Darwinian medicine: Nothing in cancer makes sense except in the light of [evolution]? Wow.

The essence of cancer and evolution is: "Mutations cause cancer and destroy function." DLH

cornu, Methinks that you are equivocating. There isn't anything about cancer that requires "knowing" that Common Descent is true. There isn't anything about cancer that requires "knowing" that natural selection and other blind, mindless processes produced the diversity of life. ET

Of course there's a link between cancer and evolution: "Evolution is the Cancer on the science of Biology" See? It all makes sense. Nonlin.org

Does this simply not show that population genetics is useful at the microevolutionary scale, which nobody really disputes? The problem as soon as Dobzhansky gets quoted is the old failure to define what "evolution" means in context. Does "The origin of Species" cast any light on cancer, or cancer on the history of life? No. Does the way genes vary in populations give insights that apply to cancer? Yes. Hooray for Gregor Mendel. Jon Garvey

Using "evolutionary principles" in the research of cancer, to the extent they are believed to be true for how all life came to be on earth, are only bound to mislead researchers rather than inform successful treatments:

Jonathan Wells Dismantles Joshua Swamidass’s Argument for Evolution from Cancer - September 11, 2017 https://evolutionnews.org/2017/09/jonathan-wells-dismantles-joshua-swamidasss-proof-for-evolution-from-cancer/ Mutant Destruction: Does Cancer Really Innovate? by Jonathan Wells - 2017 Excerpt: computational biologist Joshua Swamidass argues that "cancer regularly innovates with proteins of novel function."2 He calls this "neo-functionalization." According to Swamidass, this "casts serious doubt on the ID arguments from molecular biology," namely, that proteins cannot evolve novel functions without the aid of intelligent design. He concludes that if ID were true, "then cancer as we know it would be mathematically impossible, or regularly require the direct intervention of God to initiate and be sustained."3 Innovation or De-regulation? But is it true that "cancer regularly innovates with proteins of novel function?" Many cancers have alterations in their DNA that are called "gain-of-function" mutations. But how novel are the functions that are gained? Two classes of "genes" (protein-coding regions of DNA) that have been widely studied in cancer are "proto-oncogenes," which, when mutated, lead to the uncontrolled growth that characterizes cancer cells, and "tumor suppressor genes," which normally prevent cancer but when mutated fail to block it. The former include genes of the Ras family, while the latter include the TP53 gene. Ras genes produce signaling proteins that induce cells to divide. In normal cells, Ras proteins (gene names are italicized, while the proteins encoded by them are not) are turned off much of the time, but when mutated, they get stuck in the "on" position (a condition called "constitutive activation"). So they induce cells to divide without stopping.4 Although this is called a "gain-of-function" mutation, the Ras protein hasn't actually gained a new function. It has simply lost the ability to regulate its old one.5 The TP53 gene encodes a protein called p53 that has many functions. It binds to specific DNA sequences, but it also interacts with many other molecules involved in cell metabolism.6 In normal cells, the functions of p53 prevent the cell from becoming cancerous, but when TP53 mutates, this function is abolished. The mutant protein still binds to DNA, but it has lost its ability to target specific sequences, so it interacts with regions of DNA that are unaffected by normal p53. The mutant protein (designated mutp53) also accumulates at a much higher concentration than normal p53 (designated "wild-type" p53, or wtp53). Like wtp53, mutp53 continues to interact with many other molecules in the cell, but those interactions are now perverted to the point where the cell becomes cancerous and invades other tissues.7 This does not necessarily mean that mutp53 acts through mechanisms different from those of wtp53. The mutant protein binds to more regions of DNA than wtp53, not because it has gained anything, but because it has lost its sequence specificity. And the other effects of mutp53 are not as novel as they seem. According to Israeli cancer researchers Moshe Oren and Varda Rotter, "given the high concentration of mutp53 protein in tumor cells, relatively weak molecular interactions, which are marginal within the wtp53 protein, may now be amplified by mass action and reach a threshold that allows them to exert a measurable impact on biochemical processes within the cell."8 In 2012, philosopher of biology Pierre-Luc Germain emphasized that the "new" functions in cancer cells "are not complex adaptations; in other words, they are not the result of cumulative evolution. . . . Instead, it is the pre-existing wiring of the cell which best accounts for these features." In other words, "healthy cells—their structure, possible states, pathways, and weak spots—already contain the resources to be drawn upon and developed by cancer cells."9 So the neo-functionalization that Swamidass attributes to cancer cells is really the de-regulation and perversion of existing functions, rather than the creation of new ones. Polar Opposites Swamidass goes on to argue that "evolutionary theory 'makes sense' of cancer." We see "all the same genetic patterns in cancer tumors that we see in, for example, humans [and] the great apes."10 Most DNA changes in cancer cells are not "driver" mutations that contribute to malignancy, but "passenger" mutations that simply go along for the ride. This is consistent with the modern "neutral theory of evolution," which says that most DNA mutations have little or no effect and persist because they are not eliminated by natural selection. According to Swamidass, "this is true for cancer, and it is also true for the evolution of new species." In other words, "cancer evolves with the same evolutionary mechanism that drives the evolution of new species."11 But we don't actually know what drives the evolution of new species. Except for some examples of chromosome doubling in plants (which can lead to reproductive isolation, though not to new organs or body plans), the origin of species is as much a mystery today as it was when Charles Darwin wrote his book by that name. No one has ever observed the origin of a new species by mutation and selection—certainly not by the accumulation of neutral mutations. What we do observe is cancer. http://www.salvomag.com/new/articles/salvo42/mutant-destruction.php

Again, as mentioned in post 3, In so far as knowledge of Darwinian processes allows advances in medicine, those advances come solely from the realization that Darwinian processes are excellent at breaking things in biology but are woefully inadequate when it comes to creating any new functional complexity in biology. It is in realizing the strict limits of Darwinian processes to ever create new functional complexity that effective medical treatments can be developed to combat diseases. This is since medicines can be administered in precise, and knowledgeable, ways that ‘destructive’ evolutionary processes will never be able to overcome.

Fighting Cancer with Intelligent Design – Casey Luskin – December 25, 2015 Excerpt: “In fighting antibiotic resistance, Darwin’s theory actually provides little guidance. Indeed, quite the opposite. As SUNY Professor of Neurosurgery Michael Egnor has written here, “Darwinism tells us that … bacteria survive antibiotics that they’re not sensitive to, so non-killed bacteria will eventually outnumber killed bacteria. That’s it.” To create drugs that outsmart evolving bacteria or cancer cells, biomedical researchers must use a process of intelligent design. They create drug cocktails that bank upon the fact that there are limits to how much living things can evolve on their own. Far from being evidence for Darwinian theory, antibiotic resistant bacteria point to what Michael Behe has called “the edge of evolution,” beyond which unguided Darwinian processes are powerless.” In simple terms, Darwinian evolution tends to work fine when only one mutation is needed to give an advantage. But when you need multiple mutations to gain an advantage, the process tends to get stuck. By throwing lots of antibiotic drugs at an organism, we force it to evolve lots of mutations — more than Darwinian evolution can produce — in order to survive. In this way, we can beat antibiotic-resistant microbes.,,, Dr. M. William Audeh at UCLA School of Medicine. He makes the same point with regard to fighting cancer.,,, He says we kill cancer cells by using many (“combinations of”) drugs — more than they can possibly evolve resistance to. When he says that we can “overcome the adaptive potential of the population,” he means there are limits to how much cancer cells can evolve. If we intelligently design combinations of drugs that would require more mutations than could possibly arise via Darwinian evolution, then we kill cancer cells before they evolve mutations to evade our therapy techniques. - per ENV

A particularly clear example of 'evolutionary principles' misleading researchers is in animal testing (including testing on monkeys), where billions of dollars have been wasted because of the false Darwinian assumption of common descent:

What scientific idea is ready for retirement? – Mouse Models Excerpt: A recent scientific paper showed that all 150 drugs tested at the cost of billions of dollars in human trials of sepsis failed because the drugs had been developed using mice. Unfortunately, what looks like sepsis in mice turned out to be very different than what sepsis is in humans. Coverage of this study by Gina Kolata in the New York Times incited a heated response from within the biomedical research community. AZRA RAZA – Professor of medicine and director of the MDS Centre, Columbia University, New York http://www.theguardian.com/science/2014/jan/12/what-scientific-idea-is-ready-for-retirement-edge-org Animal Testing Is Bad Science: Point/Counterpoint Excerpt: The only reason people are under the misconception that animal experiments help humans is because the media, experimenters, universities and lobbying groups exaggerate the potential of animal experiments to lead to new cures and the role they have played in past medical advances.,,, The Food and Drug Administration (FDA) has noted that 92 percent of all drugs that are shown to be safe and effective in animal tests fail in human trials because they don’t work or are dangerous.,,, Physiological reactions to drugs vary enormously from species to species. Penicillin kills guinea pigs but is inactive in rabbits; aspirin kills cats and causes birth defects in rats, mice, guinea pigs, dogs, and monkeys; and morphine, a depressant in humans, stimulates goats, cats, and horses. http://www.peta.org/issues/animals-used-for-experimentation/animal-testing-bad-science.aspx Comparing the human and chimpanzee genomes: Searching for needles in a haystack – Ajit Varki1 and Tasha K. Altheide – 2005 Excerpt: we have many characteristics that are uniquely human. Table 1 lists some of the definite and possible phenotypic traits that appear to differentiate us from chimpanzees and other “great apes”2. For the most part, we do not know which genetic features interact with the environment to generate these differences between the “phenomes”3 of our two species. The chimpanzee has also long been seen as a model for human diseases because of its close evolutionary relationship. This is indeed the case for a few disorders. Nevertheless, it is a striking paradox that chimpanzees are in fact not good models for many major human diseases/conditions (see Table 2) (Varki 2000; Olson and Varki 2003). http://genome.cshlp.org/content/15/12/1746.full

i.e. The overall physiology of different species are drastically different:

Mouse gene expression reveals “widespread differences” from humans - Nov. 22, 2014 Excerpt: an international group of researchers has found powerful clues to why certain processes and systems in the mouse — such as the immune system, metabolism and stress response — are so different from those in people.,,, Mice are widely used to model human metabolism, disease, and drug response. But results published today (November 17) in PNAS reveal widespread differences between human and mouse gene expression, both in protein-coding and noncoding genes, suggesting that understanding these disparities could help explain fundamental differences in the two species’ physiology. Michael Snyder of Stanford University and his colleagues compared how genes are expressed in 15 different human and mouse tissues, including brain, heart, liver, and kidney. They found that gene expression patterns clustered by species rather than tissues. For example, gene expression in a mouse liver more closely resembled the patterns observed in a mouse heart than those observed in a human liver. https://uncommondesc.wpengine.com/genetics/mouse-gene-expression-reveals-widespread-differences-from-humans/

This drastic difference in physiology includes humans and chimpanzees:

Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012 Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,, A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species. On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,, http://www.the-scientist.com/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%2F Frequent Alternative Splicing of Human Genes – 1999 Excerpt: Alternative splicing can produce variant proteins and expression patterns as different as the products of different genes. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC310997/ Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing - 2016 In Brief Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,, Page 806 excerpt: As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms (Smith and Kelleher, 2013). http://iakouchevalab.ucsd.edu/publications/Yang_Cell_OMIM_2016.pdf

bornagain77

ET, The paper in the OP includes some of the information. This older review is a nice summary of how evoluionary principals can be brought to bear on cancer biology. Here is a recent review of how using phylogenetics in tumour biology has helped us understand the progression of cancers. The first paper to take this phylogenetic approach has been cited > 4,000 times, which suggests it's been a useful method! There are many more studies on these topics if you want to search for them. cornu

Cancer most definitely sheds light on evolution. Variation offers immediate selective advantage. Variant exploits selective advantage, resulting in extinction of not only itself and its base type, but its entire ecosystem. Wait, what? LocalMinimum

The application of evolutionary biology methods and principals to cancer biology have become increasingly important in recent years.

Your say-so is meaningless. Try to actually make your case. ET

as to his claim from Greaves's article:

"Dobzhansky’s insight applies not just to biology but to much in medicine."

Actually, it might interest Mel Greaves to know that Dobzhansky’s famous article, "Nothing in Biology Makes Sense Except in the Light of Evolution," is actually a Theological argument that has little to nothing to do with actual biology:

Nothing in biology makes sense except in light of theology? - Dilley S. - 2013 Abstract This essay analyzes Theodosius Dobzhansky's famous article, "Nothing in Biology Makes Sense Except in the Light of Evolution," in which he presents some of his best arguments for evolution. I contend that all of Dobzhansky's arguments hinge upon sectarian claims about God's nature, actions, purposes, or duties. Moreover, Dobzhansky's theology manifests several tensions, both in the epistemic justification of his theological claims and in their collective coherence. I note that other prominent biologists--such as Mayr, Dawkins, Eldredge, Ayala, de Beer, Futuyma, and Gould--also use theology-laden arguments. I recommend increased analysis of the justification, complexity, and coherence of this theology. http://www.ncbi.nlm.nih.gov/pubmed/23890740

Realizing that, then it makes perfect sense that Darwinists would claim cancer as proof of evolution. The argument from Darwinists goes like this, "Evolution must be true because a loving God would never allow such a evil thing as cancer to exist." And their you go, no experimental or mathematical proof needed. Just claim that you know exactly what God would and would not allow and call it a day. In so far as knowledge of Darwinian processes allows advances in medicine, those advances come solely from the realization that Darwinian processes are excellent at breaking things in biology but are woefully inadequate when it comes to creating any new functional complexity in biology. It is in realizing the strict limits of Darwinian processes to ever create new functional complexity that effective treatments can be developed that combat diseases. This is since medicines can be administered in precise, and knowledgeable, ways that 'destructive' evolutionary processes will never be able to overcome.

Guide of the Perplexed: A Quick Reprise of The Edge of Evolution - Michael Behe - August 20, 2014 Excerpt: If there were a second drug with the efficacy of chloroquine which had always been administered in combination with it (but worked by a different mechanism), resistance to the combination would be expected to arise with a frequency in the neighborhood of 1 in 10^40 -- a medical triumph. http://www.evolutionnews.org/2014/08/guide_of_the_pe089161.html

Using Behe's 'Edge of Evolution' to Fight Disease (even Cancer):

Fighting Cancer with Intelligent Design - Casey Luskin - December 25, 2015 Excerpt: "In fighting antibiotic resistance, Darwin's theory actually provides little guidance. Indeed, quite the opposite. As SUNY Professor of Neurosurgery Michael Egnor has written here, "Darwinism tells us that ... bacteria survive antibiotics that they're not sensitive to, so non-killed bacteria will eventually outnumber killed bacteria. That's it." To create drugs that outsmart evolving bacteria or cancer cells, biomedical researchers must use a process of intelligent design. They create drug cocktails that bank upon the fact that there are limits to how much living things can evolve on their own. Far from being evidence for Darwinian theory, antibiotic resistant bacteria point to what Michael Behe has called "the edge of evolution," beyond which unguided Darwinian processes are powerless." In simple terms, Darwinian evolution tends to work fine when only one mutation is needed to give an advantage. But when you need multiple mutations to gain an advantage, the process tends to get stuck. By throwing lots of antibiotic drugs at an organism, we force it to evolve lots of mutations -- more than Darwinian evolution can produce -- in order to survive. In this way, we can beat antibiotic-resistant microbes.,,, Dr. M. William Audeh at UCLA School of Medicine. He makes the same point with regard to fighting cancer.,,, He says we kill cancer cells by using many ("combinations of") drugs -- more than they can possibly evolve resistance to. When he says that we can "overcome the adaptive potential of the population," he means there are limits to how much cancer cells can evolve. If we intelligently design combinations of drugs that would require more mutations than could possibly arise via Darwinian evolution, then we kill cancer cells before they evolve mutations to evade our therapy techniques. http://www.evolutionnews.org/2015/12/merry_christmas_1101861.html

The multiple drug cocktail that has been so effective in controlling HIV uses much the same strategy of being beyond the 'edge of evolution' that Dr. Behe has elucidated:

When taking any single drug, it is fairly likely that some mutant virus in the patient might happen to be resistant, survive the onslaught, and spawn a resistant lineage. But the probability that the patient hosts a mutant virus that happens to be resistant to several different drugs at the same time is much lower.,,, it "costs" a pest or pathogen to be resistant to a pesticide or drug. If you place resistant and non-resistant organisms in head-to-head competition in the absence of the pesticide or drug, the non-resistant organisms generally win.,,, This therapy has shown early, promising results — it may not eliminate HIV, but it could keep patients' virus loads low for a long time, slowing progression of the disease. http://evolution.berkeley.edu/evolibrary/article/medicine_04

bornagain77

Dobzhansky's Phrase should be rewritten as: "Nothing in biology makes sense except in the light of reproduction." ...then, "Nonthing in cancer makes sense except in the light of reproduction." Now it makes sense. Peer

Not sure why this headline needs the "wow". The application of evolutionary biology methods and principals to cancer biology have become increasingly important in recent years. I think much of Darwinian medicine is pretty useless (at least clinically) but evolutionary epidemiology and the evolutionary biology of cancer are two obvious exceptions. cornu