I'll read the publication in the coming days and report back, but don't get your hopes up. There's a "breakthrough" in cancer research every few months and it leads to nothing. And this study was done in mice which are a bit different to humans (citation needed)

[–] chosensilence@pawb.social 30 points 2 weeks ago (1 children)

while you're not wrong i do want to reiterate that mRNA vaccines are likely going to be how we treat and cure cancers so there is precedent at least for this to be massive news. if not this there will likely be a real announcement one day.

[–] tburkhol@lemmy.world 21 points 2 weeks ago (1 children)

The likelihood that all cancers express a common surface marker that is never expressed by any non-cancerous cell seems pretty low. Not a cancer biologist, but there's all kind of different genetic paths to cancer - why would they all cause some specific molecule to be expressed and why would no other cell ever use it?

[–] AmidFuror@fedia.io 24 points 2 weeks ago

Your instincts are correct. The approach in the paper is more complicated than this. Here is the abstract:

Abstract The success of cancer immunotherapies is predicated on the targeting of highly expressed neoepitopes, which preferentially favours malignancies with high mutational burden. Here we show that early responses by type-I interferons mediate the success of immune checkpoint inhibitors as well as epitope spreading in poorly immunogenic tumours and that these interferon responses can be enhanced via systemic administration of lipid particles loaded with RNA coding for tumour-unspecific antigens. In mice, the immune responses of tumours sensitive to checkpoint inhibitors were transferable to resistant tumours and resulted in heightened immunity with antigenic spreading that protected the animals from tumour rechallenge. Our findings show that the resistance of tumours to immunotherapy is dictated by the absence of a damage response, which can be restored by boosting early type-I interferon responses to enable epitope spreading and self-amplifying responses in treatment-refractory tumours.

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