How, exactly, would you find every cancerous cell in the body and immobilize it? Not only is every type of cancer different, with each person bringing a different genetic structure to the cancer, but cancers mutate, so that there can be more than 100 different mutations in a single tumor.
So each cell will be mostly like all of your other cells genetically, but slightly different from your regular cells in thousands of different ways. And the blood isn’t just in big veins, it’s also in a network of capillaries so thin that red blood cells have to slide through single file. Even if you could design a filter that allowed healthy cells to pass while grabbing cancerous ones, you’d never get a filter into all of those capillaries.
On a related topic, mothers can have genetic material from the children they’ve borne floating in their blood up to ten years after they’ve given birth. The easiest bits to identify are Y-chromosomes from sons. No one can filter those out, either.
Thinking some more. I don’t think the process of metastasis is “known and understood” in the way you think it is.
In my sister’s case, she developed an infection in her intestines. An operation would have, in the doctor’s opinion, likely killed her. Rather than go through any more medical procedures or try more drugs, she chose to just let her life run out (with the help of painkillers). This was with chronic leukemia (CLL). Most people do not actually die from this disease but from something else due to a depressed immune system.
Does it ever happen that during an autospy of (say) a gunshot victim, it’s discovered that the deceased happened to have had advanced cancer spread throughout various parts of the body – and yet the deceased never complained of pain/discomfort, never went to the docot, and apparently lived many years with a significant number of “well-placed” tumors in their bodies?
Similarly, my father had mesotelioma (misdiagnosed as lung cancer until I asked if it was possible to have “cancer of the pleura” during his third and final bout - this led to changing local cancer-classification protocols), but the terminal CoD was an aortic aneurysm which had been discovered during his cancer-related analysis and which could not be treated while he was being treated for the cancer. And holy run-on sentence, Batman!
An incidental finding of cancer is actually quite common. What is much less common is discovering an asymptomatic yet “advanced” cancer where there has been “spread throughout . . . the body”.
Occult cancers of the thyroid gland seem to be particularly common. If you look hard enough, you will find the presence of thyroid cancer in around 25 percent of apparently healthy young people (who died from accidents, etc.). Reference 1 and reference 2.
In men over age 60, the prevalence of prostate cancer is over 40 percent. In men over age 80, the prevalence is even higher - about 60 percent. (reference)
Findings like these should compel us to think hard before treating small, asymptomatic cancers of the prostate in particular.
Advanced metastatic cancer will almost always be symptomatic in some way, and most of the time it may be apparent in some way to observers (weight loss, etc)… Some people may not report symptoms due to denial or stoicism.
I am sure that there are cases of early metastatic cancer in autopsies done for other reasons.
Numerous unsuspected cancers (that is true cancers, not benign neoplasms, at least by microscopic examination) are found in autopsy studies that may try to get at the baseline incidence of undetected cancer. This is especially true of the breast, prostate gland, and thyroid gland. The existence of so many incidental cancers indicates the existence of “benign” non-lethal cancers, fuelling controversy about cancer screening programs.
Nitpick that cancers and neoplasms mean the same, unless you’re differentiating specific lesions within a continuum of lesions (for example cervical intraepithelial neoplasia progressing to cervical cancer).
Is the immune system only attacking free floating met cells, or all cancer cells?
Interesting about the lymphatic system. Thanks. I did some wiki link jumping and got to add to my vocabulary.
If the mets (can I use that term, or is that only for cells that have implanted and grown into a tumor) travel by blood vessels, it’s Haematogenous spread. If they travel by lymph vessels, it’s Lymphatic spread. They can also float in extracellular spaces, ending up seeding all over the surface of a cavity, such as the peritoneal cavity, which is Transcoelomic spread.
None of that would be easy to filter. Two would be impossible to touch by filtering blood. Although re-reading the entry, I obviously fixated on filter, when I shouldn’t have. The real question was how to stop the free cells or keep them from re-implanting. Filtering out by the body after the cells died without a home was assumed.
There are studies aimed at interfering with the implantation and growth of mets, but they’re piggy-backing off of new research on the process of metastasis, which is not completely understood. Every new bit of knowledge discovered about the process spawns other research trying to interfere with that bit of the process. The research is sort of like a cancer that way. I guess the short answer is “they’re working on it - it’s complicated.”
Hijacking the immune system to attack free floating mets would be a very cool trick. I don’t know if the immune system gets everywhere, but it gets most places.
The problem is, “the process” is known to have incredible variety.
I think it was Dostoevsky who said something like “Every happy family is the same, but every dysfunctional family is dysfunctional in its own special way.” The same is true of cancer. For a great book for the intelligent layperson, see Cancer: The Evolutionary Legacy by Mel Greaves. A very interesting read, and one that would add significantly to any layperson’s understanding.
Greaves points out early on that we expect a DNA mutation per 100K cell divisions. Given that we have trillions of cells, why don’t we ALL have cancer? The answer is that the body has a number of mechanisms to thwart it, including:
DNA error correction
uncorrected DNA error detection causing cell suicide (apoptosis)
inhibition signals from neighboring cells causing apoptosis
limits on number of cell divisions in a cell line (e.g., telomeres)
growth limits due to needing increased blood circulation
In addition, cancers that aren’t mobile are usually easier to fight (e.g., by removing the tumor). So, to be really nasty, a cancer has to metastasize, or has to be in a cell line that is already mobile (e.g., lymphomas)
For a cancer to succeed, it has to have at least 4 and usually 5 or 6 unrelated mutations, one to overcome each limitation.
No doubt there is hopeful research into common ways in which cells can metastasize, but my guess is that it’s terribly hard to predict the results of random mutations, so that even for this one step, there would be myriads of possibilities and no silver bullet to kill them all.
My (limited) understanding is that it usually takes a concentration of foreign cells to attract the immune system cells.
That would be “supercharging” rather than “hijacking” since it would be doing what the immune system is designed to do, only with more specificity. Yes, it would be great to be able to use an actual cancer cell to train the immune system to recognize it and differentiate it from healthy cells.
If I’m correct that the immune system could be good at attacking tumors but not at attacking met cells, then that might not be sufficient for a cure, but could keep the patient alive and far less symptomatic while other measures can be employed to attack the met cells themselves. Or perhaps, if we can kill all the tumors quickly enough, there won’t be a source for new met cells.