h a l f b a k e r yIt's not a thing. It will be a thing.
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I saw part of a PBS documentary titled "Cancer, the Emperor of
All Maladies", and that has led to this HalfBaked Idea.
It was stated that a healthy cell can experience random
mutations, and if certain of them happen, then the cell becomes
cancerous. The particular mutations don't have to happen
in a
particular order, and there are multiple sequences that can lead
to cancer.
Let's assume that, generally speaking, we are talking about 5
mutations from the original healthy state to the cancer state (if I
recall right, the actual number is greater than 5).
The cell may still generally act like a healthy cell, until the last
mutation happens --but certainly WE can call it a "damaged cell".
So, what we need are specific tests for those damaged cells.
This Idea makes the HalfBaked assumption that at least one of
those damage-items causes a change in the surface properties of
the cell. We then design a special drug to take advantage of that
change. (Note our abilities to design and construct special
molecules for special purposes is steadily advancing, and already
is well-advanced.)
The drug molecule would latch onto the damaged cell, BECAUSE of
that surface change, and THEN expose an "antigen", which is a
portion of a molecule that signals the immune system to destroy
the cell. Therefore the pre-cancerous cell gets destroyed before
actual cancer occurs.
[link]
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This is not an entirely dumb idea. |
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The main problem is that it's already difficult to
design drugs that target fully fledged cancer cells
with enough selectivity - most of the changes are
quantitative rather than qualitative, so a drug that
will kill _all_ cancer cells will probably devastate the
rest of the body. Finding drugs that target
precancerous cells is likely to be even harder. |
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Ultimately, what we need is the ability to do
genomics properly. What I mean by "properly" is
"actively", as opposed to our current abilities in
"passive" genomics - reading DNA. At present,
genomics is basically the same as weather - we can
see it, understand it, and to an extent predict
outcomes, but we can't do anything about it except
carry an umbrella. |
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Active genomics would include tools to do
elementary things, such as proof-check a cell's
genome and either fix it or kill the cell. Once we can
do that, cancer's a doddle. |
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Good point, [nrm]. Was it apropos anything? |
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The immune system already detects and attempts to
eliminate damaged cells. |
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Not all damaged cells are such a big deal. Some drift along, unemployed and confused, not causing much harm. Tolerance for such probably differs from organism to organism. Certainly for the skin the immune system presides over this tolerance level which is why as the immune system wanes more such damaged skin cells are allowed to persist. |
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I have never been clear as to whether smoking leads to increased rates of cancer by damaging DNA, or whether it is the increased repair and turnover of tar-damaged cells that leads to cancer. Any situation where there is increased cell turnover can increase cancer risk: a low frequency outcome of a given event will happen more often if the underlying event happens more often. |
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The proposed idea also invokes the "gold rush" from the caspase related idea. How to specifically identify the bad ones. Maybe under hypnosis they will fess up? |
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//Good point, [nrm]. Was it apropos anything? |
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Yes, as a way to get cancer, smoking is pretty much
up in 1st place, so smoking counts as a "pre-cancer
treatment" ne? |
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