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. ..."
David Steffen replies:
> 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. ...
Well, let me join you by sticking my neck out (are two necks really
better than one?)
> ... 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 working model I have to explain this ... is that this
> limit to proliferation represents a defense against cancer. Should a
> cell begin proliferating inappropriately, its growth will ultimately
> be limited. ... 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.
Perhaps there is another way to view this. We age as a result of
selective evolutionary pressure. Perhaps early in the evolutionary
history of our pre-cursors the incidence of early age cancer was high.
A mutation developed that caused senescence in cell reproduction,
limitting the effect of certain cancers. If the typical onset age
of cancers was prior to breeding age of the individual, the evolutionary
pressure to select for the mutation is obvious.
