RAD51

If your cancer happens to be deficient in one of the homologous recombination pathways.

If you have BRCA1, BRCA2, RAD51, any of the other mutations that mess up that system and make you and your cancer a candidate for PARP inhibitors like oliparib or rucoparib, those pair incredibly well with immunotherapy.

They actually prime immunotherapy responses.

And so those are much more likely to get you an abscopal effect.

And the patients were selected.

For HRR, HRR includes PALB2, ATM, CDK12, RAD51.

There's about 12 genes.

And what they found was that the patients that had BRCA1, BRCA2, okay, that received avidarone with norepinephrine, versus Aviron alone with ADT, there was actually an improvement in PFS of 0.52 with a 48% reduction.

So this recombination process and the repair mechanisms that are going to be important for stitching these things together, is it pretty similar in humans? It's not something that we could target necessarily in the parasite?

It's a homologous recombination mechanism, but whether, I guess if you could disrupt, RAD51 is one of the key enzymes, for example, that's responsible for this process.

If you could block VSG recombination, I guess it's...

I think actually, yeah, probably the mechanism is going to bypass this.