Yeah, more or less. A risk assessment for the study is done and submitted and there's many more layers of beurocracy (both the good human-protective kind and the less-good regulatory capture kind). Providing things like information on effects and generalized consent forms and whatnot are included so the patient is given prior understandings of what the effects might be, from animal studies or previous human studies in some cases if you're testing for a novel effect in an existing treatment, for example, have determined might occur. You then, ideally, do a double blind study on the group of participants.

You missed my point, how would you safely analyze aspirin mechanism over t-cell in humans, without relying on genetically engineered humans with suppressed genes ?

If the scientist went to use genetically modified mice, I assume it's because there is no easier, non invasive test, to analyze the influence of platelets over the T-cell behavior. Like using a microscope or chemicals.

I'm not talking about signing a form but the technical aspect. However if you know how, please share, it would be interesting.

It was an honest misunderstanding. I am completely ignorant on this subject, honestly trying to understand something.

Like, why would the humans need to have a specific generic configuration? Only with some specific genes the T-Cells are affected by platelets? This is not something that happens on every human?

I just reread the article and went to look for the publication.

> The discovery, published in the journal Nature, happened by accident as the scientists were not researching aspirin.

> The team in Cambridge were investigating how the immune system responded to cancers when they spread.

> They were using genetically engineered mice and found those lacking a specific set of genetic instructions were less likely to get metastatic cancer that had spread.

From the publication : > Here we show that inhibitors of cyclooxygenase 1 (COX-1), including aspirin, enhance immunity to cancer metastasis by releasing T cells from suppression by platelet-derived thromboxane A2 (TXA2).

Safe to say my assumption was wrong, they didn't use generally modified mouse because they had no other choice but because they were looking for something else.

> This is not something that happens on every human?

It's usually much harder in science to understand and prove the 'how' than it is to check the 'if'. To prove a mechanism you got to be able to track it, for instance by using radioactive product, or use such a way that you refute all other casualties.

I think in that case, it would have been possible to prove the mechanism by using several different inhibitors of cyclooxygenase, checking if the effect on spreading cancer is still there. If yes, it's a good indication of casualties.

I see! Thanks for the detailed response, it is much clearer now. I couldn't glean as much detail reading it myself.

Sounds promising, honestly, obviously having to weigh in the risks of using medication that inhibits the action of platelets.