“If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based.” — Denis Noble
Excerpt: “In a new study, UCLA researchers analyzed the gene-expression profiles of more than 2,000 patients and were able to identify cancer-specific gene signatures for breast, lung, prostate and ovarian cancers. The study applied an innovative approach to gene-array analysis known as “surprisal analysis,” which uses the principles of thermodynamics—the study of the relationship between different forms of energy—to understand cellular processes in cancer.”
My comment: This article “miRNA and mRNA cancer signatures determined by analysis of expression levels in large cohorts of patients” integrates what is known about RNA-directed DNA methylation and the RNA-mediated DNA/RNA protein synthesizing system and biological information with the thermodynamics of intercellular interactions. A robust microRNA/messenger RNA (miRNA / mRNA) balance exemplifies a finely tuned, calibrated, and standardized reference state. Deviation from the finely tuned miRNA / mRNA balance exemplifies the cancer-specific disease pattern. The deviation is “…a signature comprised of unique mRNAs and miRNAs capable of distinguishing diseased patient samples from normal controls.” Thus, the importance of Nutrient-dependent / Pheromone–controlled thermodynamics and thermoregulation to distinguishing between an atypical or typical miRNA / mRNA balance becomes more important to the diagnosis and treatment of cancer, or to prevention. For example, I wrote: “Disease is associated with mutations exemplified in cancer where perturbations of the glucose-dependent thermodynamic/thermoregulatory equilibrium are equally clear (Locasale, 2012).”
However, it is simply not possible to differentiate bottom-up nutrient-dependent epigenetic effects on thermodynamics and stochastic gene expression from top-down pheromone-controlled epigenetic effects on organism-level thermoregulation until others realize that common molecular mechanisms are involved across species and that only one neuronal signaling pathway is required in mammals. The gonadotropin releasing hormone (GnRH) neuronal system is responsible for thermodynamically controlled organism-level thermoregulation in mammals. Yet the origins of this neuronal system can be traced back to single-celled yeasts at the advent of sexual reproduction that predicts sex differences in hormone-linked cancers and other disease states. This means thermodynamics alone cannot help us better understand human cancers. Cancer must be understood in the context of organism-level thermoregulation and adaptive evolution by differentiating it from theories that incorporate mutation-initiated natural selection. Mutations perturb the thermodynamics of intercellular signalling, and no organism naturally selects for anything involved in cancer.
Researchers must begin to popularize biological facts and continue to fight against the popularity of mutations theory. We can then better teach others to understand the epigenetic effects of nutrient stress and social stress on cancer, which is not adaptive, and also help others to begin to better understand many things about adaptive evolution. See, for example, this 5.5 minute video representation from my 2013 International Society for Human Ethology Summer Institute Poster presentation: “Nutrient-dependent / pheromone-controlled adaptive evolution: (a mammalian model of thermodynamics and organism-level thermoregulation)”