full/10.4161/cc.11.2.19006

    http://www.nature.com/ncomms/2013/130806/ncomms3268/full/ncomms3268.html

     

     Cytotoxic T Cells on Patrol

    http://www.zmescience.com/science/physics/cancer-safe-mode-mechanism-402343/

    Sudbury Impact: Extraterrestrial demise of banded iron formations 1.85 billion years ago

    Iron: A biological element?

     

     

    No Apoptosis on quantum level
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    Join Hixgrid Group: Cancer Research by Systems and Quantum Biology