I am not aware of which ones could potentially reach every cell type but so long as you have a library of methods capable of carrying a large enough payload, and the scope of the library covers every cell type, then you do have a “universal method”.
No, because cancer can mutate to invalidate ways of passing through the cell wall.
I am claiming a generalized solution to cancer that is still customized for every tumor is possible. Are you claiming otherwise and why?
I described a generalized solution in the post you were replying to that’s customized. You described a different one and one that does not actually work as a universal solution.
Such a mutation has to be possible. (in a probabilistic sense—if it requires hundreds of bases of change, and there is not an evolutionary vector pointing that way (microevolution for the cancer) it will not occur in meaningful numbers to matter)
Your solution fails because it’s the “perfect traitor” problem. It is possible for a cancerous cells to display all the right flags the immune system cannot tell it’s part of the tumor.
It sounds to me like you are thinking about this in the abstract without really thinking through the actual biology.
Substances cross the cell wall because cells have mechanisms to transport them through the cell wall. If the proteins necessary for those mechanisms get disjunctional because of mutations, the mechanism stops working.
A cancer cell has no way to stop bunch of random mutations from happening. The idea that it could sounds to me like it misrepresents what cancer is about by a lot.
I would argue every criticism you make can aim at yourself. Obviously viruses have injection mechanisms that can bypass most defenses. If they didn’t virii wouldn’t work.
The rest of it shows a poor understanding of evolutionary algorithms.
Basically, you don’t understand enough biology to see the difference between the two.
Viruses are evolved to interact with relatively stable targets. If we take COVID-19 for example, the ACE2 receptor is used by the virus. If all human cells would stop producing ACE2 receptors the infection doesn’t work.
There are mechanisms to present peptides or protein fragments on the cell wall. Those can break down, but that’s detectable by the immune system because the cell wall look differently.
If they are not broken down they will display any protein fragments that float around in the cell. It’s the nature of cancer that a lot of what floats around within a cell has mutations.
Not having a bunch of random mutations is the one thing that a cancer cell can’t do due to evolutionary pressure.
No, because cancer can mutate to invalidate ways of passing through the cell wall.
I described a generalized solution in the post you were replying to that’s customized. You described a different one and one that does not actually work as a universal solution.
Such a mutation has to be possible. (in a probabilistic sense—if it requires hundreds of bases of change, and there is not an evolutionary vector pointing that way (microevolution for the cancer) it will not occur in meaningful numbers to matter)
Your solution fails because it’s the “perfect traitor” problem. It is possible for a cancerous cells to display all the right flags the immune system cannot tell it’s part of the tumor.
It sounds to me like you are thinking about this in the abstract without really thinking through the actual biology.
Substances cross the cell wall because cells have mechanisms to transport them through the cell wall. If the proteins necessary for those mechanisms get disjunctional because of mutations, the mechanism stops working.
A cancer cell has no way to stop bunch of random mutations from happening. The idea that it could sounds to me like it misrepresents what cancer is about by a lot.
I would argue every criticism you make can aim at yourself. Obviously viruses have injection mechanisms that can bypass most defenses. If they didn’t virii wouldn’t work.
The rest of it shows a poor understanding of evolutionary algorithms.
Basically, you don’t understand enough biology to see the difference between the two.
Viruses are evolved to interact with relatively stable targets. If we take COVID-19 for example, the ACE2 receptor is used by the virus. If all human cells would stop producing ACE2 receptors the infection doesn’t work.
There are mechanisms to present peptides or protein fragments on the cell wall. Those can break down, but that’s detectable by the immune system because the cell wall look differently.
If they are not broken down they will display any protein fragments that float around in the cell. It’s the nature of cancer that a lot of what floats around within a cell has mutations.
Not having a bunch of random mutations is the one thing that a cancer cell can’t do due to evolutionary pressure.
The lipid nanoparticle mechanism used by the mRNA vaccines could have had a cancer destroying payload.
As I understand it the lipids merge with cell membranes, it’s receptor independent.
So unless the cancer cell can evolve to not have a cell membrane it’s vulnerable.