My understanding is that cancer cells become dangerous when they figure out a way to divide without shortening their telomeres. This makes them effectively immortal.
How long does it take a normal cell to loses its telomeres, degrade and die?
If a cancer wasn’t immortal, would it disappear when the rogue cells reached the end of their natural lifespan? Could this be a reason behind spontaneous remission?
Do I have a correct understanding here, or am I totally pulling this out of my rear (more likely)?
All cell types are different. We have cells in our body that divide quickly and are quickly replaced. Certain cells in the intestinal epithelium divide and replace themselves every 10-ish hours, mouse skin stem cells divide every 200 hours.
I use human T cells in culture. Normal T cells have to be stimulated to divide. If I put them in the incubator, they will live, but not divide unless “activated”. Cancerous T cells do not need to be activated to divide. Normal and cancer will all die at the same rate, but the cancerous cells will replace themselves without any prompting. Some of the checkpoint mechanisms in these cells is defective. The T cell should only be active if it has a job to do, but the cancerous cell T cell is fooled into thinking it has something to do, so it divides.
Cancer cells do die. There just happens to be so many of them dividing and proliferating in contrast to the normal cells that they overwhelm the normal cells.
You might not be quite as full of shit as you think. That is, you could still be totally wrong, but someone could probably start a legitimate research project along these lines. But I should note that I am not a cancer biologist*.
The bit of info you’re probably thinking is the number of cell divisions that can occur before telomeres are too short. This is the Hayflick Limit, and tends to be around ~40 divisions for most cell types. My understanding is that some more benign tumors do stop growing when they hit this limit. It’s conceivable that a more aggressively dividing tumor could grow enough to make a patient very sick, but then hit the Hayflick limit and stop.
A quick look around Pubmed shows that a lot of cancers are associated with odd telomere dynamics, but at first glance I don’t see anything about the telomere dynamics of cancers that go into remission.
Note that there is a large array of different cancer mutations that make telomeres irrelevant. Generally, the idea is that a too-short telomere will lead to DNA damage and trigger apoptosis (cellular self destruct). Cancers can get around this in many ways, either by finding a normal or abnormal way to lengthen telomeres, or by losing anything along the signalling pathway that leads from DNA damage detection to apoptosis. There’s lots of ways for a cancer cell to go wrong, and each cancer is practically unique.
*I do hang out in a department full of them and have managed to soak up a bit of cancer biology along the way.