Is this a reasonable way to think of cancer? The immune system is important, so, what would the immune system do with cancer? It would identify little runaway cells or groups of cells. What’s the difference between such a tiny runaway, and a tiny tumor? Do our immune systems wage frequent war with microscopic malignancies, and almost always win? And perhaps what we think of as having cancer is really the occasional case of one of these microscopic tumors surviving and winning its battle with the immune system. So, if there was some magical test that could detect even a single cell whose regulation of division had failed, that test would alarm frequently, but almost always going silent again.
If not, how should we think of the immune system’s involvement in cancer?
Perhaps this is just a definitional thing. Perhaps runaway cell division in little clusters happens all the time, but it isn’t defined as “cancer” until it reaches some size threshold or something.
Cancer is essentially a mutation in the nuclear genome of a cell. Despite the self-correction mechanisms in the process of mitosis, sometimes genes can be damaged in ways that they are still functional, or latent genes can be activated and expressed by various environmental or endogenous factors. This occurs quite frequently (estimated to be tens of thousands of occurrences per day, though it is difficult to find a definitive basis for estimate) but most of the time, these mutations are not fully functional and cause the cells to either repair the mutation (essentially slicing it out) or cause the cell to naturally die off (senescence mechanisms) without propagating. However, some mutations are robust against repair mechanisms or occur within those repair mechanisms and will grow and reproduce in an unchecked fashion beyond the normal passive nutriet diffusion they would receive; in essence, they start to consume neighboring cells and replace them with cancerous ones. In particular, cancer cells ignore normal hormonal growth factors that govern metabolic activity and cell lifecycle, and lose their normal regulation for senescence. If growth is left unchecked long enough, many carcinomas (epithelial tumors) will further mutate and metastasize, spreading from the origin site to other organs of the body.
There are a number of competing hypotheses of oncogenesis but there is not one fully accepted primary theory, and different types of cancer may have somewhat different mechanisms though all are essentially failures in the appropriate regulation of gene growth and sensecence mechanisms. One hypothesis that is gaining some traction is the reversion of normal cells to a pluripotent state where it becomes a stem cell for the colony of cancerous cells. It would explain why some cancers take so long to spread and are difficult to cultivate in lab animals while others grow rapidly and metastasize readily (differing levels of pluripotency) and why certain cancers tend to occur in specific age ranges rather than more uniformly across lifespan. However, this has never been directly observed in a lab (as far as I’m aware) and many cancers have other external causal factors that do not seem to require pluripotency, particularly oncoviral-induced tumors. We tend to lump “cancer” in one big box because all cancers kill by the same essential mechanisms—consuming all possible nutrients to grow in uncontrolled fashion, and starving the affected organs of nutrients and blood flow—but it is likely that there are different root causes and mechanisms by which different types of cancer originate.
So to address the o.p., we have a lot of mutations mitogoing on in the genome during normal cell mitosis, but that only very rarely results in ‘cancer’ unless there are external factors which reinforce the development of carcinomas. The normal cellular growth and sensescence mechanisms prevent most defective genomes from expressing dysregulation in those factors. Cancers have been known to go into sponteneous remission; essentially, just dying off without any apparent external intervention, and nobody really knows why, but it is presumbly some reactivation of sensecence mechanisms. Our only other ways of treating cancer are to excise is surgically and/or attack it with targetted toxins and radiation (chemotherapy and radiotherapy). The immune system, by the way, generally has little to do with any of this; the active immune system recognises most cencer cells as bing part of the body, although there are some types of cancer it can recognize (which is not always a good thing, paerticularly in scarcomas), and some cancer treatments can activate and target immune factors toward cancerous cells.
On the specific question of the role of the immune system: since it constantly monitors the entire body for aberrations that indicate the presence “non-self” (i.e. pathogens), it’s natural that the surveillance role has evolved to also help monitor aberrations that are early markers of dysfunctional proliferation in cells. It makes sense to use the same surveillance system to police both infection and cancer.
But it’s an integrated system in which ordinary cells actively monitor themselves, and will often help kill themselves if mutations give rise to a threatening problem. So, most of the time, it’s not right to think of it as an antagonistic process where the immune system is watching out for good cells gone bad. It’s an integrated regulatory and monitoring system in which all cells actively participate and also communicate with and cooperate with the immune system. Cancer only takes hold when the multiple regulatory and surveillance systems all fail.