Who Has Been Visiting This Site?

Now that the site has accumulated a few thousand page-views, it might be interesting to view a summary of visitors' geographic location.

    USA                               57.4%
    Russia                           10.8
    Germany                      10.6
    France                             4.8
    United Kingdom             4.0
    Ukraine                           4.0
    China                              4.0
    All Other                         4.4 
    
    Total                           100.0%

On the Origin of Bilateral Symmetry

It is a fundamental principle of evolutionary theory that Nature never anticipates. A gene pool cannot plan for changes in the environment, for the possible future emergence of new predators or any other contingency; the existential threats any gene pool ever encountered existed in the here-and-now. In this posting I propose that bilateral symmetry was originally selected, not for its future mobility-enhancing potential, but because it functioned as a cancer-preventing device in the earliest Bilaterians. 

Those familiar with my published theory know it asserts that all multicells can be divided into two mega-groups: those constructed of somatic cells which all contained functioning cancer triggers (oncogenes) and those that were incapable of dying of cancer. As my peer-reviewed 1984 Letter in the Journal of Theoretical Biology stated succinctly, "This theory states that oncogenes, thus defined, have been present in every cell of every specimen of every species of the Bilateria that ever existed, and that they have existed nowhere else in Nature."

My 1983 Letter asserted that evolutionarily significant lethal cancer did occur in developing Bilaterians in numbers sufficient to create selection pressure for the accumulation of anti-cancer mechanisms and, because cancer begins with replication error, that all those defenses " ... enhanced the ability of the genomes to create organisms in which the genetic program is expressed with great fidelity in all somatic cells." (1)
 

I am convinced that one of the earliest anti-cancer adaptations was rejection of the radial symmetry found in other multicells (including the likely ancestors of Bilaterians) and selection of symmetry along a longitudinal axis, a radical departure that enabled gene pools to produce sufficient numbers of animals free of cancer during development.

Cancer Discovered in Hydra?

It has recently been reported here and here that scientists at Kiel University in Germany claim that cancer has been found in Hydra.

Anyone familiar with my published theory knows it asserts that lethal juvenile cancer occurred in all Bilaterians and only in Bilaterians, that other multicells including cnidarians like Hydra did not experience it during evolution.

So does this report from Kiel University conflict with my theory? 

On Peto's Paradox

"Peto's Paradox is the observation ... that at the species level, the incidence of cancer does not appear to correlate with the number of cells in an organism."

Do blue whales seldom get cancer?

Being a cautious fellow I don’t know whether or not it is true that blue whales get less cancer than (say) mice but I do accept that fewer cases of cancer have been reported in blue whales than in smaller vertebrates. Caution also tells me that neither I (nor anyone else) has, at present, access to technology that enables one to observe an animal’s somatic cells as they are transformed to the cancerous state. Nor can we observe whether such cells are promptly extinguished by agents of an adaptive immune system (which all vertebrates possess) before producing cancerous daughter cells in sufficient numbers. Sufficient, that is, to cause death from cancer or to produce detectable symptoms. 
  

So, my starting point is different from others who have written extensively on this subject. My view is that—most probably—blue whales, because they consist of greater numbers of somatic cells, produce a greater number of cells transformed to the cancerous state than do mice but, as I will explain below, their greater size enables them to minimize production of detectable cancer.

Starfish Secrets: Did Echinoderms Cure Cancer? [New Material Added]

Since my theory does say that all Bilaterians accumulated defenses against cancer is it possible that other animals have defenses that might be adaptable to treating or preventing human cancers? Interestingly, researchers at the University of Rochester recently identified a chemical in naked mole rats that seems to make them “cancer-proof.” Although Dr. Vera Gorbunova, one of the lead investigators, had access to my book and cited it in some of her earlier papers, I am certain that neither she nor her colleagues needed guidance from me or from  any evolution theorist to prompt their interest in naked mole rats. After all, researchers have established that other rodents not only experience cancer but may be especially susceptible to it: as mentioned on p134 of Cancer Selection two National Cancer Institute investigators [Anderwont and Dunn] found tumors in more than 40 percent of randomly gathered wild mice. Considering the widely known facts about cancer in rodents the Rochester investigators did not need any evolutionist to suggest that it might be worthwhile examining the rare rodent species that seems not to experience any cancer. Nor would they need much thought to suspect that those cancer-free rodents may even have acquired, over evolutionary time, an efficient anti-cancer mechanism.  

However, I think there may be other animals that might warrant investigation as possible possessors of potentially useful cancer defenses: the echinoderms. These Bilaterians (1) exhibit a characteristic which, according to my theory, complex animals ought not to possess: they regenerate damaged parts with spectacular efficiency. In my book (pp 79, 83 and 144) I argue that the reason most Bilaterians (and especially the more complex ones) do not regenerate as routinely and as competently as, for example, Hydra, is that regeneration involves increased production of somatic cells, each possessing cancer-triggering mechanisms embedded in oncogenes. (My theory asserts that only Bilaterians can die of cancer.)  To prevent death from cancer natural selection would have favored strict limits over regeneration despite its obvious survival benefit. Although I did note (on p79) that starfish can regenerate an entire animal complete with internal organs from one amputated arm, I may have underestimated the significance of that fact.   

To give some sense of the echinoderms’ regenerative powers, consider this quotation from the abstract of University of Milan’s Dr. Candia Carnevali’s 2006 paper Regeneration in Echinoderms: repair, regrowth, cloning.

Regenerative potential is expressed to a maximum extent in echinoderms. It is a common phenomenon in all the classes, extensively employed to reconstruct external appendages and internal organs often subjected to amputation, self-induced or traumatic, rapidly followed by complete successful re-growth of the lost parts. Regeneration has been studied in adult individuals as well as in larvae. In armed echinoderms, regeneration of arms is obviously frequent: in many cases, the detached body fragments can undergo phenomena of partial or total regeneration independently of the donor animal, and, in a few cases (asteroids), the individual autotomised arms can even regenerate to produce new complete adults, offering superb examples of cloning strategies.

Aside from the theoretical consideration—if I am correct to claim that avoidance of flamboyant regeneration is a cancer defense, does that imply that any Bilaterian exhibiting such activity has solved its cancer problem?(2)—what do observable facts say about cancer in echinoderms? Well, a search of Google Scholar shows no reports of echinoderm cancers and Wellings reported unsuccessful efforts to  initiate it artificially: “A number of attempts were made to induce neoplasia in post-embryonic echinoderms by the injection of carcinogenic hydrocarbons, or other substances, but there are no recorded examples of a successful result.”

If modern echinoderms are indeed free of cancer what is the evolutionary explanation? I believe there are two possibilities: they have completely lost the ability to trigger cancer (if they once possessed functional oncogenes those cancer triggers have since been altered to such an extent that cancer cannot even be induced) or they do possess functioning oncogenes but their gene pool discovered, as did that of the naked mole rats, a way to avoid the initiation of detectable cancer.

March 2018 Addition: Starfish display another characteristic that may suggest the presence of defenses against cancer: their abandonment of bilateral symmetry. If I am correct in believing that bilateral symmetry originated as a de facto anti-cancer mechanism then the reversion to radial symmetry in pre-adult echinoderms strengthens the suggestion that this lineage acquired especially effective cancer defenses.

Notes

1. Although starfish and other echinoderms display radial symmetry as adults they are bilaterally symmetrical as larvae and are thus classified as Bilaterians.

2. I also use the logic of my theory to suggest in another posting that the apparent absence of cancer in certain rodents is related to their extraordinary life span: Do Naked Mole Rats Confirm That Senescence is a Cancer Defense?

Do Naked Mole Rats Confirm That Senescence is a Cancer Defense? - See more at: http://cancerselection.blogspot.com/2013/08/do-naked-mole-rats-confirm-that_20.html#sthash.KfZ444k7.dpuf

References

Carneveli, M. D. C. "Regeneration in Echinoderms: repair, regrowth, cloning." Invertebrate Survival Journal 3 (2006): 64-76.

Wellings, S. R. "Neoplasia and primitive vertebrate phylogeny: echinoderms, prevertebrates, and fishes--A review." National Cancer Institute Monograph 31 (1969): 59.

Comments and questions are welcomed here.

At this site you will find links to additional material including my original Letters to the Journal of Theoretical Biology and  the 1992 Nature review of my book.

Copyright © 2014 by James Graham

This page was archived at The WayBack Machine on April 21, 2015.

Did a Carcinogenic Crucible Produce the Human Brain?

In writing my 1992 book Cancer Selection I had several objectives. I wanted to introduce to a wider audience the essential core of my peer-reviewed theory—that defenses against lethal juvenile cancer enabled precise construction of complex animals. My theory says that if cancer did not exist the Bilaterians would not exist. I also wanted to argue vigorously in favor of its acceptance as a major amendment to evolutionary theory, hoping for its adoption. Finally, I wanted to extend the theory, explain why I thought certain phenomena no one else associates with cancer actually originated as defenses against it. I wrote that sleep, animal senescence and the human brain originated largely because they defend against lethal juvenile cancer.

Regarding sleep, I wrote in the book that any future discoveries of increased immune activity during sleep, which is when somatic cells divide, would support my idea. Subsequent research seems to have done that. 

Although I am not aware of any published research supporting my proposal that animal senescence originated as an anti-cancer mechanism, an American scientist has informed The New York Times that he had reached the same conclusion. 

In the remainder of this posting I will concentrate on my third proposal, that cancer played a major role in the origin of the human brain. Much of what follows is an adaptation of material appearing in Chapter Nine, pages 105-108.

The Chapter Five Argument: Explaining Two Megafacts

This is a re-posting in a slightly different form, of an essay originally published in 2009.

I present several arguments in Cancer Selection in favor of my theory, and devote an entire chapter to what I consider the strongest. It’s Chapter Five.

The argument is based on two, to coin a phrase, megafacts about the history of the Bilaterians – the complex animals – that now exist or that existed in the past.

This is the first megafact: No Bilaterian animal that bred—no animal that left behind any descendants —died as a juvenile. Not a single one. Juvenile animals—by definition—are incapable of sexual reproduction, therefore every one of those breeders—all the ancestors of every animal alive today, every ancestor of every dinosaur or other extinct animal—survived into adulthood. Every breeder, in other words, was the beneficiary of meticulous—perfect—development. [See Note.]

Every statement in the prior paragraph is true for the simple reason that each is tautological.

The Axillae of San Stefano

I have only ever attended two scientific meetings, both of them annual conferences of AAAS, The American Association for the Advancement of Science. The first meeting was in 1982 and it was held in Washington DC. 

 

The reason I traveled from Manhattan to attend that conference stemmed from the discovery of oncogenes which had recently been reported in several newspapers. I had begun writing in 1978 my theory about lethal juvenile cancer’s role in the origin and evolution of complex animals and by 1982 I had written seven or eight versions. In all of those drafts I postulated the existence of cancer triggers in all Bilaterians’ normal somatic cells and after reading that some cancer theorists (but no evolution theorists) had also postulated the existence of such triggers, I started to call them by the scientific term, oncogenes.  

Pleased to learn that my hypothesized genes had actually been identified, I sent a copy of my latest draft to the reporter at New York’s Newsday who had written one of the earliest reports. My hope was that he might publish something about my idea. A few days later I telephoned him and after saying he did not understand my theory he made a suggestion. He told me about the annual conference of AAAS which included something called a “poster session.” He explained that the standards for acceptance in poster sessions were not very high and that I could probably have no difficulty “posting” my theory which could then be read by conference attendees. It was too late for me to post my paper at the 1982 meeting, but he suggested I  visit it anyhow with a view of submitting something for the 1983 meeting. I took his advice and arranged to attend for a single day to find out what a “poster session” was all about. I picked a day on which several prominent evolutionary biologists would be giving presentations in commemoration of the centennial of Charles Darwin’s death.