From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Tue Jun 17 2003 - 12:51:22 MDT
On Wed, 18 Jun 2003, Brett Paatsch wrote:
> So the question seems to be how do we target the cancerous cells
> that are seeking to furnish themselves with a necessary blood supply
> from healthy dividing cells that are doing the same thing.
Fortunately in adults there is very little angiogenisis taking
place. So it is reasonable to use anti-angiogenisis drugs without
having to worry too much about side effects.
> I imagine we are probably building up a catalog of cancer cells in
> petri dishes somewhere.
Oh, there are large libraries of cancer cells, presumably at
the NCI and elsewhere. HeLa cells being the prototypical example.
> Anyone know what the technological bottleneck is on identifying
> markers of tumor cells (or even cells generally)?
The problem is basic biology. Proteins that control cell division
generally operate only within the cell or within the nucleus,
not on the cell surface. One doesn't need cell surface proteins
to mutate (usually) to cause excessive cell division. Sometimes
one gets mutations for secreted proteins that cause the cell
to stimulate itself into dividing -- but then they aren't attached
to the surface of the cell. The internal proteins are digested
and are often displayed on cell surface, but exactly which fragments
get displayed (and these are small 9-12 amino acids) depends on
which set of MHC genes one has. If the mutations responsible
for cancer are not those that one can display in the MHC proteins
then it is very difficult to detect cells that are in the process
of becoming cancerous and eliminate them. In effect, it is true
for many cancers that the same reason one cannot develop a monoclonal
antibody is the same reason your immune system doesn't eliminate
the cancerous cells -- one cannot "see" what has gone wrong
*inside* the cell.
Its going to take nanorobots to solve that problem.
Robert
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