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Doctor X, a scientist who has
been aware of my work for several years, has emailed some “friendly,” but
unsolicited, advice about this blog. He suggests that I “tone down” my
rhetoric. He claims my proposal is merely a modest extension of conventional
evolutionary theory; it may add to our understanding of cancer but that’s all
it does. The citations it has received appear primarily in journals devoted to
cancer not evolution and, according to him, that is as it should be; my claim to
have developed an alternative to conventional evolutionary theory is wrong.
Oh, dear me!
Where shall I begin?
What if I review, not this blog’s
language or what I wrote in my 1992 book Cancer
Selection, but the exact wording of the two Letters published in the Journal of Theoretical Biology? That’s it. Let’s see if I managed to
surreptitiously sneak past the JTB
reviewers some wild and crazy “rhetoric.”
Before quoting the Letters I
think it worthwhile to briefly review my dealings with the JTB.
In my initial cover letter I made
clear, as I had in prior submissions to other journals, that I had no scientific
credentials, that I was a rank amateur. In due course I received a response
enclosing JTB’s reviewer’s evaluation
of my proposed full-length paper: he deemed it unsuitable for publication.
Somewhat cheekily, I then telephoned the late Doctor James F. Danielli, Editor
of JTB, and asked if it were possible
to receive a second opinion. He agreed, telling me it would be reviewed by him
and by a member of the journal’s Editorial Board. A few weeks later I was told they
would consider publication providing I shortened my manuscript and submitted it
as a Letter. I accepted their decision and a Letter was published in April
1983. Unfortunately, in reducing the text I had deleted an essential part of my
theory. In an attempt to correct the omission I wrote a second Letter which was
accepted and published in JTB in
March, 1984.
Following the first Letter’s
appearance Nicholas Rothwell, a journalist for The Australian wrote:
Mr. Graham’s appearance in the journal is
itself rather bizarre since this scientific publication is not normally given
to printing theories by New York businessmen who happen to be amateur
evolutionary theorists.
Indeed. I think it probable that
because of my complete lack of scientific background and the nature of my idea,
as well as the initial reviewer’s negative opinion, those two senior scientists
at that respected journal (which had, and continues to have, a policy of not
publishing speculation) gave my proposal an exceptionally careful reading.
So what did Dr. Danielli and his
colleague agree was worthy of appearance in their journal? A proposed modest
extension of conventional theory that might explain something or other about
cancer’s evolutionary history? Or did they approve a far more radical idea?
Let’s peek at those Letters and see what they in fact approved for publication.
Starting with the opening
sentence in the first paragraph of the 1983 Letter I made clear that mine was not
a modest proposal: “Cancer…played a major
role in the origin and evolution of the Bilateria…” And in the
final sentence of that opening paragraph I make the point that is essential to
the core of my theory “all selected
defenses against cancer would have enhanced the ability of the [Bilaterian]
genomes to create organisms in which the genetic
program is expressed with great fidelity in all somatic cells.” [Emphasis added.]
As for my amplifying 1984 Letter,
I not only confirmed my fundamental position—“Because
the process leading to [lethal juvenile cancer in Bilaterians] is believed to
begin with imprecise replication of
the genetic program in a single cell, I conclude that all anti-oncogenes also
function as enhancers of precise
replication” [emphasis in the original]—but
even asserted that “Those [Bilaterian] germ lines that created the most complex
animals endured the most genetic losses to cancer and vice versa.”
To summarize, my published theory
not only says that cancer defenses enabled precise cell replication during
development—precision absolutely essential to
the existence of all Bilaterians—but that those
Bilaterian lineages that “benefited” from higher historical rates of lethal
juvenile cancer were—as a result—able to produce animals of greater complexity.
Any truncation and distortion of
my theory that excludes those two conclusions might render it more acceptable to
Doctor X and others but if it does they are embracing a theoretical proposal they created, not me.
So, how, if I were so inclined,
could I possibly follow Doctor X’s advice? Shall I approach the current editors of JTB (with cap in hand and feet ashuffle) and humbly apologize for
having foisted on their esteemed publication two Letters laden with irresponsible
rhetoric? Should I beseech them to permit me— please?—to rewrite the Letters to
reflect Doctor X’s view: that evolution may have managed to—well, to do something or other to the cancer mechanism—but that anti-cancer adaptations could not possibly have also enabled
the Bilaterian gene pools to control with precision the production of somatic
cells during development. Of course the complete avoidance of somatic mutations
during all stages of development would have eliminated the possibility of
lethal juvenile cancer while also (it is a tautological certainty) enabling precise
replication of cells but … (I need to think of something to follow that “but”).
As for my proposal that the most complex Bilaterians were products of higher
levels of cancer selection than their simpler brethren, well I have no idea
what I could have possibly been thinking when I wrote that. It is, of course, ridiculously
wrong.
All kidding aside, Doctor X, it
is not rhetoric. It’s logic.
As the recipient of unsolicited
advice I will now return the favor and respectfully offer this suggestion to
Doctor X: Give this matter further thought.
Perhaps on your next long flight
you might contemplate what must have been involved in the manufacture of the
airplane you’re seated in and in all the airplanes constructed in all the
world’s factories over the past 100-plus years. You wouldn’t seriously consider
it possible that the people in charge of those manufacturing facilities did not
employ procedures to ensure, with high probability, that the individual working
parts were fabricated with precision. The cumulative result of aviation history
makes clear that as the planes became more complex and flew greater distances
at higher altitudes and at greater speeds the rate of fatal quality-control
failures—crashes caused not by poor design or extreme
weather or pilot error but by a particular type of imperfect manufacture, the
malformation of a specific individual part—became almost non-existent. Once you
have an accurate appreciation of the essential role of quality control in the
history of airplane manufacture turn your thoughts to the most precisely “manufactured”
objects on the plane: the bodies of the humans on board, each of which is far
more complex than any airplane and consists of many more working parts. A
Boeing 747 consists of about five million parts. We humans have about ten
trillion somatic cells and every adult (and every ancestor of every adult) was
constructed of precisely-made individual cells. As I explain in recent posts to
this site (here and here) the number of those “perfect” cells in
all the Bilaterian breeders that ever existed was uncountably high (trillions
of trillions?). Such perfection must, in my view, be explained by
evolutionarily-effective mechanisms. As you intensify your thinking about those
perfect cells keep in mind two facts about cancer that no evolutionist should
ignore: (1) all Bilaterian somatic cells contain cancer triggers (oncogenes) and
(2) lethal juvenile cancer is initiated by things that interfere with precise
replication: mutagens are carcinogens. Wouldn’t even the earliest Bilaterian
gene pools have quickly “discovered” that the simplest solution to the problem of
lethal cancer during development was not to suppress non-existent tumors but to
avoid completely the possibility of tumor formation? And how could they do that?
By executing the development program with great precision. If mutagens are carcinogens then the avoidance
of the molecular events caused by mutagens avoids cancer; perfect cell
replication is a perfect anti-cancer mechanism.
My theory
says that anti-cancer selection pressure occurred in Bilaterian lineages from
the time of their origin and that it occurred in no other multicells. To anyone
who thinks my idea is a minor matter, another ho-hum revision of conventional
theory, I quote from the final paragraph of the 1983 Letter where I assert that
if my proposal were adopted evolutionary theory “would offer, as it does not now,
a mechanistic explanation for a generally ignored, but nonetheless perplexing
problem: why, if they had access to the same mechanisms as the Bilateria, did
the germ lines of [cell colonies] not create multicells with complex vital
organs? Or, conversely, if tissue-level multicells were sufficiently adapted to
ensure the survival of their germ lines for hundreds of millions of years, why
do organisms of so much greater complexity exist in such abundance in the
Bilateria?” No rhetoric I’ve posted to this site or wrote in my book says more
clearly and with greater emphasis that my proposal is radically different from
conventional theory.
Although my
theory is ignored in evolution textbooks and journals the idea that cancer
defenses enhanced replicative efficiency and thus enabled complexity received some
notice in Crespi and Summers’ 2006 review article Positive selection in the evolution of cancer where, in a paragraph
beginning, “As first described by Graham (1992) in his book Cancer Selection,” the authors note that evolutionary changes may lead to increased
cancer rates and “Such [cancers]…may lead to…greater developmental precision and complexity…” [Emphasis added.] The sequence Crespi and
Summers describe actually appeared, in succinct form, in my 1984 Letter:
“Selection of adaptive pro-oncogenes would have increased the pressure for more
effective anti-oncogenes, which, because of their inherent replication
enhancive properties, would have enabled the surviving gene pools to create the
more complex (or larger or more exposed) animals whose development was by then
imbedded in the genetic program.”
Finally, is
it possible that although mine may indeed be a radical proposal it is simply
wrong? That anti-cancer defenses were not necessary for the emergence and evolution of the
Bilaterians? Might not evolutionary mechanisms, as is implicit in conventional
theory, that produced jellyfish and other cell colonies have been entirely
responsible for Bilaterian evolution? I invite anyone who thinks that to
compose a plausible explanation of how that may have happened. Simply take pen
(or pixels) in hand and describe how the mechanisms that enabled the jellyfish
gene pools to produce nothing but jellyfish for more
than 500 million years also managed to produce blue whales, butterflies—and
thee and me.
REFERENCES
Crespi, B. & K. Summers. 2006. Positive selection in the evolution of
cancer. Biol. Rev. Camb. Philos. Soc. 81:407-424.
Graham, J. 1983. Cancer
and Evolution: Synthesis. J. theor.Biol. 101, 657.
Graham, J. 1984. Cancer and Evolution: Amplification. J. theor.Biol. 107, 341.
Rothwell, N. 1983. Cancer sparked human evolution, claims researcher. The Australian.
April 26.
Thompson, A. 2007. Oldest Known Jellyfish Fossils Found.
Live Science.com. October 30.
Copyright © 2012 by James Graham
