Discussing the Immune System and Improving Outcomes in AML

One of the interests of Daniel Peters, MD, is to evaluate the drivers of immune dysfunction and identify the immune cells in a patient with acute myeloid leukemia (AML) that can be targeted to generate less intensive cellular therapy strategies. CancerNetwork® spoke with Peters, an assistant professor of Hematology and Oncology in the Department of Medicine at the Medical College of Georgia of Augusta University and bone marrow transplant & cellular therapy faculty member at Georgia Cancer Center, during a site visit to Georgia Cancer Center.

As Peters stated, AML is a disease that leads to a lot of immune dysfunction. For patients who are being treated for their disease with azacitidine (Vidaza) and venetoclax (Venclexta), one question that Peters noted was whether there are autologous cell therapies that could mitigate some major toxicity that may stem from graft-versus-host-disease or bone marrow transplant.

Additionally, at Georgia Cancer Center, Peters highlighted his unique role to both diagnose and treat patients while also guiding them through the transplantation process. He noted that many other centers don’t offer the same opportunity, as leukemia and transplantation care are separated. With his role, he is able to conduct translational projects and research that explores new ways to help patients with AML.

Transcript:

AML causes a lot of immune dysfunction, and by immune dysfunction, I mean dysfunction in the normal patient’s immune system that’s just trying to live its life and do its job. One of my interests is to look at what these drivers of immune dysfunction are; what cellular components or subsets are dysfunctional in a patient’s immune system; and which of these cells can be targeted, exploited, or removed in hopes that we can create less intensive cellular therapy approaches for patients with AML. For patients who are going down this pathway of receiving the azacitidine and venetoclax, are there perhaps autologous cell therapies that we could use that would avoid some of the big [adverse] effects that you’d get with graft-versus-host-disease or bone marrow transplant? Or are there other ways to exploit the host immune system to augment or improve outcomes with standard allogeneic stem cell transplant?

Another thing I’ll just say is that I uniquely have the opportunity and privilege here at the Georgia Cancer Center, with my position, to both diagnose and treat patients with AML and take them up to and through the transplant process in and of itself. In a lot of other centers, the leukemia care and the transplant care are partitioned, but here, I can actually do both. That enables me to do some of these translational projects and some other research that I’m interested in.

How would this translate into benefiting patients? Essentially, what I’m hoping to do is find new therapies that are going to improve outcomes, cause fewer [adverse] effects, and be more accessible to a variety of patients who have AML.