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hkhenson@rogers...
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virus: Unpublished 1977 letter to Science
« on: 2003-11-30 21:31:40 » |
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Last night in chat I mentioned this letter.
I had not thought about this for a long time. Science didn't publish the
letter. Dr. Hayflick wrote me asking for a copy of the bamboo article. (I
still have a copy of his letter.) After I wrote it, someone pointed me to
another source where someone had proposed very close to the same rational
for cell limits.
Still, given what we can do with reading genes nowadays, there is a PhD
thesis out there for the person who identifies the counter mechanisms for
bamboo or the 13/17 year cicada.
I came reasonably close to describing the way telomers function, something
that was not well understood until the early 1990s. Figured I would put it
up for your amusement and the public record value.
Keith Henson
******************
[Address and telephone long out of date!]
ANALOG PRECISION INC
1620 N. Park Tucson, AZ 85119 Tel: 602-622-1344
Aug 2, 1977
Letter Editor
Science
American Association for the Advancement of Science
151.5 Massachusetts Ave., NW
Washington D. C. 20005
HENSON'S Hypothesis--"Cellular aging may be a defense against cancer"
Two puzzling features of cellular in normal and cancerous
cells have been known for more then a decade (1) . These are,
1. a limit on the number of times normal cells will divide in
culture before "senescing" (i.e., they quit dividing), and 2.
the observation that cancerous cells or cells transformed by
viruses or chemical agents are not subject to this limit. To my
limited knowledge neither a generally accepted mechanism nor a
satisfactory evolutionary reason has been proposed for cellular
aging. One theory, that of molecular clocks and programmed
aging readily accounts for both phenomena but evolutionary
objections have been raised to this theory. (2).
Briefly stated the molecular clock theory proposes that
cells have a counter (perhaps built into the chromosomes)
which is decremented one count division. In this way,
a cell "knows" how many divisions have occurred since the
sperm/egg fusion or some other event. Programmed aging
refers to the concert that cells would be inhibited from
further division or killed when the count reaches zero.
One of many possible physical methods by which this could
be accomplished would be through the action of enzyme which
cleaves a DNA base pair from the end of a chromosome at
each division until the coding for a critical
sequence was destroyed . (Some way to restore or reset this
hypothetical "chromosomal counter would also be required,
otherwise each generation would he shorter than the proceeding
one!) Molecular clocks per se almost certainly exist,
there seems to be no other way to explain the accuracy
of the reproductive cycles of certain bamboo species, one
of which, Phyllostarchy bambusoides waits 120 years between
flowerings and then flowers world wide (3). The obvious
difficulty with which a molecular clock explanation for cellular
aging is that a complex method to cause an organism's death,
long after the usual end of the reproductive period, seems
unlikely to evolve unless is serves some other purpose.
I believe a good case can be made for cellular senecesence
(and possibly aging itself) being a side effect of one of the
defences organisms have against cancer.
(page 2)
There are evidently a number of checks that inhibit cells
from becoming cancerous and evidence exists that several
mutations are required to transform cells into cancerous
types. (4). A limit on the number of normally permitted
divisions may be one of these mechanisms. If so, a cell
could lost contact inhibition and begin to grow in a cancerous
fashion, but unless it had also lost the division inhibit
codon or was continuously resetting the counter, growth
would stop when the remaining permitted divisions were
used up. Microscopic invasive growths which might represent
this class of limited cancers are reported to be 100 times
more common than unlimited cancers (5). The advantages in an
evolutionary sense of this line of defense from cancerous
cells might outweigh the obvious disadvantages of cellular
aging.
H. Keith Henson
BSEE (University of Arizona)
1620 N. Park Ave.
Tucson, AZ 85719
1. Hayflick, L. "The Limited In Vitro Lifetime of Human Diploid
Cell Strain," Expl. Cell Res. 37: 614-663 (1965).
2. Orgel, L. E., "Aging of Clones of Mammalian Cells," Nature,
Lond. 243, 441-445 (1973).
3. Jazen, D. H. "Why Bamboo Waits So Long To Flower," Ann. Rev.
Ecol. Syst. 1976 7:347-91.
4. Emmelot, P. and Scherer, E. "Multi-Hit Kinetics of Tumor
Formation, with Special Reference to Experimental Liver and Human
Lung Carcinogenesis and Some General Conclusions," Cancer Res.
37, 1702-1708, (June 1977).
Carnes, J. "The Cancer Problem," Sci. Amer. Vol 233, Nov. 1975.
cc to referenced authors.
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David Lucifer
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Enlighten me.
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Re: virus: Unpublished 1977 letter to Science
« Reply #1 on: 2003-12-02 13:18:58 » |
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Keith Henson wrote:
> Last night in chat I mentioned this letter.
>
> I had not thought about this for a long time. Science didn't
> publish the letter. Dr. Hayflick wrote me asking for a copy of the
> bamboo article. (I still have a copy of his letter.) After I wrote
> it, someone pointed me to another source where someone had proposed
> very close to the same rational for cell limits.
This is the same Hayflick who is recently the subject of an article:
"Everything in the universe ages ... why people believe they can somehow
make themselves immortal and violate the fundamental laws of physics is
beyond my understanding," said Hayflick, author of "How and Why We Age"
(Ballantine Books, 1994). "I don't see any scenario that would benefit
individuals or society in general by having the power to increase human
longevity."
That sentiment applies to his own.
"My ideal goal is to live until the age of 100 and drop dead on my 100th
birthday with full cognitive and physical abilities," confided the
75-year-old past president of the Gerontological Society of America,
who also is a founding member of the Council of the National Institute
of Aging and professor of anatomy at the University of California,
San Francisco, School of Medicine.
http://www.upi.com/view.cfm?StoryID=20031124-034745-5824r
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