A new bigger cluster of cells emerging that divides forming.
What happens once such a cluster is formed.
I think it’s plausible that 1) happening more frequently in older people is due to a weaker immune system as the largest factor.
As 2) happens and a tumor develops more mutations it activates telomerase production (which results in the cancer keep on growing), develop drug resistence, create some attack surfaces for the immune system and also remove attack surfaces for the immune system.
The interaction between the immune system and a tumor is that every cells automatically presents subchains of it’s proteins on it’s sell surface as antigens. It’s the nature of a tumor that some tumor cells have protein sequences that differ from the other cells in the organism due to mutations. When the part of the sequences that’s mutated gets presented on the cell wall, the immune system can attack the tumor cells.
If a tumor mutates in a way to shut down the process of antigen’s being presented on it’s outside, other immune system processes are there to kill those cells.
One theory would be that the primary aging clock is reduced thymus size. A smaller thymus means a weaker immune system and it’s plausible that this is the primary reason cancer develops more often in older people.
Interesting! Can you give me some background on where those ideas come from? I haven’t specifically studied cancer biology yet so I don’t know if this is something an intro textbook on the subject would cover, or whether they’re to some extent your original ideas?
The fact that immune function is worse in older people is standard knowledge and johnswentworth wrote a post about the thesis that the thymus might be a central factor here.
The fact that cancers have to mutate to activate telomerase production to be able to constantly replicate seems to me like a cancer 101 thing. There might be some cancers that happen in stem cells that actually produce telomerase naturally but it’s necessary for normal cells.
A decade ago, cancer vaccines were targeting single targets and usually proteins that are developed in the fetus but not in adults. The personalized cancer vaccines currently in development are about sequencing the cancers of a patient and then creating vaccine’s to targets a bunch of different mutations. I got that knowledge from an explanation about cancer vaccines.
This process of antigen presentation is done by MHC (Major Histocompatibility Complex)-molecules.
Lastly, as complete abrogation of antigen presentation can lead to natural killer (NK) cell-mediated tumour killing, we also discuss how tumours can harbour antigen presentation defects and still evade NK cell recognition.
Here it seems that it’s possible for a cancer to mutate in a way where it has some antigen presentation defects and still avoid NK cell recognition but it doesn’t seem to be the standard case.
One distinguishing factor of cancer cells is that they either have to present antigens of their mutations on their cell walls or fail to present some antigens that normal cells present on their cell wall.
Given cancer patients NK cells is one way of cancer immunotherapy that’s currently studied. There’s recent research on artifical NK cells.
There’s the general issue of biology usually being complex and there being a lot of unknowns, so when I say it’s plausible that reduced immune function is the most important reason for more cancers in old people, I’m not claiming that we currently have evidence for that thesis but that what we know is compatible with the thesis.
Cancer was two levels that are quite distinct.
A new bigger cluster of cells emerging that divides forming.
What happens once such a cluster is formed.
I think it’s plausible that 1) happening more frequently in older people is due to a weaker immune system as the largest factor.
As 2) happens and a tumor develops more mutations it activates telomerase production (which results in the cancer keep on growing), develop drug resistence, create some attack surfaces for the immune system and also remove attack surfaces for the immune system.
The interaction between the immune system and a tumor is that every cells automatically presents subchains of it’s proteins on it’s sell surface as antigens. It’s the nature of a tumor that some tumor cells have protein sequences that differ from the other cells in the organism due to mutations. When the part of the sequences that’s mutated gets presented on the cell wall, the immune system can attack the tumor cells.
If a tumor mutates in a way to shut down the process of antigen’s being presented on it’s outside, other immune system processes are there to kill those cells.
One theory would be that the primary aging clock is reduced thymus size. A smaller thymus means a weaker immune system and it’s plausible that this is the primary reason cancer develops more often in older people.
Interesting! Can you give me some background on where those ideas come from? I haven’t specifically studied cancer biology yet so I don’t know if this is something an intro textbook on the subject would cover, or whether they’re to some extent your original ideas?
What I wrote isn’t very original.
The fact that immune function is worse in older people is standard knowledge and johnswentworth wrote a post about the thesis that the thymus might be a central factor here.
The fact that cancers have to mutate to activate telomerase production to be able to constantly replicate seems to me like a cancer 101 thing. There might be some cancers that happen in stem cells that actually produce telomerase naturally but it’s necessary for normal cells.
A decade ago, cancer vaccines were targeting single targets and usually proteins that are developed in the fetus but not in adults. The personalized cancer vaccines currently in development are about sequencing the cancers of a patient and then creating vaccine’s to targets a bunch of different mutations. I got that knowledge from an explanation about cancer vaccines.
This process of antigen presentation is done by MHC (Major Histocompatibility Complex)-molecules.
Searching a bit gives me https://pubmed.ncbi.nlm.nih.gov/33750922/ for the thesis about complete stop of antigen presentation:
Here it seems that it’s possible for a cancer to mutate in a way where it has some antigen presentation defects and still avoid NK cell recognition but it doesn’t seem to be the standard case.
One distinguishing factor of cancer cells is that they either have to present antigens of their mutations on their cell walls or fail to present some antigens that normal cells present on their cell wall.
Given cancer patients NK cells is one way of cancer immunotherapy that’s currently studied. There’s recent research on artifical NK cells.
There’s the general issue of biology usually being complex and there being a lot of unknowns, so when I say it’s plausible that reduced immune function is the most important reason for more cancers in old people, I’m not claiming that we currently have evidence for that thesis but that what we know is compatible with the thesis.