Cellular Senescence = Tumor Control ?

Timothy R. Hughes th035681 at mbcr.bcm.tmc.edu
Sat Sep 18 17:07:49 EST 1993

While the idea that cellular senescence has
evolved as a means of containing morphological
or metastatic malignancies is attractive and 
obviously cannot be disproven, I am not convinced
that it is accurate.  The immune response
is supposed to eliminate errant cells, and
in the event that malignant cells have escaped
the immune reponse and are proliferating when they
shouldn't, they have definitely abandoned their normal
growth controls, and the senescent property is
certainly no guarantee.  This is in fact how
transformed cells are identified in cell culture -
they don't senesce.  I have personally never heard
of a tumor ceasing growth and upon inspection it
was found that all of its cells had senesced, and
I would sure be interested if anyone had.     

If humans _were_  to depend on senescence to control
tumorous growth of cells escaping both the immune 
system and their normal growth restrictions,
we would wind up with pretty big tumors anyway,
judging from the division potential of fibroblasts
in vitro (a model which is another issue
entirely).  Roughly estimating that fetal fibroblasts
have a division potential of 100 and lose 
one division per year, at the age of forty
a malignant growth could still
reach 2^60 cells, which is a pretty
big tumor.  (As age reaches 100, of course, the possible tumor
size decreases exponentially.  I chose 40 as the age
at which selective pressure was probably largely removed
during most of human evolution.)

Tim Hughes

(I am a first-year graduate student 
at the Baylor College of Medicine.
I am hoping to do my thesis work in
Jim & Olivia Smith's lab, where I worked
over the summer.  I am fascinated by the
aging process and would be interested in 
corresponding with anyone in a similar




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