Summary: The nutrient-dependent microRNA/messenger RNA balance links virus-induced entropic elasticity and the anti-entropic epigenetic effects of nutrient-dependent protein biosynthesis and degradation to everything that is currently known about RNA-directed DNA methylation and RNA-mediated amino acid substitutions. The substitutions differentiate the cell types of all genera. That fact is not being reported in most of the extant literature on healthy longevity and/or pathology.
Here is another example of the failure to report facts about biologically-based cause and effect. Note, specifically, this statement (below): “While the test itself is simple, the science behind it is remarkable” Compare the simplicity of the test to the systems complexity of the science, and you may realize why many current misrepresentations of top-down causation continue to link mutations to evolution. Obviously, the systems complexity must be studied by serious scientists and reported to the biologically uninformed in terms that allow them to continue thinking that species evolve from other species despite the fact that mutations perturb the biophysically constrained chemistry of RNA-mediated protein folding and lead to pathology.
Researchers have found that a genomic biomarker can accurately determine the likelihood of a lung lesion being malignant. The findings that appear online in the New England Journal of Medicine are from two large, prospective, multicenter studies…
“While the test itself is simple, the science behind it is remarkable,” added Spira who also is the Alexander Graham Bell Professor in Health Care Entrepreneurship at BUSM. Previous work by Spira found that the pattern of gene activity in cells lining the upper respiratory tract can identify cancer that is developing deeper in the lung. “The ability to test for molecular changes in this ‘field of injury’ allows us to rule out the disease earlier without invasive procedures. Conceptually, this may have significant implications for other diseases.”
My comment: What is the genomic biomarker that validates the effectiveness of the genomic test for lung cancer detection, which may also “… have significant implications for other diseases.”? Why not tell us what the biomarker is?
See: A Bronchial Genomic Classifier for the Diagnostic Evaluation of Lung Cancer
The use of gene expression in the classification of biologic disease states in clinical specimens is well established.11
My comment: Use of gene expression to classify disease has been well established by experimental evidence of biologically-based cause and effect. See, for example: Biomarkers and microRNAs as Biomarkers in Plasma (below)
The NIH officially defines a biomarker as “a characteristic that is objectively measured and evaluated as an indicator of normal biologic processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention”.
MiRNAs regulate gene expression by targeting individual or multiple messenger RNAs (mRNAs). Perfect or partial base pairing with the target mRNA promotes cleavage of the RNA in plants and inhibition of protein translation in animals. Many studies have demonstrated that dysregulation of these miRNAs is associated with various diseases suggesting there is potential for use of miRNAs in diagnosis and treatment.
A Bronchial Genomic Classifier for the Diagnostic Evaluation of Lung Cancer Revisited
In this study, we describe the evaluation of a bronchial genomic classifier for lung-cancer diagnosis among patients undergoing bronchoscopy in two independent prospective cohorts. We found that the gene-expression classifier had high sensitivity across different lesion sizes, locations, stages, and cell types of lung cancer.
My comment: There is no mention in this article of the fact that microRNAs are biomarkers of gene regulation. MicroRNAs link the nutrient-dependent microRNA/messenger RNA balance from RNA-mediated cell type differentiation to virus-driven pathology or to healthy longevity. There are no citations that link what is known about microRNAs to the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding via amino acid substitutions that stabilize the organized genomes of all genera.
Researchers who bury facts about cell type differentiation in the rhetoric of their reports, or fail to mention anything that might allow others to link their results to what is currently known about biomarkers and gene expression, are not likely to be among those who are Combating Evolution to Fight Disease.
See for contrast: SNPs in MicroRNA Binding Sites as Prognostic and Predictive Cancer Biomarkers
Until recently, the predominant focus for cancer causing SNPs has been limited to nonsynonymous SNPs, those within the protein coding domain that alter the amino acid sequence and, therefore, the protein structure and function of a gene. The majority of SNPs, however, do not alter the amino acid sequence. More and more we are finding that these so-called silent polymorphisms, many of which reside in non-coding regions of the genome, are actually functional. Importantly, these non-coding regions include microRNAs and microRNA target sites.
Since miRNA regulation is dependent on sequence complementarity, it follows that variation in either the mRNA or miRNA sequence will have significant effects.
My comment: Viral microRNAs epigenetically effect sequence complimentarity. That fact links viruses to entropic elasticity. The entropic elasticity is linked to genomic entropy and to cancer via microRNAs in plasma that are biomarkers of pathology and health. Nutrient-dependent microRNAs are the biomarkers of heath and longevity. The anti-entropic epigenetic effects of nutrients are linked to the physiology of reproduction and the fixation of amino acid substitutions that stabilize the organized genomes of all genera.
This leads me to suspect that researchers have identified more microRNAs that can be clearly linked to cancer via A Bronchial Genomic Classifier… If they have, why aren’t they telling us that is what they have done? If they have not, why aren’t they telling us what they have linked to cancer via their classifier?
See for comparison: 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.