I doubt "10s of millions of Americans" can describe the core functions of the NIH

> when scientists are hired because they know someone, or are part of some “group” rather than being the best choice.

How do you think new appointees and hires in the NIH/HHS are selected? Political loyalty seems to be a better predictor than scientific impact or output.

> Also not interested in funding anything not research related, including various “offices” that have nothing to do with supporting research. Lots of things to like about these cuts.

The cuts and changes are dramatically impacting research support. Grant money is not being disbursed at the same rate since the new review changes began. You can more plainly characterize the changes as harmful to research in general than focused on removing whatever specific things you don't like.

The political left, of course, is the opposite and obsesses over Type I error. Accepting the wrong people and ideas is less important than getting good results. This leads to things like Lysenkoism, but also tends to reject less successful research, given the other checks and balances built into a healthy system.

Prove it. Prove this happens at a large scale. This is just nonsense talking points.

That is not true for most cancers, though.

However this is just the first version of the drug, it can be combined with other modalities to allow more selective targeting of cancer versus not cancer cells (e.g antibody-drug conjugation). And when used in earlier stage cancers, rather than the advanced cancers in this first clinical trial, there's the possibility of lower dosing that has less strong side effects.

This is just the first attack that has ever broken through to hit a key weakness of some cancers. It's the start of learning, a breakthrough that will launch refinements, enhancements, and a ton of innovation. That sort of innovation is sometimes derided as "me-too" drugs, and not meaningful, but some of the biggest advancements in cancer care have been from taking very hard to tolerate treatments and making them more tolerable and refined and better for patients, allowing longer and more thorough killing of cancer cells. I would expect we will see a lot of that here, as well as work towards combinations with other drugs.

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.)

When we first started getting good at sequencing the DNA of tumors, I remember initial reports of taking samples across the 3D space of a tumor and finding great spatial heterogeneity in the tumor genomes.

I'm actually most excited for using this drug in combination with colon cancer, where KRAS mutation is a common drug resistance evolution in response to drugs that target the gene EFGR (though cancer researchers may all have their favorites to go after, colon cancer went after my family especially hard).

Ways to avoid specific resistance include multiple treatments simultaneously, since the probability of generating resistance to both is the product of the probability of resistance either.

We'll just use you!

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.

> 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.

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.

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

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.

This is very true. It was certainly a lot of work for us, and a lot of work for them.

In the first months I was cooking everything.

By the end of the chemo treatment the patient had learned to cook these new meals for themselves.