X-Message-Number: 12979
Date: Tue, 21 Dec 1999 21:30:10 -0500
From: Jan Coetzee <>
Subject: Aging and Darwin

Several years ago people scoffed at my theory that aging is the
consequence of "evolution" taking place in the organism. E.g.. elastin
cells are replaced by collagen cells in the older organism. Well I think
the following abstract not only supports the idea but actually suggest
prevention. Stabilize the DNA of cells that one associate with youth and
aging can not only be prevented but actually be reversed. Aging is the
consequence of  somatic cell evolution.

"              Darwinian tumors
                Comparing malignant colorectal tumor and polyp DNA to
that of normal tissue,
                a new study found that as many as 11,000 individual
 genomic events  had
                occurred in each tumor cell. The authors of the study
assert that cancer
                therefore arises from a decade or more of cellular
changes, due to a profound
                loss of DNA stability. In other words, the authors say,
malignancy is not the
                end result of a few mutations, but rather the
consequence of exceptionally
                unstable cells that have had years to evolve into cancer
via natural selection.
                The authors conclude that one of the best therapeutic
approaches to cancer thus
                appears to be prevention in the form of stabilizing the
genome before
                progression to cancer can be completed.


The onset and extent of genomic
instability in sporadic colorectal tumor
progression

Daniel L. Stoler*, Neng Chen, Mark Basik, Morton S. Kahlenberg , Miguel
A.
Rodriguez-Bigas , Nicholas J. Petrelli , and Garth R. Anderson, , 

Departments of * Experimental Pathology,   Surgical Oncology, and
Cancer Genetics, Roswell
Park Cancer Institute, Buffalo, NY 14263; and  University of Montreal
Hospital Center,
Montreal PQ, Canada H2W1T8

Edited by Alfred G. Knudson, Jr., Institute for Cancer Research,
Philadelphia, PA, and approved
October 1, 1999 (received for review October 12, 1998)

Cancer cell genomes contain alterations beyond known etiologic events,
but their total number
has been unknown at even the order of magnitude level. By sampling
colorectal premalignant
polyp and carcinoma cell genomes through use of the technique
inter-(simple sequence repeat)
PCR, we have found genomic alterations to be considerably more abundant
than expected, with
the mean number of genomic events per carcinoma cell totaling
approximately 11,000. Colonic
polyps early in the tumor progression pathway showed similar numbers of
events. These results
indicate that, as with certain hereditary cancer syndromes, genomic
destabilization is an early
step in sporadic tumor development. Together these results support the
model of genomic
instability being a cause rather than an effect of malignancy,
facilitating vastly accelerated
somatic cell evolution, with the observed orderly steps of the colon
cancer progression pathway
reflecting the consequences of natural selection.


  To whom reprint requests should be addressed at: Department of Cancer
Genetics, Roswell
Park Cancer Institute, Buffalo, NY 14263. E-mail:


Copyright   1999 by The National Academy of Sciences
0027-8424/99/9615121-6$2.00/0

Related Commentary in PNAS:

How many mutations does it take to make a tumor?.
    C. Richard Boland and Luigi Ricciardiello
    PNAS 1999 96: 14675-14677. [Full Text]

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