Deacon Sweeney wrote (to Damien Broderick):
> Would you mind more thoroughly explaining the importance, as you
> understand it, of contact inhibition in the relevant pathway?
to which Damien invited me to reply, since I had mentioned contact
inhibition to him. The confusion arises from Damien's over-brief
wording: his query to me concerned the RATE of cell division of
Geron's cells by comparison with fibroblasts in vivo, because he
didn't appreciate that a division rate of about once per day is
perfectly normal for fibroblasts in culture irrespective of their
telomerase status. I described contact inhibition as the reason
(not the only one of course, but I kept it simple) why fibroblasts
don't divide once a day in vivo. I may have confused Damien by
banging on about the difficulty this raises for in-vitro to in-vivo
inferences, which was the basis for his original question to me.
I do quite agree with Deacon that the difference between 220+ and
300 divisions is a lot less interesting than the difference between
75-80 and 220+, and also that the absence of immediate cancer in
human cells introduced into mice means rather little. I have yet
to see the Nature Genetics papers though; I may be maligning them
(OK, pun intended, I admit it). Tom Mahoney and I had a rather long
exchange on s.l.e in mid-October about whether malignancy would be
promoted or inhibited by constitutive telomerase expression, which
those who are new to the group may find useful (viewable at DejaNews).
Aubrey de Grey