Bacterial ‘communication system’ could be used to stop, kill cancer cells, study finds

Excerpt: “During an infection, bacteria release molecules which allow them to ‘talk’ to each other,” said the lead author of the study. “Depending on the type of molecule released, the signal will tell other bacteria to multiply, escape the immune system or even stop spreading.”

My comment: Nutrient-dependent cell type proliferation is pheromone-controlled during health and infections — and in other diseases and disorders. The conserved molecular mechanisms of RNA-directed DNA methylation link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. Health and pathology are determined by atomic-level competition for nutrients, which are required to support thermodynamic cycles of RNA-mediated protein biosynthesis and degradation of the proteins. Controlled protein biosynthesis and degradation enables organism-level thermoregulation.

Infections associated with fever are manifestations of how the morphological and behavioral phenotypes of bacteria can kill us if the bacteria can tolerate higher body temperatures than the human body can produce. Cancers associated with local perturbations of seemingly futile thermodynamic cycles of protein biosynthesis and degradation are manifestations of what occurs in the context of one-carbon metabolism of nutrients.

When the cycles of protein biosynthesis are not controlled by nutrient uptake, cell type differentiation is not controlled. For example, vitamin-dependent DNA repair fails when dietary intake prevents microbes from establishing the delicate balance of microRNAs to messenger RNA that typically results in amino acid substitutions that stabilize cell type differentiation. Stabilized cell types resist stress in the context of atoms and ecosystems.

Evolutionary theorists ignore the requirement to link atoms to ecosystems in species from microbes to man. Instead, they claim mutations and natural selection lead to the evolution of antibiotic resistance in bacteria. They also claim that mutations lead to the evolution of biodiversity. Those claims ignore biophysical constraints on nutrient-dependent pheromone-controlled cell type proliferation. That’s how the ignorance of evolutionary theorists has contributed to deaths from cancer. They ignore biologically-based cause and effect in the context of how atoms and ecosystems must concurrently interact to facilitate ecological adaptations.

Meanwhile, medical laboratory scientists support accurate representations of biologically-based cause and effect. Accurate representations are required so that physicians can diagnose and treat disorders of organism-level thermoregulation that include infections and cancer. Cancers may metastasize and lead to death via the same perturbed molecular mechanisms that lead to death by bacterial or viral infections. When their cell types reach the critical mass required to overcome the immune system-wide defenses of the organisms they infect or infest, the microbes control what researchers have not — until now — noticed are the result of conserved molecular mechanisms, which are perturbed by nutrient stress and social stress.

“Under such circumstances,  the synergistic use of tissue diagnostic techniques and microbiology is paramount to render an accurate diagnosis (p. 92).” Patel, R., Rhodes, J., Spicknall, K. E., & Mortensen, J. (2014). Case Twenty NIne: The synergistic role of microbiology and pathology. Journal of Continuing Education Topics & Issues, 16(3), 88-92.

An accurate diagnosis leads to proper treatment. Under all circumstances of nutrient-dependent pheromone-controlled cell type proliferation and diagnostic medicine, the failure to consider the synergistic role of microbiology and pathology can be attributed to evolutionary theorists. It seems that most of them would rather contribute to the death of us all rather than admit that mutations cause disease, not the evolution of biodiversity.

Biodiversity arises in the context of nutrient-dependent RNA-directed DNA methylation and RNA-mediated events that stabilize cell types via amino acid substitutions. Cell type proliferation is controlled by the degradation of proteins to species-specific pheromones that control the physiology of reproduction in species from microbes to man via conserved molecular mechanisms. Killing cancer requires integration of what is already known about stress and pheromone-controlled cell type proliferation.

Additional resources:

“Bacteria that use quorum sensing constitutively produce and secrete certain signaling molecules (called autoinducers or pheromones). These bacteria also have a receptor that can specifically detect the signaling molecule (inducer).”

Bacterial Quorum Sensing Molecule N-3-Oxo-Dodecanoyl-L-Homoserine Lactone Causes Direct Cytotoxicity and Reduced Cell Motility in Human Pancreatic Carcinoma Cells

“In a process called inter-kingdom signaling, bacterial QS molecules may modulate or influence the behavior of eukaryotic cells… It also appears that O-DDHSL can inhibit mammalian cell proliferation and cause cell death in certain cell types….”

Epigenetic Vestiges of Early Developmental Adversity: Childhood Stress Exposure and DNA Methylation in Adolescence “Biological embedding is said to occur when: experience gets under the skin and alters human biological processes; systematic differences in experience, under different nurturant conditions, lead to different bio-developmental states; the differences are stable and long term; and these differences influence health, well-being, learning, or behavior over the life course.

Human pheromones: integrating neuroendocrinology and ethology

Kumar, A., Dudley, C. A., Chackravarty, S., & Moss, R. L. (2010). Pheromones. In G. Fink (Ed.), Stress Science: Neuroendocrinology (pp. 746-753). San Diego: Academic Press.

 

 

 

 

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