Yi-Bin Chen, MD: We should talk a little about the fact that not everybody gets graft-vs-host disease after transplant. The big reason is because every recipient receives some prevention or prophylactic strategy. Nelson, do you want to take us through the different ways people can be prophylaxed against graft-vs-host disease?

Nelson J. Chao, MD, MBA: Everybody gets a graft-vs-host reaction because there are allogeneic cells going into an environment that’s inflamed. But clearly, not everybody gets graft-vs-host disease. Historically, it was primarily methotrexate initially, and then cyclosporine became available in the late 1980s. The combination of cyclosporine-methotrexate, or a calcineurin inhibitor and methotrexate, has remained the standard in many practices. There have been multiple variations around it. There have been attempts in making calcineurin-free regimens. Probably the most recent is post-transplant cyclophosphamide, which has changed the field in our ability to do haploidentical transplants. That’s on the pharmacological side.

There has been lots of interest in doing graft manipulation by trying to delete T effectors, CD20-positive cells, and CD69-positive cells, using CD34 selection as a way of improving this, and there have been a lot of data on ATG [anti-thymocyte globulin] for many decades. None of these have been shown to be much better in overall survival than the standard approaches.

Yi-Bin Chen, MD: It’s exciting, and I’m looking forward to seeing how this field develops. There are ongoing trials comparing calcineurin inhibitor–based to post-transplant cyclophosphamide-based regimens, and we may have a new standard of care. At the same time, other agents have shown promise added on, such as abatacept recently, and other agents and trials as well.

Transcript Edited for Clarity