Is This An Old Wives Tale about cancer?
Peter C. Everett
pce at world.std.com
Wed Apr 4 22:59:17 EST 2001
Martin E. Lewitt (lewitt at swcp.com) wrote:
: Once they stop regulating the expression of their genes they have
: the whole normal genome at their disposal. However, they can
: stimulate angiogenesis by acting normal without needing any abnormal
: gene expression. -- Martin
Yes and no. A tiny mass of cancer cells usually will not
produce enough angiogenic signal to overcome the background
inhibition no matter how hypoxic they become. (Whereas a larger
chunk of ischemic tissue resulting from an injury will.)
Most cancers never escape this bottleneck of proliferation
balanced with apoptosis, perhaps a millimeter in diameter,
eventually dying when the cell division limit is reached.
However, if during this period, an errors of gene expression
upregulate telomerase (creating an immortalized clone) AND
increase the angiogenic output or decrease the antiangiogenic
output, the resulting blood vessel growth will support exponential
tumor growth and result in clinically observed disease.
The key observation is that angiogenesis is the determined by
the balance of proangiogenic factors and antiangiogenic factors,
which can change over time and location. The background inhibition
prevents the decendants of a single deranged cell from ever becoming
a tumor before the Hayflick limit catches up with them. It takes
multiple low-probability events for this physiological protection
against cancer to be defeated. It almost always works. Perhaps we
can make it always work with pharmacologic doses of natural
inhibitors of angiogenesis.
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