I guess there could be many genes that affect the “grow uncontrollably” part or the “refuse to die” part, but can’t we just target all of them?
In: Biology
You could, if you can extract literaly every cell with that mutation in the body, apply your crispr process to all 10 billion of them and then put them back…
CrisprCAS is something you do in the lab to individual cells or smal groups of cells, its not a liquid you drink and that does all that for you.
Crispr isn’t a magic wand. You can’t wave it over the body and somehow change all the defective cells DNA perfectly. There is a Nobel prize and billions of dollars in royalties waiting for someone to figure out how to apply gene editing to all cancers.
Ok, you can do that. You just need to identify the exact gene in every individual cancer patient that is causing the cancer patient (every cancer and cancer patient is different). Remember the human genome is 3 billion base pairs long, in which there can be thousands of mutations that don’t cause cancer at all, and most of these genes are aren’t even sure of what they do, or if they are even being expressed.
And then you need to deliver the crispr in such a way that it definitely reaches every single cancer cell, but doesn’t damage the DNA in any other healthy cells and possibly cause a new cancer
Or why can’t we use crispr to cause cancer?
The short answer is that the technology and implementation isn’t there yet. But the actual research focus currently isn’t preemptively altering genes in this way, but rather to create therapeutic treatments. Making permanent genetic changes to a patient is an ethics nightmare. While the human genome has been sequenced, we don’t really have a user guide saying what does what – current science showing confidence in what a particular gene does is based on testing, observation, and experimentation. For every gene that’s been identified with any level of certainty, there are thousands more that are still a mystery.
Imagine being given an extremely detailed map of a foreign land, that contains intricate drawings of every house, street, town and geographical feature, but features no labels, no scale, and no compass to help you navigate. That’s where gene mapping is today, and we are quickly learning to fill in the legend ourselves, but it will take time.
You can and there’s lots of research trying exactly this. Two problems though, it has very low in-vivo efficiency, so getting the plasmid to the cells is hard. And basically if you don’t kill a vast majority of cancer cells they will come back, so that’s a fundamental problem that needs to be solved. The other issue is the off-target rate. Something like 60% have at least one off-target splice and can have up to three off target splices. This can obviously be fatal to cells or exacerbate cancer.
I have a better question…if everything has its own resonance frequency even cancer cells, why can’t we use the resonance frequency of the cells against themselves to destroy them which wouldn’t harm the other healthy cells around them?
There’s a number of challenges with that. First, you have to identify what gene has the harmful mutation. This is already super difficult – people have been researching this for decades and we’re still very far from mapping every possible gene mutation that can cause cancer. It’s also worth noting that it normally takes a number of mutations across several genes in order for a cell to become cancerous, so that raises the question of which one to target (or else you’d have to target all of them, making your job that much harder). Usually earlier mutations switch off the cell’s own safety protocols that are supposed to defend against cancer, while later ones actually cause the cancerous behavior, but so it’s not as easy as just comparing a cancer cell to a healthy one and finding the places in the DNA that are different.
Second, you have to find a way to program CRISPR to reliably target the bad genes and not other genes that happen to be similar. This may take a lot of trial and error (using tissue samples from the patient), if it is even possible on a patient-by-patient basis. Get it wrong, and you may end up damaging other genes and thus causing side effects that could be severe.
Third, you then have to be able to replace the mutated sequence with a healthy alternative, which is another thing you have to get right based on the individual patient’s genome.
Fourth, you have to be able to deliver your treatment to every cancer cell (or at least to enough of them that the patient can go into remission for a long time before needing treatment again). This is also really difficult. You either need a way to target cancer cells specifically (which, if you have that, that in itself would be a much more direct route for treatment), or you need to be able to target every cell within the area that is known to be affected, e.g. entire organs or bodily systems.
There are gene-editing based cancer treatments being researched, but they tend to have a different approach: programming some of your own immune cells to target the cancer.
In general, trying to turn cancer cells back into healthy cells is kind of overkill. In the vast majority of cases, you can survive losing each and every one of those cells. So why not just destroy them? In fact, not only can you typically live without the affected cells, but often their very presence is a problem, because they are taking up space and using up resources in places where they aren’t needed. You’re not going to be healthier after turning a colon tumor back into a big lump of “normal” colon cells, because it’s not healthy to have a lump in your colon to begin with.
genetic engineering on grown humans is very inefficient, at best we can hit 1-2% of target cells, or something like that. For some diseases and indications, that is enough to make a difference. For a cancer treatment to work though, we would need to be able to reliably hit every single one.
Because cancer is not a DNA mutation.
In a.test where the nucleus of a cancer cell was transplanted (both ways) with the nucleus of a normal cell, the normal cell with the cancer nucleus reproduced normal cells, while the cancer cell with the normal nucleus reproduced cancer cells. This proves that it’s NOT a mutation of nucleic DNA
Cancer is a metabolic disease.
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493566/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493566/)
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