The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
but what's interesting about that is that some people develop resistance because the engine cancer cells evolve and they find a way of resisting but that resistance it becomes a linear problem you figure out what the mechanism the resistance is and you drive a second stake through cancer heart and when it becomes resistant to that he drive a third stake and so forth
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Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
so what is the probability that there are going to be cells present that are resistant to both still high you have a big denominator you know so but now let's say you you have a million so let's say you give one drug you get it you know you really do a great job you're down to a million cells let's say 10 million cells now you add the second drug and so now it's what's what is the probability that within this 10 million uh that you you will have some resistance knock it down again give a third drug now what's the probability let's say of a hundred thousand so you see what i mean
remember that that the ones that are resistant are also have to deploy mechanisms of resistance