would you mind more thoroughally explaining the importance, as you
understand it, of contact inhibition in the relevant pathway?
Specifically, how the expression of telomerase in a cell whose cycle is
being inhibited because of cell-cell contact might possibly lead to
I think that one thing that we really should be looking for is an
examination of 'telomerase active' cell lines which, under exposure to
normal environmental conditions, do not suffer a dangerous level of
unlimited, uncontrolled tumor growth.
Any other treatment of this paper, I gather from the impressions that
I've noticed in this newsgroup, misleads one to assume that somatic
expression of telomerase is a safe and effective way to deal with the
problems of cell death due to loss of telomeres.
This is simply not true, as I'm sure you've gathered from the research
that you've done for the book which you so rudely decided to use me to
plug. (is there really this much difference between 220+ and 300?)
Damien Broderick wrote:
>> Deacon Sweeney wrote:
>> > It's good to hear that the cells are still alive after 220+ generations.
>> No - look again:
>> > telomerase, now more than 220 generations past their normal life span
> > of 75 to 80 divisions, remain young and vigorous.
>> They're now at around 300 divisions. (Due, as Aubrey de Grey kindly
> explained to me offline, to the absence in vitro of contact inhibition, so
> the salience to in vivo avoidance of senescence is still unproved. But at
> least their telomeres haven't packed in.)
>> BTW, my forthcoming book THE LAST MORTAL GENERATION (Sydney: New Holland)
> will go to printers in Australia next week, due out in February. Good timing
> from Geron and Shay & Wright... :)
>> Damien Broderick