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September 6, 2014

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%

For a more up-to-date summary go here.

August 8, 2014

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.

July 6, 2014

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? 

May 28, 2014

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.

May 15, 2014

An Open Letter to Armand Marie Leroi (Continued, With a New Postscript)

The first part of the Open Letter is available here

Dear Armand,

Connections you fail to make.

1. What I think will be eventually judged as twentieth century Biology’s most embarrassing episode was the publication and enthusiastic receptionit's received nearly five thousand citations—of Gould and Lewontin’s Spandrels paper. 

Now, Armand, consider this. As lead author of a 2003 paper in Nature Reviews Cancer you expressed agreement with a fragment of my theory—that following adoption of physiological modifications lethal juvenile cancer rates increased—but, unlike me, you ignore the import of that fact to evolutionary theory.
Those increased cancer rates demolish the Gould-Lewontin notion that non-adaptive physical modifications could have played a significant role in Bilaterian evolution. If a prospective new feature offered no immediate survival benefit whatsoever, but increased the incidence of lethal juvenile cancer that feature would not have been selected.

Armand, you hold a university title that includes the word “evolution.”  You could have written a publishable paper pointing out the significance to evolutionary theory of those pediatric cancer rates: they nullify anti-adaptationist notions as they pertain to the bilaterian phenotypes. Instead, your paper appeared in a cancer journal where it was classified as "Opinion" and ignored by evolutionists.

As I wrote in the rejected TREE manuscript, “Neo-Darwinism is insufficiently Darwinian,” meaning that in Bilaterian evolution natural selection in the form of cancer selection explains the heretofore inexplicable: the unbroken chains of perfect construction of the most complex things in the universe. But you managed to ensure that no one will read those words in that journal.

March 12, 2014

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.

February 28, 2014

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 bredno animal that left behind any descendants died as a juvenile. Not a single one. Juvenile animalsby definitionare incapable of sexual reproduction, therefore every one of those breedersall the ancestors of every animal alive today, every ancestor of every dinosaur or other extinct animalsurvived into adulthood. Every breeder, in other words, was the beneficiary of meticulousperfectdevelopment. [See Note.]

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

January 1, 2014

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.