Pheromones and cancer

By: James V. Kohl | Published on: April 30, 2013

Transcription Factor-MicroRNA-Target Gene Networks Associated with Ovarian Cancer Survival and Recurrence

Excerpt: “MicroRNAs (miRNAs) are small, non-coding RNA molecules that bind to complementary sequences on target mRNA transcripts, and thus, regulate gene expression at the post-transcription stage. Transcription factors (TFs) are a different type of regulator. These proteins bind to specific DNA sequences in the promoter region, promoting or repressing transcription into mRNA, and thus, regulate genes at a pre-transcription stage [4]. TFs and miRNAs can regulate each other and both can regulate the expression of target genes. TF-miRNA-target genes can function as onco or tumor suppressor networks, triggering global alterations of genetic programs implicated in cell proliferation, differentiation, apoptosis, and invasiveness in cancer.”
My comment: Nutrient-dependent pheromone-controlled seemingly futile cycles of themodynamically regulated protein biosynthesis and degradation alter cellular-level and organism-level thermoregulation. This enables the nutrient-dependent microRNA/messenger RNA balance to modulate 1) cell proliferation 2) cell differentiation 3) unicellular and multicellular ecological niche construction 4) social niche construction 5) neurogenic niche construction (e.g., via synaptogenesis, synaptolysis and apoptosis) and 5) socio-cognitive niche construction in my model of adaptive evolution. (The honeybee is a model organism for many of the factors involved in adaptive evolution).
Nutrient stress and social stress alter the finely tuned microRNA/messenger RNA balance, which helps to explain the link from life’s stressors to mutations, abnormal cell differentiation, and abnormal cell proliferation. The point can now (i.e., again) be made that there is a difference between typical and atypical fine-tuning of the microRNA/messenger RNA balance.
What’s typical does not involve mutations because mutations are not adaptive. Furthermore, as we see in the disease processes they cause, mutations are not finely-tuned as is required for them to be beneficial. Besides, there is no means known by which one organism can naturally select for a mutation (or select for accumulated mutations) in another organism.
What’s typical does involve nutrients and their metabolism to pheromones that control reproduction because the common molecular mechanism of species from microbes to man ensure the required species-specific niche construction (i.e., ecological, social, neurogenic and socio-cognitive). Typically, natural selection is for nutrients (food) and species-specific pheromones control reproduction, which is why I detailed those facts in the context of an explanation for the socioaffective nature of evolved behaviors (sans mutations theory).
What happens in cancer:
“The relationships among transcription factors, microRNAs and target genes can be visualized as interconnected networks. These intricate webs are often used to determine how diseases such as cancer proceed. Analyzing how these networks function in cancer can offer insight into how tumor cells proliferate and differentiate, undergo (or resist) programmed cell death, and how likely they are to become invasive.”
What happens in evolutionary theory.
Others denigrate my works and attack me personally for my Christian beliefs, my commercial involvement, my profession (medical laboratory scientist) et al. They do not address the content of my model and now one antagonist claims that: “Finally, someone provides an explanation of how environmentally-induced and epigenetically employed phenotype change can result in evolutionary change, and which utilizes our current understanding of biological processes.” This fool, has also been personally responsible for misrepresenting cause and effect to members of groups like evol-psych and human-ethology. With enough people like him misleading others, scientific progress comes to a halt. So, ask yourself, how many people are there like Clarence ‘Sonny’ Williams. Are all of them delaying progress with cancer research? Could evolutionary theorists, in general, someday return us to the ‘dark ages’ of medical practice? Or are they merely slowing scientific progress and thereby causing only a little more human suffering?

My comment to the discussion groups: Williams must certainly know how much I resent his implication that: “Finally, someone provides an explanation of how environmentally-induced and epigenetically employed phenotype change can result in evolutionary change, and which utilizes our current understanding of biological processes.”
Most participants here also realize that my model provides a detailed “…explanation of how environmentally-induced and epigenetically employed phenotype change can result in evolutionary change, and which utilizes our current understanding of biological processes.” However, lest anyone think that Williams is providing new information, here are two links that note the importance of switching between epigenetic states, which is obviously not done via random mutations.
Reversible switching between epigenetic states in honeybee behavioral subcastes
Abstract: In honeybee societies, distinct caste phenotypes are created from the same genotype, suggesting a role for epigenetics in deriving these behaviorally different phenotypes. We found no differences in DNA methylation between irreversible worker and queen castes, but substantial differences between nurses and forager subcastes. Reverting foragers back to nurses reestablished methylation levels for a majority of genes and provides, to the best of our knowledge, the first evidence in any organism of reversible epigenetic changes associated with behavior.
News release:
“What is exciting is that the genes that change back are the same genes that changed in the other direction initially — and the same ones that would regulate epigenetic behaviour,” says Feinberg. Gene Robinson, a bee researcher at the University of Illinois at Urbana-Champaign, who was not involved in the research, says that although the paper does not necessarily prove that epigenetic mechanisms cause behavioural differences, “it demonstrates for the first time that if behaviour is reversible so is the methylation”.  A greater understanding of how epigenetics affects behaviour may lead to insights into human biology, Feinberg says, noting that epigenetic effects on human behaviour might express themselves in addiction, learning and memory. If the link between behaviour and methylation patterns “is true in a bee, it is likely to also be true in us”, he says.
My comment: Robinson (from above) with Elekonich (2000): Organizational and activational effects of hormones on insect behavior, extended our 1996 model of hormone-organized and hormone-activated mammalian behavior to the honeybee model organism. Thus, since 1996, we have known that the mutations theory of adaptive evolution was on its way out. Now we can see why it has taken so long to remove it from any consideration whatsoever. We have people telling us that “Finally, someone provides an explanation of how…” —-when the explanation of how has been available since 1996. See for example: From fertilization to adult sexual behavior. 
Molecular epigenetics
“Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA…”

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