Emerging Therapies for Acute Myeloid Leukemia

Transcript:Elias Jabbour, MD: Marty, I want to ask you about Mylotarg; Mark mentioned Mylotarg. Do you think it’s time for Mylotarg to come back? I know you’re involved in the SWOG trials. What do you think: will Mylotarg ever come back?

Martin S. Tallman, MD: I think that it may come back. I think there are several exciting roles. One is less important today, and that is in APL. It’s a very effective agent in APL. APL cells actually express CD33 among the most extensively among many other AML. So, it’s possible, although our therapy today for APL is so good that I’m not sure it’ll be needed there. But there are data, particularly from the British group, suggesting that Mylotarg, or an anti-CD33 antibody, may play a role in core-binding factor leukemias. So, I think either Mylotarg or, perhaps as Mark suggested, the new cytogenetics anti-CD33, may play a role.

Mark J. Levis, MD, PhD: If you’re in the UK and you have core-binding factor leukemia, that’s actually part of the standard of care in the UK.

Elias Jabbour, MD: And in the most conservative place. Richard, before we conclude this session today, we hear about immune therapy a lot—nivolumab, pembrolizumab, and other agents. Do you think there’s a role for the drugs in factor leukemia?

Richard M. Stone, MD: I think there’s a role to study them. Right now, the signal is not great enough to write a prescription for pembrolizumab, which will be extremely expensive, for example, in AML, except for one important area. People from our place, Matt Davids and others, published a paper in NEJM and describe the use of ipilimumab in people who have relapsed after transplant. It was in other diseases, too, but there were some responses, particularly in people with extramedullary leukemia. So, that’s something we need to learn more about obviously. The milieu is completely different in the post-transplant relapse setting where there are some donor cells around. But, I think we need to look into those.

Elias Jabbour, MD: Well, this has been extremely informative. Before we end this discussion today, I’d like to get final thoughts from each of our panelists. I want to start with Dr. Erba.

Harry P. Erba, MD, PhD: I think, again, the challenge that we’re going to have now is trying to decide how to combine these agents. But, more importantly, as we look at targeted therapies, really trying to better define who are the patients who are going to benefit is going to be a challenge because, as we heard from Rich, AML is very heterogeneous with small subsets. And it may be that we can move away from chemotherapy in very defined subsets like we have in APL, which was one of our major advances. But, for the time being in the management of AML, I see chemotherapy is not going away, as excited as I am with all of these other agents.

Elias Jabbour, MD: Dr. Levis?

Mark J. Levis, MD, PhD: So, the cynic is tempted to say that we’re still using 7+3. What has really changed? I actually remain remarkably optimistic. I think the survival curves are going up, not just because of supportive care, but because we understand the disease better and know who to treat. And so, I think, in fact, we are going to continue to push the survival curves up and up, in an incremental fashion, but I’m a patient man.

Elias Jabbour, MD: Okay. Dr. Stone?

Richard M. Stone, MD: I share the optimism of my colleagues. The challenge is going to be proper use of these agents, and in a carefully designed rational way. Yes, it’s great that some of these drugs are approved for other cancers, but we have to be careful about using them in a willy-nilly fashion because we might be harming patients, adding the cost to medical care, and not learning anything. So, I certainly support prospective clinical trials to figure out what’s what in this disease.

Elias Jabbour, MD: And Dr. Tallman?

Martin S. Tallman, MD: I continue to also believe that there really has never been a more exciting time in our field. I think the future will be about combinations and collaborations, as we are dissecting cytogenetic, molecular genetic subsets of AML into smaller groups. And we’re going to have to continue to collaborate around the world.

Elias Jabbour, MD: That’s great. Well, thank you all for your contributions to the discussion. On behalf of our panel, we thank you for joining us, and we hope you found this Peer Exchange® discussion to be useful and informative.

Transcript Edited for Clarity