Question

[In this post, I may ascribe agency to processes, inanimate objects or microorganisms: this is rhetorical, I know they don't intend anything. I will also use evolution in a fairly loose sense of learning (again, rhetorical agency) to overcome obstacles to survival].

Assumptions:

Cancers are caused by mutations of cells, and successful cancers are caused by mutations that result in a, sometimes literally, killer combination of

Suppression of their own apoptosis
Invisibility to the immune system or resistance to immune attack
Ability to co-opt biological resources such as bloody supply so they don't starve
The various types of cancer that we know and give names to are the end-points of available mutation pathways that cells can take to get to such a successful cancer state. Because lots of mutations result in cancers that don't work for some reason (e.g. immediately shut down by an immune response), they just don't result in a noticeable tumor. Therefore, we end up with a discrete set of familiar cancers, each representing a different path, and their frequency related to how likely it is that path is hit (i.e. how many mutations needed, etc).

Some cancers, the malignant ones, happen also to spread very effectively, though this is not specifically required by the above success criteria, so we also see benign tumors which don't spread but still can be said to succeed in that the cells survive.

Once mutated, cancers are presumably fairly genetically static within a single case, otherwise we'd see a storm of cancer variants developing within patients over a relatively short period as an evolutionary arms-race took place, much like the race between antibiotics and bacteria.

However:

Some cancers have quite advanced mechanisms for spreading1
Some cancers are extremely resistant to human treatment
The question:

How did these dangerous cancers becomes so dangerous? A dangerous cancer seems to be fully capable of effective spread in the first instance, rather than undergoing a complex evolutionary battle with the host's own anti-cancer abilities or some exogenous treatment.

Furthermore, even cancers that succeed can't effectively propagate themselves like bacteria, because they're always in the same body2. If anything, cancers that do not kill the host should be selected for, since people with genes near dangerous mutation opportunities would be less likely to reproduce effectively3. So (naively, since it's clearly not the case), if people do evolve such that they can get cancer4, cancers would tend towards being both benign and generally non-life threatening.

Even if they do somehow evolve to spread and threaten the host (as they indeed evidently have), why are they then also often so good at evading non-host treatment?

It seems like two warring armies (host vs. cancer) that have evolved together using hand weapons, evenly matched for centuries. The cancer invents the crossbow (mutates) and starts to win the war. Then, aliens (doctors) suddenly turn up with UAV surveillance and cruise missiles (imaging and treatment) and side with the host, but the cancer still wins much of the time, even though they're facing an Outside Context Problem that by rights they have no innate ability to counter.

So what results in these cancers being so adept at spreading themselves without some adversarial evolutionary process (à la bacteria vs. antibiotics)? Furthermore, how are they so often also resistant to human-directed treatment? Is it just because the human treatment is crude (i.e. not so much aliens but a large but unruly peasant milita that often doesn't really help that much)? Is there more evolution going on within a single cancer patient than I imagine?

Expansion in response to comments: if my assumption that the cancer cells are not usually evolving once formed is indeed incorrect: is that evolution then usually the cause of treatment escape? And does that mean that treatment-escaping cancers are freely evolving, in that they could take a number of case-dependent paths to escape (as opposed to the original recognizable cancer type which took one of a limited number of available mutation pathways through the fairly static environment of human biochemistry to become that cancer in the first place)?

Answer 1

Dangerous cancers become so adept at spreading and resisting treatment due to the inherent complexity of cancer biology. The mutations leading to a successful cancer are multifaceted, involving suppression of apoptosis, immune system evasion, and resource co-option. While the initial mutation pathways are somewhat limited, the variability in cancer behavior arises from ongoing evolution within the tumor microenvironment. Evolutionary pressures, both from the host and medical interventions, contribute to the adaptability and resilience of certain cancer cells, making them highly effective at spreading and surviving despite treatment.

Step-by-step explanation:

The development of dangerous cancers involves a combination of mutations that confer survival advantages, such as apoptosis suppression, immune system evasion, and resource utilization. While the initial cancer types follow distinct mutation pathways, ongoing evolution within a tumor allows for diversification and adaptation to the host's defenses. Treatment-resistant cancers often emerge from this dynamic evolution, as cells with advantageous mutations survive therapeutic interventions. The adaptability of cancers to both the host environment and medical treatments contributes to their dangerous nature.

The dynamic nature of cancer evolution within a single patient and the interplay between cancer cells and treatment strategies. Understanding the molecular mechanisms driving cancer evolution and resistance can inform the development of more targeted and effective therapies.