In article <adavison.696842042 at fraser.sfu.ca> adavison at fraser.sfu.ca (Allan Davison) writes:
"I'd like to see some discussion of the similarities between aging and
"cancer. Cancer is clearly a disease which primarily affects the aged.
"To some extent this may simply reflect lifelong accumulation of
"insults: initiators and promoters. However, loss of DNA repair
"mechanisms may produce both progeria and cancer susceptibility (ataxia
"telangiectasia or bloom's syndrome). Similarly loss of
"immunocompetence may contribute to both aging and cancer.
Well, in the spirit of David Kristofferson's lust of discussion of
IDEAS on bionet, I will stick my neck out and risk making a fool of
myself. My research area is cancer (oncogenes specifically) and not
ageing. What I know about ageing is attributable to the friendly
folks at the Huffington Center on Ageing here at Baylor.
When I listen to the Huffington Center people talk, I am always struck
by the similarity between their work and mine. However, the working
model I am left with is a bit different than what you seem to be
describing. My working model is that ageing occurs, at least in part,
as a result of defenses against cancer. The clearest example of this
is the limited proliferative potential of normal cultured cells.
Cells put into culture will not proliferate indefinitely, but will
become senescent. The proliferative potential of a cell put into
culture is related both to the lifespan of the organism from which it
comes (e.g. human cells proliferate longer than do mouse cells) and
the age of the organism from which they were obtained (e.g. cells from
a young animal proliferate longer than cells from an old animal). On
the surface, this sounds perverse; every cell in our body contains a
time bomb, telling us when we will die. The working model I have to
explain this (this model is certainly not my invention) is that this
limit to proliferation represents a defense against cancer. Should a
cell begin proliferating inappropriately, its growth will ultimately
be limited. [There is a problem, in that the number of generations
allowed by this limitation is sufficient to produce a tumor many times
larger than that needed to kill the animal. I do not have the space
to resolve that dilema here]. Thus, my model is that we age, in part,
because of this limit to proliferation. In the absence of this limit,
we might age more slowly, but would be much more likely to die of
cancer, so that our average lifespan would be less.
My favorite explanation for the increase of cancer incidence with age
is a statistical one. If it takes six mutations to convert a normal
cell to a cancer cell, incidence of cancer should go up with the sixth
power of age, approximately what is observed.
--
David Steffen
Department of Cell Biology, Baylor College of Medicine, Houston TX 77030
Telephone = (713) 798-6655, FAX = (713) 790-0545
Internet = steffen at mbir.bcm.tmc.edu
