From: Brett Paatsch (paatschb@optusnet.com.au)
Date: Tue Jun 17 2003 - 23:43:59 MDT
Robert J. Bradbury writes:
> 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.
Cool. I guess the little that is happening that is healthy
is an acceptable loss considering.
> > 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.
I did a bit of reading last night (not much) to see how many
different *types* of cancers there actually are.
It was interesting. Tumors can be benign or malignant and only
the malignant are cancers.
Malignant tumors (cancers) are classified in accordance with
the embryonic tissue of origin. Most (>80%) are carcinomas,
from endothermal or ectothermal tissues such as skin or the lining
of internal organs and glands. Colon, breast, prostate and lung
cancers are carcinomas.
Leukemias and lymphomas are cancers of the hematoietic cells
of the bone marrow and make up 9% in the US. Leukemias
proliferate as single cells, lymphomas grow as masses.
Finally sarcomas, ~1% are dervied from tissues such as bone,
fat and cartilage.
>
> > 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.
Makes sense.
> 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.
Yep.
> 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.
Yep. But there seems to be one positive thing at least. Given
nanobots, all malignant tumors, are likely to be directly abutting
the vasculature not two or three cells away from it so it should
not be necessary to pass through healthy cells to get at the
cancerous ones.
Tumorous cell two or three cell widths away from the
vasculature are likely to be benigh, ie, not dividing very fast
and ignorable. By the time the rate of division gets to be
a problem the nanobots will find a vasculature access point
to the cancer mass.
A good early project for nanobots. Kicking cancers butt.
Regards,
Brett
>
> Robert
>
>
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