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Pre-Cancer Treatment

A number of genetic mutations cause a cell to become cancerous, so...
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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.

Vernon, May 11 2015


       This is not an entirely dumb idea.   

       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.   

       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.   

       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.
MaxwellBuchanan, May 11 2015

       We call this "smoking".
not_morrison_rm, May 11 2015

       Good point, [nrm]. Was it apropos anything?
MaxwellBuchanan, May 11 2015

       The immune system already detects and attempts to eliminate damaged cells.
Voice, May 12 2015

       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.   

       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.   

       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?
bungston, May 12 2015

       //Good point, [nrm]. Was it apropos anything?   

       Yes, as a way to get cancer, smoking is pretty much up in 1st place, so smoking counts as a "pre-cancer treatment" ne?
not_morrison_rm, May 12 2015


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