3 ms·
This isn’t ‘evolution busting’, have to laugh at university PR. The drug has modest single agent activity, and is additive with a chemotherapy drug in an animal
by Gatsky 7y ago
This isn’t ‘evolution busting’, have to laugh at university PR. The drug has modest single agent activity, and is additive with a chemotherapy drug in an animal model (not synergistic). The mechanism of action is a bit interesting, it seems to make cells rush through the cell cycle.
The drug development is going to be complicated. The drug doesn’t work well by itself, so getting the right combination dosing and schedule is crucial. It also only works in some tumours and there is a candidate biomarker, so a clinically meaningful assay has to be developed. There is also no idea about toxicity yet. Long road ahead.
- executive 7y agowhat a downer
- gus_massa 7y agoI agree. It looks promising but IIUC it is just a new chemotherapy drug. The general idea of killing cells that reproduce is common in many (most?) of the chemotherapy drugs, so they produce nasty side effects like perhaps killing the bone marrow that also have (healthy) cells with a fast preproduction cicle. I really don't understand the evolutionary/Darwinian spin. It doesn't make sense, it looks like a buzzword. They just (try to) kill all the cells that reproduce like other chemotherapy drugs.
- entee 7y agoThere are even DNA and cell division targeted agents. Colchicine kills cells by messing with DNA segregation between dividing cells. This one appears to promote division? Though I haven’t read all the details.
- gus_massa 7y agoI think it doesn't promote cell division directly. IIUC this make the cell during the division to not wait until the chromosomes are correctly split, so the new cell have a high chance of getting a wrong number of chromosome and die. Since the cell doesn't wait until everything is in order, the division is faster. Form the abstract: https://mct.aacrjournals.org/content/18/10/1696 https://mct.aacrjournals.org/content/18/10/1696 > In in vivo pharmacodynamic experiments, BOS172722 potently inhibits the spindle assembly checkpoint induced by paclitaxel in human tumor xenograft models of TNBC, [....] I think the key part is "spindle assembly checkpoint" https://en.wikipedia.org/wiki/Spindle_checkpoint https://en.wikipedia.org/wiki/Spindle_checkpoint
- entee 7y agoOh interesting. It's basically working in a similar way to Colchicine then. Colchicine blows up the microtubules so the chromosomes don't segregate properly. The combination of the two might be effective, though I suspect there's a toxicity issue or something else I'm missing.
- rubatuga 7y agoI mean, every cancer therapy drug would be 'evolution busting' if this was the case.
- dang 7y agoOk, we've busted that bit out of the title above.