3 ms·
> The hope is that, without PD-1, the edited cells will attack and defeat the cancer. It seems that we already have good drugs which inhibit interaction betwee
by yread 10y ago
> The hope is that, without PD-1, the edited cells will attack and defeat the cancer.
It seems that we already have good drugs which inhibit interaction between PD-1 and PD-L1 is there really enough benefit from this?
- psychometry 10y agoThe effectiveness of drugs like pembro varies with cancer type and other factors. Here's a recent study where patients exhibited only a 56% response rate: http://www.nejm.org/doi/full/10.1056/NEJMoa1603702 http://www.nejm.org/doi/full/10.1056/NEJMoa1603702 The field is extremely promising and it's worth exploring fully, especially considering that even good responders can suffer relapses due to subclonal evolution.
- Gatsky 10y agoThose drugs cost $100K+ per year, and have toxicity.
- ejstronge 10y agoI can't imagine that personalized gene editing therapy will ever be cheaper than the current checkpoint blockade agents. It will be interesting to see if there are differences in side effect profiles in the PD-1 knockout T-cells vs our current biologicals, however.
- Gatsky 10y agoI took the original comment to be asking why bother taking out PD-1 from the T-cells. The answer is that it obviates the need for checkpoint inhibitors, which you would otherwise need to administer together with the CAR T-cells for best efficacy. Maybe they meant something different. Checkpoint blockade alone is a great development, but having treated patients with these drugs, I can tell you it is far from a cure for 80% of people.
- refurb 10y agoAgree with the other comment that CRISPR is unlikely to cost less. Also, there is toxicity associated with gene modification. Take a look at the patient deaths with CAR-T therapy.