A failed theory of cancer: two more decades of pseudoscience
Cancer is evolution taking place inside multi-cellular organisms. Cancer cells are perversely adaptive and proliferate faster than normal cells. Since evolution has no foresight, it doesn’t matter that the end result of cancer evolution is the death of the cancer along with its host. But cancer cells are subject to the same evolutionary pressures as other cells. Amazingly, only a tiny group of researchers are taking this approach to cancer.
Conclusion by David Sloan Wilson:
The idea that something as scientific and biological as medicine might not be evolutionary has to be explained to a lot of people. It’s wonderful to get this snapshot of cancer research from an evolutionary perspective and congratulations for all the great successes you’ve been having.
My comment: Defects in the atomic structure of tungsten are not beneficial. Many people may not understand an explanation of evolution that links point defects in physics to point mutations and cancer.
See: Three-dimensional coordinates of individual atoms in materials revealed by electron tomography reported as Researchers Determine the Three-Dimensional Positions of Individual Atoms for the First Time
These imperfections, known as point defects, can weaken materials, which can be dangerous when the materials are components of machines like jet engines.
See also: Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA reported by John Hewitt as: Mitochondrial DNA mutations: The good, the bad, and the ugly. (See also: Attempts to discuss his report degrade into opinionated comments on my published works and expertise.)
My comment: The question remains: “How could defects in the DNA that encodes key proteins in the mitochondrial machinery that converts energy from food to a form of chemical energy required for RNA-mediated cell type differentiation be beneficial?”
No matter what they are called, point defects and/or point mutations, are not beneficial. The defects alter energy conversion in materials or hydrogen-atom transfer in DNA base pairs in cell types.
That is why all the serious scientists I know are “Combating Evolution to Fight Disease.” They have learned the difference between a mutation and an RNA-mediated amino acid substitution. And they are citing Dobzhansky (1973), which included an important example of that difference.
With an afterword by E. L. Doctorow—the Pulitzer Prize-winning novel of one man’s pursuit of intellectual freedom in the face of ignorance and corruption, from the author of Babbit
Arrowsmith, the most widely read of Sinclair Lewis’s novels, is the incisive portrait of a man passionately devoted to science. As a bright, curious boy in a small Midwestern town, Martin Arrowsmith spends his free time in old Doc Vickerson’s office avidly devouring medical texts. Destined to become a physician and a researcher, he discovers that societal forces of ignorance, greed, and corruption can be as life-threatening as the plague.
Part satire, part morality tale, Lewis’s Pulitzer Prize-winning novel illuminates the mystery and power of science while giving enduring life to a singular American hero’s struggle for integrity and intellectual freedom in a small-minded world.
My comment: The “… societal forces of ignorance, greed, and corruption…” are still the driving force behind some important aspects of healthy longevity. For example, please see again this claim (above): ‘Cancer is evolution taking place inside multi-cellular organisms.” I do not think cancer is not a part of healthy longevity — except to teleophobic neo-Darwinian theorists. A teleophobe might also exclaim:
For contrast, a serious scientist might complain.
See also: Thanks academia, soon I will join a generation of jobless PhDs
After entering a PhD programme, it became obvious that when in academia, the only respectable future job is in academia. Becoming an academic is typically considered the holy grail for PhDs in the sciences.
My comment: Denis Noble, is an academic. See: OBC | The Music of Life
Denis Noble is one of the pioneers of Systems Biology and developed the first viable mathematical model of the working heart in 1960. His research focuses on using computer models of biological organs and organ systems to interpret function from the molecular level to the whole organism. Together with international collaborators, his team has used supercomputers to create the first virtual organ, the virtual heart. He is also a philosopher of biology, and the author of :”The Music of Life.”
My comment: He introduces his lecture and his biased perspective with the caveat “The Music of Life” has no conductor. In Physiology is rocking the foundations of evolutionary biology, he makes it clearer.
The twenty-first century can look forward to a new synthesis that will reintegrate physiology with evolutionary biology.
My comment: Nothing could be further from the truth.
As with the evolution of other complex structures and processes (29–32), we have shown the bacterial flagellum too originated from “so simple a beginning,” in this case, a single gene that underwent successive duplications and subsequent diversification during the early evolution of Bacteria.
My comment: No experimental evidence of biologically-based cause and effect links successive duplications and subsequent diversification to the evolution of Bacteria. Like all living genera they must ecologically adapt to variation, and the adaptations are nutrient-dependent. The adaptations also are controlled by the physiology of reproduction. Is the nutrient-dependent physiology of reproduction what Denis Noble claims leads to evolution? How long does he think it takes a different species to evolve?
After 96 hours of incubation of AR2 and Pf0-2x at room temperature on SMM, two breakout mutations were visible, conferring first slow (AR2S and Pf0-2xS) and then fast (AR2F and Pf0-2xF) spreading over the agar surface (Fig. 1A). The AR2F strain produces flagella, but we could not detect flagella in electron microscopy samples for AR2S (Fig. 1B). Genome resequencing revealed a single-nucleotide point mutation in ntrB in strain AR2S, causing an amino acid substitution within the PAS domain of the histidine kinase sensor NtrB [Thr97→Pro97 (T97P)] (13). The fast-spreading strain AR2F had acquired an additional point mutation in the σ54-dependent EBP gene ntrC, which alters an amino acid (R442C) within the DNA binding domain (Table 1 and table S2).
My comment: They also reported this:
Although de novo origination of new functions in nature is likely to take longer and involve more mutational steps, this system enables us to understand the adaptive process in detail at the genetic and phenotypic level. We identified a tractable model for gene network evolution and observed, in real time, the rewiring of gene networks to enable the incorporation of a modified component (NtrC′) creating a novel regulatory function by a highly repeatable two-step evolutionary pathway with the same point mutations often recurring in independent lineages.
My comment: Others claimed that this functional structure was irreducibly complex. The nutrient-dependent pheromone-controlled weekend evolution placed that complexity into the context of reintegrating physiology with evolutionary biology. The example of weekend evolution occurred in the context of only two nutrient-dependent amino acid substitutions and the RNA-mediated events that linked them to the physiology of reproduction. The physiology of reproduction is linked to chromosomal rearrangements, which are required for the biodiversity of morphological and behavioral phenotypes to exist in all living genera.
Metaphorically, this chain of events is like playing your favorite symphony or “Unchained melody” in a split second and enjoying it as much as a lifetime of epigenetically-effected transitions in your morphology that must be linked from affects of hormones to RNA-mediated amino acid substitutions and your behavior.
…33% of the human population present a BDNF Val66Met SNP that leads to a valine-to-methionine substitution in the BDNF protein at codon 66, and this SNP has been associated with increased susceptibility to development of stress-related disorders (21, 22).