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] Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=12979