The next 1-5 years will tell us which cancers this new drug will work well on, right now it's only been tried in pancreatic cancer when people have failed their first treatment. The new drug from the article, daroxonrasib, has nine trials i see currently, here:

https://clinicaltrials.gov/search?intr=daraxonrasib&viewType...

The first two are the trial that just completed and showed success: people that have pancreatic cancer that failed other treatments, then a "trial" that is meant to give quick access to more people now that it's been shown to work.

Then there's a trial for using it as the first-line treatment for pancreatic cancer, one for lung cancer (NSCLC), and also various combinations with other drugs. I expect we'll see a ton of new trials registered in the coming year. Especially something in combination with colon cancer, because a common drug resistance mechanism in colon cancer is to develop KRAS mutation.

The thing is that we don't really know which cancers it will work well in until we try. And there's limited number of people with cancer that enter clinical trials, and we want to give each person their very best chance at survival, and then there's the massive expense of running the clinical trial itself, so learning happens slowly, one month of survival at a time, or one cancer recurrence at a time, or one death at a time. Patients that take part in clinical trials really are the heroes here. (Especially with the side effects of this new drug, which are horrible. It is a revolutionary drug, but we need to learn how to manage the other things it does as well, and that's going to take time.)

I think the meaning is that because we can see success with KRAS mutation of pancreatic cancer, we can now begin clinical trials for other cancers that may have KRAS mutation (colorectal, lung) and see if there is success there. If there is success in treating other cancers during clinical trials, it could be fast tracked through FDA to be more generally available and then become part of the national treatment option (ideally in 1-5 years after clinical trials).

It seems relevant here because the question was “How will this potentially help me if I get cancer?” and the answer is “Not at all unless you get a particular form of cancer that this applies to”.

> Bacteria are also all different, but still they are "one thing", and despite their diversity, antibiotics exist that can deal with many species of them at once.

Except people don’t ask “what if I get bacteria” the way they ask about cancer. If the story was about a new antibiotic that only affected 20% of common infectious bacteria strains and someone asked “in laypersons terms, how will this help me if I get a bacterial infection”, it would be appropriate to clarify that it only applies to some bacteria.

I understand where you are coming from here, but I think it is helpful for people to overtly grasp that there are very different cancers, very different treatments, and indeed very different outcomes.

Without this understanding it becomes a quick jump from "we're spending all this money on cancer" to "we've made no progress"

An example of the nuance plays out in the common cancers (like breast and prostrate). These have between 90 and 100% 5 year survival rates. Others (like the one in this article, pancreatic) have very poor survivability.

As you note, it's very unlikely that we'll "cure cancer". But we already "cure" (for some definition of cure) some cancers. Progress is slow, methodical, and incremental. It can feel like a lost cause when viewed from afar, but up close very real progress is being made. And that's an important message to pass along.

> I truly hope cancer will meet its "penicillin" one day (yes I know this is unlikely).

Penicillin blocks a specific enzyme (transpeptidase).

https://en.wikipedia.org/wiki/Penicillin-binding_proteins

Cancer cells, by definition, are not a uniform mass. It will depend on the cancer type, which in turn is defined by the properties those cells have. And mutations happen all the time, often more in cancer cells when their repair systems also have mutations, e. g. are less efficient. By that definition alone, there can never be a wonder-cure for all cancer types. At best you can find some proteins more important (p53 for instance) and while more than 50% of cancer cells have some form of mutation in p53, others simply don't. By that definition there will never be a penicillin-equivalent to all cancer types.

The problem is the similarities of cancer to normal cells. We have penicilin that works against all human cells. We call that poison.

Now, "no, i mean poisons that attack the special chemistry of cancer," oh yes, those we call chemo.

You've been downvoted but I would say you are right. It would be more accurate to say "cancer does not have one cause".

Benign cancers are a thing. They might not kill like they show in the Hollywood movies, but your quality of life will be significantly diminished.

For every cell mechanism that's being abused by cancer to fuel its growth, there are other cells in the body for which that mechanism is crucial for their correct functioning. Wholesale editing every cell in the body mostly guarantees that the patient does not die of cancer -- the cure will kill them before the disease does.

I have an even better proposal.

We'll just use you!

I don't much care what happens to most inmates but those with really long sentences should probably not be released early (or at all!) because they pose too much of a risk to the rest of us.

Are you going to give them cancer first too?

This is a horrifying proposal not only on the ethics front but also in the scientific uselessness of it.

This is exactly the type of thing that gave the Nazis the bad name they deserve.