A physicist clueless about cancer lectures cancer biologists on...cancer!

There's a good rule of thumb about headlines (other than Betteridge's Law of Headlines) that I use when perusing articles. It's particularly useful for evaluating headlines about medical and science stories. Basically, if a headline says something like, "everything you know about X is/might be/could be wrong" or "everything scientists know about X is/might be/could be wrong," it's a highly reliable indication that much of what is in the article that follows is very likely to be unmitigated, grade-A bullshit. I realize that it might be confirmation bias on my part (I am, after all, a skeptic), but it's a rule of thumb that has rarely let me down. It is, after all, a very lazy trope on the part of editors and journalists designed to pique the reader's interest and imply that there's been some sort of radical new finding that's overturned much of what scientists thought about a topic before. Science, of course, doesn't usually work that way. Findings that totally overturn a scientific paradigm are rare; most new findings are evolutionary, not revolutionary. This is good for science. It's not so good for news stories and headline writers.

My rule definitely didn't let me down yesterday, too, as I started seeing on my social medial an article in Newsweek by Jessica Wapner that definitely follows it. Oh, sure, there's a paragraph or two out of a very long article presenting one scientist criticizing the crank idea presented, but for the most part the article is all credulous praise. Entitled, A New Theory on Cancer: What We Know About How It Starts Could All Be Wrong, the title fits the pattern, as does the article that follows. It is unmitigated, grade-A bullshit. Not only that, to the lazy trope of lionizing a "scientific maverick" (whose ideas are, of course, what show us that "what we know about how cancer starts could all be wrong") who is most unworthy of lionization. Unsurprisingly, it is a theoretical physicist. It could be confirmation bias on my part again, but it sure does seem that physicists seem particularly prone to entering a new field, coming up with a new "insight" in it, and then wondering why all the scientists there hadn't thought of the insight he's had and indeed reject it. In any case, it's a physicist we have met before, Paul Davies, who three years ago with his partner in crime Charles Lineweaver (another physicist, in this case an astrophysicist) made a splash with his idea that cancer is a throwback to an ancient genetic “sub-routine” where the mechanisms that usually instruct cells when to multiply and die malfunctions, thus forcing the cells to revert back to a default option that was programmed into their ancestors long ago, or, as it's called, an atavism, a "reawakening" of ancient genetic subroutines. I wrote about it then. I described why his ideas are wrong and how they've inspired a quack. So did biologist P.Z. Myers (multiple times) Nothing's changed since then, except that Wapner cranked up the worship of the Brave Maverick Scientist to a cringe-inducing 11.


Paul Davies knows what’s wrong with cancer research: too much cash and too little forethought. Despite billions of dollars invested in fighting this disease, it has remained an inscrutable foe. “There is this assumption that you can solve the problem by throwing money at it,” he says, “that you can spend your way to a solution.” Davies, a theoretical physicist at Arizona State University (ASU)—and therefore somewhat of an interloper in the field of cancer—claims he has a better idea. “I believe you have to think your way to a solution.”

Bloody hell. As a cancer surgeon and biologist, I couldn't help but be monumentally pissed off when I read this paragraph. The hubris just oozes from every word of Davies' quoted. So does the condescension and contempt for us poor, poor, oncologists, surgeons, and cancer biologists, who (or so Davies apparently thinks) are so deeply embedded into the existing paradigm that they can't appreciate the brilliance of his insights. ""I believe you have to think your way to a solution"? What does he think cancer biologists have been doing for well over a century now, dating back to the 1800s? Sitting around in their labs waiting for that sweet, sweet grand money to flow in, so that they can do whatever experiment that pops into their heads on any given day?

He also betrays the bias of his background as a theoretical physicist. Let me give him an education. To make progress against cancer takes a lot more than "thinking." Yes, thinking is important, but it's worthless without actual experimental evidence from the laboratory, which is then translated into the clinic and validated through clinical trials. This is a process that can take decades, of which "thinking" is only the first step. The hard work of cancer biology, like any science, is not necessarily coming up with ideas and insights. The real thinking that has to be done is to design strategies to assess which ideas lead to testable hypotheses that can result in a better understanding of cancer and, at least as importantly, identify mechanisms that can be targeted for therapy. The hubris that Davies demonstrates is breathtaking, and Wapner doesn't call him out on it in the least.

If you don't believe me that Davies is peddling grade-A bullshit, then check out this next passage:

Over the course of several years spent pondering cancer, Davies has come up with a radical approach for understanding it. He theorizes that cancer is a return to an earlier time in evolution, before complex organisms emerged. When a person develops cancer, he posits, their cells regress from their current sophisticated and complex state to become more like the single-celled life prevalent a billion years ago.

But while some researchers are intrigued by the theory that cancer is an evolutionary throwback, or atavism, plenty more think it’s silly. That theory suggests that our cells physically revert from their current form—a complex piece in the even more complex puzzle that makes a lung or a kidney or a brain—to a primitive state akin to algae or bacteria, a notion that seems preposterous to many scientists. Yet gradually, evidence is emerging that Davies could be right. If he is—if cancer really is a disease in which our cells act like their single-celled ancestors of eons ago—then the current approach to treatment could be all wrong.

"Gradually evidence is emerging that Davies could be right"? No. It's not. Really, it's not. Nothing Davies has thought of is remotely new. As I discussed a long time ago, it is not surprising that the hallmarks of cancer described by Douglas Hanahan and Robert Weinberg in 2000 and updated in 2011. The original six hallmarks were:

  1. sustaining proliferative signaling
  2. evading growth suppressors
  3. resisting cell death
  4. enabling replicative immortality
  5. inducing angiogenesis
  6. activating invasion and metastasis

Cancer biologists have known for a long time that the genes involved in developing cancer control cellular processes like these, and these processes are very ancient ones. Just because these processeas are ancient, however, does not mean that Davies is correct. His first line of argument is that cancer is found in virtually all multicellular organisms have cancer, which is true but basically irrelevant. Then he argues:

The evidence that cancer is an evolutionary regression goes beyond the ubiquity of the disease. Tumors, says Davies, act like single-celled organisms. Unlike mammalian cells, for example, cancer cells are not programmed to die, rendering them effectively immortal. Also, tumors can survive with very little oxygen. To Davies and his team, which includes Australian astrobiologist Charles Lineweaver and Kimberly Bussey, a bioinformatics specialist at ASU, that fact supports the idea that cancer emerged somewhere between 1 billion and 1 and a half billion years ago, when the amount of oxygen in the atmosphere was extremely low.

Tumors also metabolize differently from normal cells. They convert sugar into energy incredibly fast and produce lactic acid, a chemical normally resulting from metabolism that takes place in the absence of oxygen. In other words, cancer cells ferment, and scientists don’t know why. This phenomenon is known as the Warburg effect, named for Otto Warburg, a German biochemist who won a Nobel Prize in 1931 for his discoveries about oxygen and metabolism. Up to 80 percent of cancers display the Warburg effect. Researchers know that many cancers depend on the Warburg effect for their survival, but they don’t know why. To Davies, the strange way in which tumors metabolize also speaks of cancer’s ancient past: They are behaving as if there were no oxygen available.

Yes, tumor cells are not programmed to die (a process called apoptosis, or programmed cell death), an essential process in building multicellular organisms, particularly of keeping cells under control and from proliferating outside of control of the organism. However, as P.Z. Myers notes, there are normal cells that have the same ability, such as germ line cells. As a cancer biologist myself, I can't help but note that another relevant cell type is the stem cell. Stem cells are cells that can differentiate into any cell type and have in essence unlimited replicative potential. It would make more sense to say that cancer cells in some ways resemble stem cells, and, yes, cancer stem cells are a hot (if controversial) area of research. Just ask Max Wicha, a pioneer in the field. Unlimited replicative ability is not an atavistic property.

As for surviving in very little oxygen, mammalian cells do the same thing. It is not an atavistic property. When oxygen tension is low, they revert to glycolysis, which doesn't require oxygen. The disadvantage is that glycolysis produces much less energy per molecule of glucose than oxidative metabolism does. It is true that many tumor cell types do "prefer" glycolysis over aerobic metabolism. It's something that Otto Warburg observed back in the late 1920s, and it's the reason that PET scans work. PET scans use radiolabeled glucose Tumor cells, because of their dependence on glycolysis, use a lot of glucose, which means that areas with tumor cells "light up" on PET, allowing the detection of tiny tumor deposits. I've discussed the Warburg effect on multiple occasions. Again, there's nothing "atavistic" here.

It's also not as though we don't understand some of these things as well. The Warburg effect is associated with the PKM2 isoform of a key enzyme in glycolysis, pyruvate dehydrogenase. Attempts to use inhibitors of aerobic glycolysis in the clinic or other drugs that target the Warburg effect have not been dramatically successful.

Although PZ did a fine job deconstructing this nonsense, but, being a cancer physician, I found one part that really stood out to me:

Davies thinks the moneyed and narrow focus on targeted therapeutics is misguided. These new drugs tend to focus on attacking cancer’s strengths rather than its weaknesses; its muscle rather than its Achilles’ heel. For example, a medication might be designed to stop the abnormal protein that is allowing a cell to divide without stopping.

I laughed out loud when I read this. How stupid we are, we cancer biologists. We never would have thought of this without a genius like Davies to lead the way. Oh, wait. We did think of it. Long ago. Targeting mechanisms of that allow cancer cells to evade apoptosis is a major focus of cancer research. It's even listed as one of Hanahan and Weinberg's hallmarks of cancer! Bloody hell! The contempt Davies must have for the long history of cancer research is palpable. Small armies of scientists, postdocs, and graduate students have been working on just this problem for decades! Let's put it this way. I started graduate school in 1990, and apoptosis was a major focus of research. I could show Prof. Davies my Cancer Biology class notes from then if he likes. (I'm pretty sure I still have them somewhere.) Davies makes it sound so easy, doesn't he? Oh, and it's not "the abnormal protein" that allows cells to divide without stopping. It's proteins, as in many, and there are other forms of programmed cell death besides apoptosis.

It gets worse:

But, says Davies, for as long as cell division has existed, so have threats to it. “Life has had 4 billion years to evolve responses to those threats,” he says. Tumors are incredibly adept at circumventing the stress of a new drug by developing genetic abnormalities that preserve their ability to divide. Cancer patients know this strength all too well: Many once-potent therapies stop working because tumor cells become resistant, eventually exhausting all treatment options.

The atavistic theory portends new approaches. Drugging tumors with the lowest possible dose could prevent the evolution of therapy-resistant pathways that would otherwise enable the cancer to spread around the body. “You don’t have to get rid of it,” says Davies, “you just need to understand it and control it.”

Bloody hell times a thousand! Yes, tumor cells become resistant. It's what they do. They're genetically unstable and have a high rate of mutation, which leads to a lot of tumor heterogeneity, with the cells different parts of tumors often being quite different from each other, upon which selective pressures can work. Chemotherapy and other drugs are a powerful selective pressure that forces them to evolve resistance.

As for using low dose chemotherapy, Davies is behind the times, too. Has he never heard of metronomic chemotherapy? I have. Robert Kerbel first proposed it at least 15 years ago, and it is exactly what Davies describes, using the lowest possible dose of chemotherapy administered continuously or frequently. Of course, the goal here is not to keep resistance from developing. It's actually based on Judah Folkman's pioneering work on tumor angiogenesis (the ability of tumor cells to induce the ingrowth of blood vessels to supply its nutrient and oxygen needs. The idea is that low dose chemotherapy is antiangiogenic and targets the endothelial cells lining the blood vessels. There is a form of chemotherapy based on evolutionary considerations, though, known as adaptive chemotherapy. These ideas all long predate Davies' leaping into the field of cancer research as the Great Physics Hope here to save us dumb physicians and biologists from our own stupidity.

Speaking of angiogenesis, if there's a characteristic of tumor cells that is not the least bit atavistic, it's the cancer cell's ability to induce angiogenesis to feed itself. Single cell organisms have no need for angiogenesis. Nor do they have the need for the ability to evade an immune system. These are characteristics of multicellular organisms that cancer cells retain. Moreover, if you get into the weeds, you find that cancer cells interact with normal host cells and each other, and that that interaction is necessary for its spread and survival. There was just an interesting paper earlier this month that shows how cancer cells interact with host blood vessels and immune cells in order to invade the vasculature and spread via the bloodstream. When tumor cells arrive at other organs, it's their ability to adhere to the surrounding collagen and cells and begin to grow that determines whether they turn into metastases. There's a whole field known as tumor microenvironment that studies the interaction of cancer cells with the surrounding cells, structural proteins, and circulating signaling molecules of the host.

To shamelessly paraphrase Douglas Adams, cancer is complicated. Really complicated. You just won't believe how vastly, hugely, mind-bogglingly complicated it is. I mean, you may think it's a complicated to figure out your computer, but that's just peanuts to cancer. Basically Davies cherry picks aspects of cancer that are shared with ancient single-celled organisms and ignores all the characteristics that are not. He dismisses the "existing paradigm" that cancer is primarily a genetic disease and ignores very old observations that certain tumor suppressors and oncogenes are directly associated with cancer. In some cancers, targeting these genes is an effective treatment. Gleevec, for instance, targets a single abnormal protein.

Then he has the audacity to complain:

Many oncologists are skeptical that it ever will. Evolutionary biologist Chung-I Wu, at the University of Chicago, calls the atavistic theory “an extreme position.” Scientists have also criticized Davies’s reference to the discredited “recapitulation theory” that human embryos develop temporary vestigial organs—gills, a tail, a yolk sac—as support for the atavistic model. “I’ve been ridiculed by the biology community,” says Davies.

Yes, Davies has been ridiculed. I'm ridiculing him now. He richly deserves it. Like all good cranks, though, Davies views the ridicule as evidence that he's right:

Davies is unfazed by the objections. “My feeling is, Who cares? The idea was to come in from the outside and lend a fresh perspective,” he says. Davies sees the criticism as largely rooted in territoriality and financial concerns. “Cancer is a multibillion-dollar industry that’s been running for decades. There’s a lot of vested interests out there.” After five years with the NCI program, Davies is now funded by NantWorks, a sprawling private health care company owned by scientist and billionaire investor Patrick Soon-Shiong (who made his fortune reworking the breast cancer drug paclitaxel to be more effective) to continue his work developing the atavistic model.

Ah, yes. The last refuge of the crank. When scientists ridicule your ideas, attack big pharma and the "territoriality" of cancer researchers. Now, don't get me wrong. Scientists are human. They can be territorial. They sometimes protect their turf. They can have financial interests. But notice something. Davies had a National Cancer Institute grant to pursue his vision. The clear implication in the paragraph above is that he doesn't have it anymore, which means that he likely failed to renew it, which means that the NCI found his reapplication wanting. Why might that be? In fairness, NIH grants are hard to get, but the implication is that Davies failed to produce enough promising data with his approach to convince the NCI to renew his grant. So now he's in bed with big pharma himself! I wish he'd tell me: Why is it so horrible for scientists he dismisses as in the thrall of the existing paradigm and protecting their turf to be—dare I say—colluding with big pharma, but it's perfectly fine for him to be funded by a billionaire's health care company?

Of course, it's not just Davies. There's an oncologist, Mark Vincent, who should really know better but unfortunately seems to be trying to out-Davies Davies:

Vincent, who had his first atavism insight at around the same time as Davies, is also pursuing the theory. Vincent takes the single-celled phenomenon one step further, believing that cancer could be its own species. The stark difference between our healthy cells and cancerous ones looks more like a jump across the evolutionary tree rather than a hop to another branch. “It seems to me to be a different form of life,” he says. Vincent acknowledges that DNA mutations often cause cancer, but he sees the genetic paradigm as “very incomplete.”

Um, no. Cancerous cells are not their own "species." For one thing, they can't live on their own outside of the body. Yes, their genomes are screwed up. Real screwed up. And scientists would be the first to admit that the genetic "paradigm" is incomplete (although probably not "very incomplete"), because there are contributions to cancer from metabolism and the tumor microenvironment that we don't yet understand. It is, however, interesting how many of the genes mutated in cancer are intimately involved with DNA repair.

Basically, what Davies proposes is nothing more than a 100 year old idea that he resurrected and tarted up for the 21st century. Because he doesn't have a background in cancer, after finding this shiny new (to him) toy he became utterly fascinated with it and couldn't understand why cancer biologists don't find it as fascinating as he did. The reason, of course, is because it's a 100 year old idea that was found long ago not to be consistent with the data. Pesky that!

Look, I don't mind people from other disciplines becoming interested in cancer. Insights from physics, chemistry, and other sciences can be valuable and can shake things up. However, what makes cancer researchers grind their teeth when reading an article like this lionizing someone like Davies is being lectured by someone who didn't have the humility to actually learn the history of the field he's claiming to transform. If he had bothered to do that, maybe he wouldn't have made such a fool of himself. Or maybe he would have. He was widely castigated by evolutionary biologists and cancer researchers in 2014 when he first published his ideas, and in the interim he apparently hasn't developed any humility.

I might have to look into his tow or three most recent publications to see if his arguments have gotten any better, but PZ took care of one of those already. They haven't.


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Davies is certainly no stranger to controversy:
[from wikipedia]
An opinion piece published in the New York Times, generated controversy over its exploration of the role of faith in scientific inquiry. Davies argued that the faith scientists have in the immutability of physical laws has origins in Christian theology, and that the claim that science is "free of faith" is "manifestly bogus." The Edge Foundation presented a criticism of Davies' article written by Jerry Coyne, Nathan Myhrvold, Lawrence Krauss, Scott Atran, Sean Carroll, Jeremy Bernstein, PZ Myers, Lee Smolin, John Horgan, Alan Sokal and a response by Davies beginning I was dismayed at how many of my detractors completely misunderstood what I had written. Indeed, their responses bore the hallmarks of a superficial knee-jerk reaction to the sight of the words "science" and "faith" juxtaposed. While atheists Richard Dawkins and Victor J. Stenger have criticised Davies' public stance on science and religion, others including the John Templeton Foundation, have praised his work.

Davies wrote an article in the Wall Street Journal where he described the background to the 2 December 2010 arsenic bacteria press conference and stated that he supported the 'arsenic can replace phosphorus' idea of Felisa Wolfe-Simon because "I had the advantage of being unencumbered by knowledge. I dropped chemistry at the age of 16, and all I knew about arsenic came from Agatha Christie novels." He also made the statement, "Well, I would be astonished if this was the only arsenic-based organism on Earth and Felisa just happened to scrape it up from the bottom of Mono Lake on the first try, It's quite clear that it is the tip of an iceberg. I think it's a window into a whole new world of microbiology. And as a matter of fact, she already has 20 or so candidate other organisms that we're very anxious to take a look at. I think we're going to see a whole new domain of life here." It should be noted that it was later independently proven that the DNA of said organism contained no arsenic at all. In the same vein, in an article in The Guardian, Davies suggests that the origin of life will be uncovered through information theory rather than chemistry. Concerns have been raised about his responsibility as one of Wolfe-Simon's co-authors.[

By j a higginbotham (not verified) on 17 Jul 2017 #permalink

cancer is found in virtually all multicellular organisms have cancer

Davies' insight that where there is multicellular life requiring the cooperation of constituent cells, there are ways for that cooperation to break down... as they used to say about Micro$oft, the advice is 100% right and 100% useless.

By herr doktor bimler (not verified) on 17 Jul 2017 #permalink

Yup. That's pretty much exactly what Paul Davies has been doing since 2009.

“I had the advantage of being unencumbered by knowledge. I dropped chemistry at the age of 16, and all I knew about arsenic came from Agatha Christie novels.”

I'm pretty sure Davies meant Dorothy Sayers but got that wrong as well.

By herr doktor bimler (not verified) on 18 Jul 2017 #permalink

The biography page for Davies on the ASU web site won't be winning any awards for modesty (http://cosmos.asu.edu/about), but that's not unexpected from someone arrogant enough to think no one researching cancer has been "thinking" about cancer prior to his glorious arrival on scene.

ASU must have a soft spot for these wandering physicists who believe they're endowed with superior thought processes as ASU also has physicist JB Adams--a President's Professor-- who runs the Autism/Asperger's Research Program at ASU, believing that feeding autistic children fecal coliforms will somehow ameliorate and/or cure their autism. He's also very anti-vax (he promoted the movie Vaxxed on his ASU web pages last year) and was one of those who testified in the Omnibus hearings laughably testifying about mercury as a cause of autism (oh, and Adams did human research without an IRB once as well, but ASU let him off the hook for that). And he sells untested supplements for autism as well...

By Chris Hickie (not verified) on 18 Jul 2017 #permalink

Orac writes,

Cancerous cells are not their own “species.” For one thing, they can’t live on their own outside of the body.

@ Orac,

Does the HeLa cell line, and its history, support an example of a viral induced mechanism-of-action for atavism?

Call it "Viratavism"?

Please advise...

By Michael J. Dochniak (not verified) on 18 Jul 2017 #permalink

He's almost into "Let us assume a cow is a perfect sphere..." territory, isn't he?

And, FFS, did he really, really go for a touch of Haeckel? Haeckel? And he wants to be taken seriously?

First learn some basics of biology...Oh and stick to the day job.

@Chris: Yet the publication list I was able to find on the ASU site consists of only one paper, presumably the one that prompted the Newsweek article on which Orac is commenting. In case anyone here is curious: it's K. J. Bussey et al. (2017), Ancient genes establish stress-induced mutation as a hallmark of cancer, PLoS One 12(4), e0176258 (Davies is the last author). This may be the fault of a web programmer rather than Davies himself, but the link that ostensibly takes you to his full publication list actually points to the same place as the link in the title of the paper, a page which provides a link to a PDF of the paper. I will leave it to others more qualified than I to evaluate the paper.

Davies claims to be involved in multiple fields of research. From his biography:

Paul Davies is a British-born theoretical physicist, cosmologist, astrobiologist and best-selling author. He is Regents' Professor and Director of the Beyond Center for Fundamental Concepts in Science, co-Director of the Cosmology Initiative, and Principal Investigator in the Center for the Convergence of Physical Science and Cancer Biology, all at Arizona State University.

There are at least two yellow flags in that biography. One is his involvement in astrobiology. There are legitimate astrobiologists out there, but it is a field in which, as Mark Twain put it, one gets a wholesome return of speculation on a trifling investment of fact, to a much greater extent than most other fields. The other yellow flag is that he won the Templeton Prize in 1995.

By Eric Lund (not verified) on 18 Jul 2017 #permalink

He’s almost into “Let us assume a cow is a perfect sphere…” territory, isn’t he?

He's well beyond it. There are applications where the exact shape of the cow does not make a large difference, and one can get a suitable estimate by assuming a spherical cow. It's a useful tool for a physicist who is aware of its limitations to have in his toolbox. Davies' cows are not only spherical but infinitely massive and moving on a frictionless plane. And they don't interact with one another. Or to pursue the tool analogy, he has pulled out his nice shiny hammer without first establishing that the problem he is dealing with is a nail.

By Eric Lund (not verified) on 18 Jul 2017 #permalink

Perhaps Davies is tired of being a theoretical physicist and has realized that as our culture seems to more and more be allowing and even rewarding the proliferation of snake oil, that he can position himself to make a lot of money from the "big pharma is bad" crowd. If not intentionally, he's still doing a marvelous job of helping those who prey on that crowd.

I think the problem is that he got the cow thing backward. He's assuming that a sphere is a perfect cow.

"“I believe you have to think your way to a solution.”"

Cause yeah, all the cancer researchers and scientists have just been grinding up money and injecting it into cancer cells in petri dishes to see if that worked.

That right there is a red flag.

That was a gob-smacking read. This Davies is astonishingly arrogant. "You have to think your way to a solution."
What exactly does he think cancer researchers (of every stripe) have been doing for the past, I dunno, 100+ years? Playing tiddlywinks?

All right, Mr "cancer is a single-celled organism" - if tumors think they're single-celled organisms (which they're obviously not in the case of solid tumors) then *why* do they evade the immune system? Huh? The immune system ignores *self*, but it's perfectly happy to attack single-celled organisms (bacteria) and even multi-celled organisms (parasites).

a clear case of how one can possess a PhD and still be a gibbering idiot.

(I would include a rant about physicists and their arrogance, but then I think about the physicists I know, and how they're dedicated researchers and teachers who delight in sharing the wonders of the universe with everyone and know their limits, so I'll let it go.)

By JustaTech (not verified) on 18 Jul 2017 #permalink

Another example, this has just been accepted on a physics magazine (with several distinguished scientists on the board!):


the title and abstract:

A mathematical model for DNA
Alireza Sepehri

Recently, some authors have shown that a DNA molecule produces electromagnetic signals and communicates with other DNA molecules or other molecules. In fact, a DNA acts like a receiver or transmitter of radio waves. In this paper, we suggest a mathematical model for the DNA molecule and use of its communication to cure some diseases like cancer. In this model, first, by using concepts from string theory and M-theory, we calculate the energy of a DNA in terms of interactions between free electrons and bound electrons. We show that when a DNA is damaged, its energy changes and an extra current is produced. This extra current causes the electromagnetic signals of a damaged DNA molecule to be different when compared to the electromagnetic signals of a normal DNA molecule. The electromagnetic signals of a damaged DNA molecule induces an extra current in a normal DNA molecule and leads to its destruction. By sending crafted electromagnetic signals to normal DNA molecules and inducing an opposite current with respect to this extra current, we can prevent the destruction of normal DNA. Finally, we argue that the type of packing of DNA in chromosomes of men and women are different. This causes radiated waves from DNAs of men and women to have opposite signs and cancel the effect of each other in a pair. Using this property, we suggest another mechanism to cancel the effect of extra waves, which are produced by DNAs in cancer cells of a male or a female, by extra waves which are produced by DNAs in similar cells of a female or a male and prevent the progression of the disease.

By Jef Arenzon (not verified) on 18 Jul 2017 #permalink

Re: spherical cows: As part of my cancer-treatment research I once started a presentation with "Blood cells are not spherical cows, a 50mL conical is not a frictionless plane, and the centrifuge is not moving a 3/4C. For these reasons, this calculation is irrelevant."

By JustaTech (not verified) on 18 Jul 2017 #permalink

Jef @19: Wow. I mean wow. That's some amazing stuff right there. Actually, it reminds me of some famous scientist who thought DNA in water could "transmit' itself to another container of water. Maybe Linus Pauling?

By JustaTech (not verified) on 18 Jul 2017 #permalink

The hubris that Davies demonstrates is breathtaking, and Wapner doesn’t call him out on it in the least.

The most recent post over at Backreaction is somewhat apropos.

Yet the publication list I was able to find on the ASU site consists of only one paper

Should've checked ADS (caveat: probably not all the correct Davies, but it's a reasonable coarse filtering).

This reminds me of the creationists who claim to demolish the theory of evolution by bringing up the third law of thermodynamics. One imagines thousands of biologists reading the criticism, smacking themselves upside the head, and shouting: "Of course! Why didn't I think of that?"
Davies is more sophisticated, but just as dumb.

I have a Ph.D. in physics, and physicists like Davis embarrass the hell out of me.

What is it about a certain strain of physicist that thinks that they know everything about everything?

By Kimberly Dick (not verified) on 18 Jul 2017 #permalink

What is it about a certain strain of physicist that thinks that they know everything about everything?

It ain't just physicists, I promise.

Given all the approaches "BIG Pharma and Research" are following why does he think they wouldn't jump on any possible "new or better" idea? As you noted, they are working on "not truly atavistic" pathways already.

By Robert B Estrada (not verified) on 18 Jul 2017 #permalink

Arrrgh! SECOND law of thermodynamics. I can't even keep crackpottery straight.

No, I'm fine with it. Let him take his overly simplistic view of cancer, his private pharma funds, and crank out some diagnostics and therapeutics that turn the world of cancer biology upside down in a short period of time. Go for it, Paul. Every young research novice or grad student should have a chance to face the woodchipper of simple explanations that is gene expression, DNA methylation, driver mutations, post-translational modification, signal transduction, cell trafficking, tumor microenvironment, metabolic regulation, checkpoint control, angiogenesis, immune evasion, chromosomal rearrangements and translocations... and just to put a cherry on top, heterogeneity at the cellular level.

Go. For. It. Paul.

By c0nc0rdance (not verified) on 18 Jul 2017 #permalink

As for surviving in very little oxygen, mammalian cells do the same thing.

Exactly. Just ask Travis's naked mole rats.

Entertainment often trumps reality.

Mathematical puzzles are misused as entertainment:


Q. 1 + 7 = ?

Orac's response would likely be 8 while some may hypothesize that it's (-8) and publish their reasoning.

Q. Is Orac a scoundrel for keeping some far-to-long in auto-moderation.

By Michael J. dochniak (not verified) on 19 Jul 2017 #permalink


Well, given the lack of understanding of the laws of thermodynamics demonstrated by creationists it would not surprise me if someone hadn't claimed that the Third Law showed evolution to be impossible at some point: entropy, mumble, mumble, absolute zero, mumble, mumble, exactly equal to zero, therefore NO EVOLUTION!

Or something...

If I remember right, the question of foreign courts' jurisdiction over Americans on US soil was settled by the famous case of Geo. Washington et 13 Colonies v. Georgius III Rex By the Grace of God, King of Great Britain, France and Ireland, Defender of the Faith, Archtreasurer and Prince-Elector of the Holy Roman Empire, Duke of Brunswick-Luneburg

By Old Rockin' Dave (not verified) on 19 Jul 2017 #permalink

Your rant there reminds me of the alt-text of https://xkcd.com/1851/

Magnetohydrodynamics combines the intuitive nature of Maxwell's equations with the easy solvability of the Navier-Stokes equations. It's so straightforward physicists add 'relativistic' or 'quantum' just to keep it from getting boring.

By Jenora Feuer (not verified) on 19 Jul 2017 #permalink

Magnetohydrodynamics combines the intuitive nature of Maxwell’s equations with the easy solvability of the Navier-Stokes equations. It’s so straightforward physicists add ‘relativistic’ or ‘quantum’ just to keep it from getting boring.

The simulations also bear some remarkable anatomical similarities.

Mathematical puzzles are misused as entertainment:


Q. 1 + 7 = ?

Orac’s response would likely be 8 while some may hypothesize that it’s (-8) and publish their reasoning.

This is, bar none, the most profoundly stupid MJD comment that I've had the misfortune of seeing. How the fυck he even came across this idiotically trivial "puzzle" is the only thing that briefly caused me a fleeting moment of curiosity.

News flash, MJD @33: as far as I can tell we're *all* in moderation now, so you can stop whining.

The sciences as art:
Physics: a perfect sphere of titanium.
Immunology: Take the entire MoMA (including the building), shake it up and splat it across the sky. That's the mammalian immune system, enjoy!

By JustaTech (not verified) on 19 Jul 2017 #permalink

What? You don't have MJD in your kill file, Greasemonkey boy?

Murmur, I am reminded of this quote from the description of the Universe in H2G2:
"Population: None. Although you might see people from time to time, they are most likely products of your imagination. Simple mathematics tells us that the population of the Universe must be zero. Why? Well given that the volume of the universe is infinite there must be an infinite number of worlds. But not all of them are populated; therefore only a finite number are. Any finite number divided by infinity is zero, therefore the average population of the Universe is zero, and so the total population must be zero."

By Old Rockin' Dave (not verified) on 19 Jul 2017 #permalink

Narad (#38) writes,

How the fυck he even came across this idiotically trivial “puzzle” is the only thing that briefly caused me a fleeting moment of curiosity.

MJD says,

I figured you out instantly, Narad is simple Daran spelled backwards.

I've kept it secret all these years to protect your privacy.

Daran, why can't we be RI friends again?

Off topic, I've been asked to write a book about Integrative Medicine and would like to thank Orac and his minions for their perspective.

I'll keep ya'll updated of course, my dearest RI friends.

By Michael J. Dochniak (not verified) on 19 Jul 2017 #permalink

Oh, Timmeh, I'm not always at home. You might have attended to, you know, the actual words.

When oxygen tension is low, they revert to glycolysis, which doesn’t require oxygen.

They don't "revert" back to glycolysis; all normal cells lyse glucose. This proceeds the oxidative stage. You cannot get to pyruvate without first splitting glucose.

Yes, tumor cells become resistant. It’s what they do. They’re genetically unstable...

Not all cancer cells are "genetically unstable". You cannot explain how some carcinogens cause "genetic instability" since benzopyrenes are not DNA-reactive molecules.

Chemical carcinogenesis can can proceed faster than mitosis. This is simple and obvious proof that it doesn't always start at one mutated cell, although it can.

The latent period of 5 years for radiation-induced thyroid cancer strongly supports irradiated DNA; there is no other way to explain it. But cancer can be caused by things which disable the electron transport chain in a group of cells collectively.

By Vander Heiden (not verified) on 23 Jul 2017 #permalink

What is it about a certain strain of physicist that thinks that they know everything about everything?

Because they "understand reality at the most fundamental atomic level" and think that higher-ordered systems can simply be explained in these terms.

They probably think that physics is more hard-headed and "real" than biochemistry. They are partially correct. Most biochemistry books will give you a lobotomy with the stupid cartoonish diagrams and Fisher projections.

But there are some biochemists who would make Davies look like a little bitch. Take the Pullman's, who wrote the first book on Quantum Biochemistry. I doubt that Davies could actually read that book.

His "primordial" cancer theory is nothing new, and has been around since the 60s. Davies is merely recapitulating 1960s and 1970s books and publications by Albert Szent-Györgyi.

By Vander Heiden (not verified) on 23 Jul 2017 #permalink

They are call "promoters" by some, and capable of causing cancer without first damaging DNA:

Promoter compounds do not interact directly with DNA and unchain biological effects without being metabolically activated (Yuspa et al. 1983, Butterworth et al. 1992, Weisburger 1998, Williams 2001). These agents increase cell proliferation in susceptible tissues, contribute towards fixing mutations, enhance alterations in genetic expression and cause changes in cellular growth control (Mehta 1995, Gomes-Carneiro et al. 1997). On the other hand, these promoters may indirectly damage DNA by oxidation (Gutiérrez and Salsamendi 2001). At first, these occurrences were associated with epigenetic mechanisms, but nowadays it is widely agreed that promotion also involves genetic changes (Simons 1995, Hanahan and Weinberg 2000).

Promoters delay the natural inhibition of the quiescent cells or in G0 by gap junctions (Barrett and Anderson 1993, Simons 1999, Bertram 2001, Trosko 2001). The promoters' most important activity is mitogenesis - genotoxical and mutational actions are not necessary at this stage (Pitot and Dragan 1991). The promoter must be present for weeks, months and years in order to be effective and its effectiveness depends on its concentration in the target tissue (Butterworth et al. 1992). Promotion is a reversible stage, after a promoter's disappearance a regression in cell proliferation can occur, probably by apoptosis. It is a stage that can be moulded up by physiological factors and therefore limit the extent of experimental carcinogenesis. Some promoter agents are specific for a particular tissue, but others act simultaneously upon several tissues (Yuspa et al. 1983, Scott et al. 1984, Yuspa and Poirier 1988, Gutiérrez and Salsamendi 2001).

In studies of chemical carcinogenesis with prolonged exposure and using high doses almost all of the promoter agents induce neoplasias without initiation(Pitot and Dragan 1991, Gutiérrez and Salsamendi 2001). Exposure to phenobarbital, benzene, asbestos, and arsenic even without the previous application of initiator agents leads to neoplasic development (Melnick et al. 1996, Trosko 2001). This contradiction has two possible explanations: either the genotoxic effect was not identified by mutagenicity and genotoxicity assays, or the initiated cells emerged spontaneously. In this last case we may consider that the promoter has an indirect effect - by increasing the frequency of cellular division it encourages the appearance of errors in DNA replication, as well as mutations.

Chemical carcinogenesis
Paula A. Oliveira

Asbestos would be a particularly hard one to explain genetically.

By Vander Heiden (not verified) on 23 Jul 2017 #permalink

They don’t “revert” back to glycolysis; all normal cells lyse glucose. This proceeds the oxidative stage. You cannot get to pyruvate without first splitting glucose.

I know that (I did take graduate level biochemistry before starting medical school). Since you're new here, I'll warn you about how much I hate pedantry and pedants.

But there are some biochemists who would make Davies look like a little bitch. Take the Pullman’s, who wrote the first book on Quantum Biochemistry.

I strongly suggest that, in this context, you do not invoke texts that (1) have practically nothing to do with physics per se and (2) are ancient.

Nothing to do with physics? This is where chemistry an physics overlap. Here is a quote from a new book titled Quantum Biochemistry:

In 1929, at the dawn of the era of quantum mechanics, Paul A. M. Dirac (1902–1984) opens his paper entitled Quantum Mechanics of Many-Electron System [9] by the, now well-known, statement:

The underlying physical laws necessary for the mathematical theory of a large part of physics and the whole of chemistry are thus completely known, and the difficulty is only that the exact application of these laws leads to equations much too complicated to be soluble.

What Dirac meant is that the solution of Schrödinger equation, the wavefunction Ψ, provides a complete description and thus contains all the information that can be known about the system in a given quantum state. But since the Schrödinger equation can be solved exactly only for a very small number of very simple systems (composed of one or two particles at the most), Dirac goes on to close the opening
paragraph to his paper wishing that [9]:

It therefore becomes desirable that approximate practical methods of applying quantum mechanics should be developed, which can lead to an explanation of the main features of complex atomic systems without too much computation.

Eighty years later, today in 2009, much of Diracs wish to develop approximate methods to extend the application of quantum mechanics to complex atomic systems has been realized, but the search for better and faster approximations to solve the Schrödinger equation remains a subject of prime importance and current interest in theoretical and quantum chemical research. The need for these approximate practical methods is particularly pertinent to quantum biochemistry where quantum mechanics is applied to biological systems of staggering complexity, unimaginable just a few decades ago.
The Born-Oppenheimer (BO) approximation....


By Vander Heiden (not verified) on 23 Jul 2017 #permalink

Quantum chemistry isn't physics. Most physicists wouldn't recognize the nomenclature used for the common basis sets, for example. Get over it.

Quantum chemistry is quantum mechanics applied to molecules.

And physical chemistry and atomic physics are essentially the same thing.

Although there are may flaky biochemists, there are certainly some hard-headed biochemists whose quantum mechanical prowess would impress many physicists. That was the only point that I was trying to make.

Davies thinks he can arrogate Szent-Györgyi's speculations on cancer's evolutionary basis and repackage it as a new idea while not bothering to do enough research to realize that dicarbonyls have been used to reverse this since the 60s.

The history of life has been divided into two periods by the appearance of light and oxygen. There are reasons to believe that in the first dark and anaerobic period, which I have called the "α period," life could develop but the simplest forms, capable only of the most primitive vegetative functions. Life began to develop and differentiate, build increasingly complex forms capable of increasingly complex and subtle functions, when light and oxygen appeared. The second, aerobic and light, period of development and differentiation I have called the "β period." Accordingly, we have two problems. First, what distinguished the animate from the inanimate in the first, primitive α period? Second, what had to be changed in the basic structure of the living systems to open the way to development and differentiation, the final product of which is us?
The α–β transition
Life originated on a dark and airless globe, covered by dense water vapor. There was no light and no oxygen. Life has left behind very few traces from this first dark and anaerobic period and so we can only philosophize that under the inhospitable conditions of that period life could develop but the simplest
forms, capable of performing only the simplest "vegetative" functions. The main product of this period had to be the protein molecule which, by its specific folding, could develop a catalytic activity.
To make life perennial, the living systems, in this period, had to proliferate as fast as conditions permitted. Energy for this proliferation had to be produced by fermentation so that the a period could also be called the fermentative period of unbridled proliferation. When, owing to cooling, the water vapor condensed and light reached the surface of the earth, life started to develop and differentiate, build increasingly complex forms capable of increasingly complex and subtle functions. To guard the harmony of the whole in the midst of increasing complexity, the unbridled proliferation had to be replaced by regulation. Whatever the case may be, the inactivation of a potent enzyme within the narrow boundaries of the cell demands a high degree of order. Any disturbance of this order (say by a carcinogen) would then lead to the release or activation of the glyoxalase, the destruction of MG, and the consecutive induction of proliferation. If it was MG that brought the cell from the α to the β state, then the destruction of MG has to have the opposite effect, and bring the cell from the resting β to the proliferative α state. This could explain why my cells begin to proliferate if I cut myself; the cut is a disturbance which activates the glyoxalase; the glyoxalase destroys MG and brings about proliferation which eventually fills the discontinuity, restores order, and inactivates the glyoxalase.


By Vander Heiden (not verified) on 23 Jul 2017 #permalink
Quantum chemistry isn’t physics. Most physicists wouldn’t recognize the nomenclature used for the common basis sets, for example. Get over it.

Quantum chemistry is quantum mechanics applied to molecules.

Dawn breaks over Marblehead. In other news, mechanical engineering is physics applied to making things. Firing up MOLPRO isn't physics per se, which was my original point following on to your "little bitch" witticism.

And physical chemistry and atomic physics are essentially the same thing.

Please just quit while you're behind, already.

Although there are may flaky biochemists, there are certainly some hard-headed biochemists whose quantum mechanical prowess would impress many physicists. That was the only point that I was trying to make.

Dandy. I, in turn, think you've been using too many broad generalizations and mixed them up with overlong quote-blobs.

So Narad: Is quantum mechanics physics, or is it chemistry?

Or is it both?

There is a much greater difference between different branches of physics (such as rocketry and optics) than between quantum mechanics and quantum chemistry. This is a nexus where these two broad categories overlap.

But hey. Continue to pretend it's not. Whatever, I understand that sometimes the cafeteria is out of turmeric and bidi breaks are few and far-between.

By Vander Heiden (not verified) on 24 Jul 2017 #permalink

There is a much greater difference between different branches of physics (such as rocketry and optics)

Yah, that thar's some prime Fυcklesworth. Just enough rope, as usual.

Simple mathematics tells us that the population of the Universe must be zero. Why? Well given that the volume of the universe is infinite there must be an infinite number of worlds. But not all of them are populated; therefore only a finite number are. Any finite number divided by infinity is zero, therefore the average population of the Universe is zero, and so the total population must be zero.

Sadly, this does not follow from simple mathematics. it is perfectly possible for the set of all inhabitable planets to be smaller than the set of all planets, yet both sets are infinite. One is a smaller infinity than the other.

Consider numbers - there are infinitely more irrational numbers than rational numbers, and infinitely more rational numbers than positive integers, and precisely 10 times as many integers as integers that are even multiples of 10 - yet there are infinite even multiples of 10.

So Douglas Adams - my personal hero and, indeed, a god in the pantheon of humorous writers - was wrong.

By Mephistopheles… (not verified) on 25 Jul 2017 #permalink