Gene expression, immortality, and cancer

By: James V. Kohl | Published on: May 19, 2015

Collaborative research team solves cancer-cell mutation mystery


TERT stabilizes chromosomes by elongating the protective element at the end of each chromosome in a cell. …cells harboring these mutations aberrantly increase TERT expression, effectively making them immortal.

My comment: To an evolutionary theorist, this might suggest that protein folding instability is beneficial. For example, see: “Mutation-Driven Evolution

…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.

The ability of theorists to link genomic instability to the evolution of biodiversity attests to their ignorance of what is known to serious scientists about the biophysically constrained chemistry of nutrient-dependent RNA-mediated amino acid substitutions and the physiology of reproduction that enables fixation of the amino acid substitutions in the organized genomes of all genera.
My comment: What aspect of the cancer-cell mutation mystery was solved? The researchers showed the complexity of the interactions among factors that biophysically constrain the chemistry of nutrient-dependent protein folding. The systems complexity that links metabolic networks to genetic networks ensure that nutrient-dependent RNA-mediated amino acid substitutions help to prevent mutations.
Excerpt from the conclusion of: The transcription factor GABP selectively binds and activates the mutant TERT promoter in cancer 

Further work is necessary to elucidate which other transcription factors are interacting with GABP at the mutant TERT promoter in order to drive aberrant transcription.

My comment: They attempted to solve the funding problem that might otherwise cause an early end to their careers and the careers of future researcher who have been taught that:

…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.

For comparison, see:  Evolution of MicroRNA Research Over the Past Decade

More than 20,000 microRNA-Focused Publications Were Assessed as a Means to Characterize the Field

My comment: The microRNA/messenger RNA balance determines all downstream aspects of cell type differentiation in health and disease. That fact has become clear during the past decade. I was politely informed of that fact, when I asked Tim Bredy if that was his claim after his 2012 symposium presentation “Memories of non-coding RNA” at the Society for Neuroscience annual meeting in New Orleans. His focus was on RNA-mediated cell type differentiation in the brain. I was surprised at how closely his presentation followed what we detailed about RNA-mediated sex differences in cell types in our 1996 Hormones and Behavior review: From Fertilization to Adult Sexual Behavior.

Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans…

My comment: Clearly, I had not learned anything that was known to nearly everyone else who attended the symposium. I was embarrassed, but confirmed that fact with Gunter Eckert and several others as I continued to learn more about microRNAs and nutrient-dependent cell type differentiation. I welcomed the invitation to submit a review of nutritional epigenetics to the jounal nutrients after publication of Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
See: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.

My comment: The Evolution of MicroRNA Research Over the Past Decade has eliminated most of the pseudoscientific nonsense about mutations and evolution that has been taught by advocates of neo-Darwinism to unsuspecting students who do not realize that population geneticists bastardized everything Darwin wrote about the importance of nutrient-dependent ‘condition of life.’ Although serious scientists are now Combating Evolution to Fight Disease, evolutionary theorists still package their ridiculous claims in the context of reports on research like this one: The transcription factor GABP selectively binds and activates the mutant TERT promoter in cancer. The report reveals that mutations are linked to pathology without one word about prevention.
For comparison, two recent reports have linked everything currently known about RNA-mediated cell type differentiation to homeostatic plasticity, structural plasticity, neural development, activity-dependent plasticity, dendrite morphology, and neuronal homeostasis via what is known about the honeybee model organism and life history transitions in humans.
See: Structural homeostasis in the nervous system: A balancing act for wiring plasticity and stability  and see: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults.
The across-species link to health and longevity may be simply described as a nutrient-dependent link from the Val158Met amino acid substitution to behavior during life history transitions that help to ensure successful reproduction via nutrient-dependent microRNAs and DNA repair mechanisms that prevent the manifestations of pathology attributed to mutations.

The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012). — cited in Kohl (2013)

For more details on the obvious links from entropic elasticity to genomic stability via nutrient-dependent microRNAs and protein folding, see the individual articles published in a special issue of the journal “Nutrients.”
The details are scattered across so many articles that evolutionary theorists may continue to tout their ridiculous claims about beneficial mutations, but these published works are among others that link what is currently known about cell type differentiation to ongoing refutations of ridiculous theories.
10/2014 The Influence of Early Life Nutrition on Epigenetic Regulatory Mechanisms of the Immune System
10/2014 Nutrients Intake Is Associated with DNA Methylation of Candidate Inflammatory Genes in a Population of Obese Subjects
12/2014 Insights from Space: Potential Role of Diet in the Spatial Organization of Chromosomes
01/2015 The Interaction between Epigenetics, Nutrition and the Development of Cancer
03/2015 What Do Studies of Insect Polyphenisms Tell Us about Nutritionally-Triggered Epigenomic Changes and Their Consequences?

See also: from 2013 Amino Acid Profiles in Term and Preterm Human Milk through Lactation: A Systematic Review


Significant differences among the different geographical regions were observed for a handful of TAA (tyrosine, proline, histidine, methionine, and tryptophan) and FAA (lysine, phenylalanine, methionine, and isoleucine).

My comment: This is the missing link from an obvious explanation of how ecological variation is linked from the availability of nutrients to the pheromone-controlled fixation of RNA-mediated amino acid substitutions and ecological adaptations in morphological and behavioral phenotypes of species from microbes to man.  Dobzhansky (1973) mentioned it in the context of differences in primates.


…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla” (p. 127).

My comment: Cancer researchers are more than 40 years behind factual representations of experimental evidence that differentiates the role of mutations from the role of nutrient-dependent RNA-mediated amino acid substitutions. The substitutions stabilize the organized genomes of all genera. That fact attests to the powerful role that neo-Darwinism has played. It continues to contribute to pathology and death by theory as the contributions of those who are Combating Evolution to Fight Disease are ignored or criticized by biologically uninformed science idiots.

See for example: Criticisms of the nutrient-dependent pheromone-controlled evolutionary model and the thesis of Andrew Jones, the author. He concludes his criticisms of my model with this statement. “…James Kohl presents an unsupported challenge to modern evolutionary theory and misrepresentations of established scientific terms and others’ research. It was a mistake to let such a sloppy review through to be published.

In his thesis he claims:

Despite their challenges, ribozymes have made an interesting niche for themselves in the field of abiogenesis. The evolution of a successful RNA polymerase ribozyme is a lofty goal. While its discovery would not be the be-all and end-all of abiogenesis research, it would represent an important stepping stone between prebiotic chemistry and life. The encapsulation of such a ribozyme is also an important step, as it would enable a system of heredity and evolution through natural selection. Based on progress in current research, it is only a matter of time before that ribozyme is discovered.

Abiogenesis is to cancer as mutations and theory are to accurate representations of how nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions are to health and longevity.

Abiogenesis is a ridiculous approach to disease by theorists who think that the differences between health and pathology have not been detailed in my model of RNA-mediated amino acid substitutions and cell type differentiation in all genera. Mutations lead to undifferentiated cell types. Amino acid substitutions ensure the stability of organized genomes.

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