Complex behaviors of cell types in cancer

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Decoding the emergence of metastatic cancer stem cells

Excerpt: “By applying a physics-based approach to understand the dynamics of cancer decision-making, we were able to explain a number of recent experimental observations, including some that seemed contradictory.”

My comment: The logic of the physics-based approach links physics, chemistry, biology, and math, etc. to conserved molecular mechanisms at the same time theorists tout their pseudoscientific nonsense about “mutations.” See, for example: Cancer’s deadly mutational tug of war

Excerpt: Mutations are either driver mutations—required for tumors to progress—or passenger mutations—additional random mutations that result from such rapid adaptation.

My comment: This interpretation of the report places the emergence of metastatic cancer stem cells back into the context of evolutionary theory, which ignores the physics-based approach.

In what might otherwise become intelligent discussions, theorists cite published works that also claim that biophysically-constrained “mutations” cause what they cannot. Others have ignored the Laws of Physics and made claims about mutations since the invention of neo-Darwinism. The Modern Synthesis was invented by definitions that excluded any facts about how cell type differentiation actually occurs. Mutations somehow led to the evolution of biodiversity via what Darwin called natural selection, and theorists accepted the assumptions as if they were based on scientific facts about how cell type differentiation occurs in species from microbes to man. Indeed, a recent text went so far as to claim that “… genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.

In the context of the physics-based approach, cell type differentiation occurs via seemingly futile cycles of nutrient-dependent protein biosynthesis and degradation that lead to the pheromone-controlled physiology of reproduction. The direct link from the epigenetic landscape to the physical landscape of DNA in organized genomes is clearly via RNA-directed DNA methylation and RNA-mediated amino acid substitutions. Genomic conservation only occurs when amino acid substitutions stabilize the DNA of organized genomes. However, no matter how much accumulated experimental evidence of amino acid differentiated cell types attests to that fact, theorists believe in mutations and evolution.

See, for example, The Man Who Bottled Evolution, which is a simple-minded approach to what serious scientists have now shown in Structure and mechanism of the tRNA-dependent lantibiotic dehydratase NisB, reported as Team discovers how microbes build a powerful antibiotic.

Excerpt: Researchers have long known the sequence of the nisin gene, and they can assemble the chain of amino acids (called a peptide) that are encoded by this gene. But the peptide undergoes several modifications in the cell after it is made, changes that give it its final form and function. Researchers have tried for more than 25 years to understand how these changes occur.

My comment: This tells us that genomic conservation only occurs when nutrient-dependent changes to the amino acid sequence determine organism-level genomic stability via changes to the peptide sequence (i.e., the sequence of amino acids) that give proteins their final form and function. Constraint-breaking mutations lead to perturbed protein folding and final forms that are not functional. For example, cancer cells are comparatively undifferentiated with unstable genomes.

Pretending that cells with unstable genomes somehow could lead to the evolution of biodiversity attests to the need for a physics-based approach, which is critically important due to ongoing ridiculous speculation by theorists. For comparison to ridiculous theories about “constraint-breaking mutations”,  physicists incorporate aspects of  “arity” that link physics to the chemistry of protein folding and to the molecular biology of amino acids substitutions that differentiate cell types in my model. For example, “We show that the miR-200/ZEB module functions as a ternary switch…” Physicists are more likely than pseudoscientists to link the ternary switch to the quaternary switch detailed in the context of a report, which states that “…cryptophytes have evolved a structural switch controlled by an amino acid insertion to modulate excitonic interactions and therefore the mechanisms used for light harvesting.

Did the quaternary switch evolve before the ternary switch, which is linked to cancer. I suspect a link from the light-induced amino acid substitution and quaternary structure of the switch to cell type differentiation and/or cancer via the nutrient-dependent microRNA/messenger RNA balance whether the nutrient source is light or micro-nutrients associated with the ternary switch link to cancer. There are reasons for me to place my assertions about this link into the context of physics, chemistry, and the conserved molecular biology of cause and effect in species from microbes to man.

For example, the senior author of the article about the ternary switch and cancer is known to me via the International Paleopsychology Project, where we both participated. Eschel Ben-Jacob’s monograph(s) are also important to anyone who hopes to understand the difference between theorists and serious scientists.

See (2003): Bacterial self-organization: co-enhancement of complexification and adaptability in a dynamic environment

Excerpt: “…self-organization reflects the system’s freedom of response, which is not predetermined.”

My comment: In my model, self-organization is determined by the effects of olfactory/pheromonal input, which link the epigenetic landscape to the physical landscape of DNA in the organized genomes of microbes to man.

See also (2009): Learning from Bacteria about Natural Information Processing

Abstract excerpt: I describe how complex colony forms (patterns) emerge through the communication-based interplay between individual bacteria and the colony. Individual cells assume newly co-generated traits and abilities that are not prestored in the genetic information of the cells, that is, not all the information required for efficient responses to all environmental conditions is stored. To solve newly encountered problems, they assess the problem via collective sensing, recall stored information of past experience, and then execute distributed information processing of the…  [10,000,000,000 – 10, 000,000,000,000] bacteria in the colony—transforming the colony into a “super-brain.” I show illuminating examples of swarming intelligence of live bacteria in which they solve optimization problems that are beyond what human beings can solve.”

My comment: In the context of increasing organismal complexity, the ability of bacteria to solve their optimization problems must be linked to the ability of other organisms to solve their optimization problems via the conserved molecular mechanisms of nutrient-dependent pheromone-controlled cell type differentiation. Theorists who think mutations can lead to increasing organismal complexity via the evolution of biodiversity in bacteria ignore the fact that the biodiversity of bacteria is constrained by the Laws of Physics, and requires the chemical complexity of amino acid substitutions and proper protein folding.

(2013) MicroRNA-based regulation of epithelial–hybrid–mesenchymal fate determination

Re: “…how to distinguish between the aberrant dynamics of epithelial–hybrid–mesenchymal transitions during tumorigenesis vs. the normal programs of embryonic development and tissue regeneration.”

My comment: Mutations can play no part in the normal programs of embryonic development and tissue regeneration because they perturb protein folding. That explains why theorists who tout the link between mutations and evolution do not link ecological variation to ecological adaptations and biodiversity. Instead, they have been taught to believe in the impossible, and they believe in it because it is simple. Their explanations did not require decades of efforts to elucidate the links between physics, chemistry, and the conserved molecular mechanisms of ecological speciation.

As I mentioned before, “Researchers have tried for more than 25 years to understand how these changes occur.” Theorists, instead, cite 25 years of experiments with E. coli as the basis for claims that mutations somehow lead to the evolution of “…all biological innovations and the enormous amount of biodiversity in this world.

Do physicists believe in that utter nonsense? I doubt it!  Serious scientists are more likely to believe that “Simply put, starved cells send a chemical signal conveying their stress. Each of the other bacteria uses the information to `interpret’ the state of the colony relative to its own, and accordingly signals its peers to sporulate or not to sporulate.” So far as is known, only nutrients and their metabolism to species-specific pheromones that control the physiology of reproduction in species from microbes to man link ecological variation to ecological adaptations and ecological speciation.

See: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans. It is clear that nutrient stress acts via RNA-directed DNA methylation and RNA-mediated events that link physics to the chemistry of protein folding, which links amino acid substitutions cell type differentiation and the organism-level stability of DNA in organized genomes.

Other serious scientists, like Eshel Ben-Jacob can now join me in thanking Howard Bloom — who, unfortunately, still may be billing himself as “The Amazing Atheist” — for bringing us together in a project that has led to very thorough refutations of the pseudoscientific nonsense touted by evolutionary theorists, evolutionary theists, and many human ethologists and atheists who are among virtually all social scientists with no understanding of biologically-based cause and effect. However, that fact makes it important to note that science fiction novelist, Greg Bear, also participated in Howard Bloom’s International Paleopsychology Project, and he linked human pheromones to human species diversity in two of his novels. See his blog post entry from discussions at 05/24/2006 05:44:30 PM.

Excerpt: Acknowledgments (with my emphasis):
Special thanks to Mark Minie, Ph.D., and Rose James, Ph.D.; Deirdre V. Lovecky, Ph.D.; Dr. Joseph Miller; Dominic Esposito of the National Cancer Institute; Dr. Elizabeth Kutter; Cleone Hawkinson; Alison Stenger, Ph.D.; David and Diane Clark; Howard Bloom and the International Paleopsychology Project; Cynthia Robbins-Roth, Ph.D., James V. Kohl, Oliver Morton, Karen Anderson, Lynn Caporale, and Roger Brent, Ph.D.

My comment: My creationist views present a conflict that remains unresolved among many of the former participants in the International Paleopsychology Project. That conflict appears to be closer to revolve via the ongoing efforts of serious scientists like Eshel Ben-Jacob, who appear to have not accepted what evolutionary theorists claim is the link from mutations to the evolution of biodiversity via the perturbed protein folding associated with cancers.

Thank God someone is investigating cell type differentiation in the context of health and disease rather than attributing both reproductive fitness and disease to mutations and evolution.

See also: Complex behaviors: science fiction and scientific facts Even if Eshel Ben-Jacob has not already found it, the key to cell type differentiation in health and disease will obviously be found within the systems complexity of nutrient-dependent pheromone-controlled ecological adaptations, not in ridiculous theories about mutations and evolution. Indeed, the evolutionary theorists have probably already indirectly caused the deaths of many who believed in their theories and many who did not, but suffered and died from the consequences of ignorance. Clearly, it is past time to consider what is currently known about Downward causation by information control in micro-organisms and link it from ecological variation in the supply of nutrients to the pheromone-controlled physiology of reproduction that enables ecological speciation manifested in the morphological and behavioral phenotypes of species from microbes to man.

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