Future Treatment Landscape of AML

EP: 1.Role of Molecular Testing in AML

EP: 2.Molecular Testing in Community Practices

EP: 3.FLT3 Testing for Treatment of AML

EP: 4.Prognostic Significance of IDH Mutations in AML

EP: 5.Assessing MRD Status in AML

EP: 6.MRD Monitoring in FLT3 ITD AML

EP: 7.Role of FLT3 Inhibitors in Chemo-Ineligible AML

EP: 8.Management of AML: FLT3 Inhibitors and BCL2 Inhibitors

EP: 9.Sequencing of FLT3 Inhibitors in AML

EP: 10.Role of Dual Targeted Therapy in AML

EP: 11.Type 1/2 FLT3 Inhibitors in AML

EP: 12.BCL2 Inhibition in AML: VIALE-A Study

EP: 13.IDH1/2-Mutated Treatment-Naïve AML

EP: 14.Novel Targets and Biomarkers in AML

EP: 15.BMT CTN 1102 Study in High-Risk MDS

EP: 16.Use of Omidubicel Therapy in Hematologic Malignancies

EP: 17.Role of Transplant in AML

EP: 18.Use of APR-246 and Oral HMAs in AML

EP: 19.Maintenance Therapy Post-Transplant in AML

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EP: 20.Future Treatment Landscape of AML

Harry P. Erba, MD, PhD: This has been an amazing discussion; I have learned so much from all of you, and I have enjoyed interacting with you this afternoon as we discuss what is new for our patients with acute myeloid leukemia [AML]. Thanks to all of you for this rich and informative discussion. Before we conclude, I would like to get final thoughts from each of you on exciting new developments or emerging agents that have caught your attention, and I will start with Corey.

Corey S. Cutler, MD, MPH, FRCPC: I have learned a lot just by listening to your discussion. The fact that you are getting many more people into deeper and longer-lasting remission bodes well for the future of transplantation. The better the patients are that you send to us, the better we can perform, and hopefully, as we learn how to use your drugs better, the better our long-term outcomes will be for everybody. We are excited about the future of transplant in advanced myeloid malignancies.

Harry P. Erba, MD, PhD: Thank you, and thanks for being with us. Adam, a few words?

Adam Bagg, MD: It is self-evident that genetics in AML is complicated. It is a complicated disease. The approaches to testing are many-fold. There are cytogenetic assays, there are FISH [fluorescence in situ hybridization] assays, there are single-gene assays, and there are NGS [next-generation sequencing] multi-gene assays. It would be wonderful if, in the future, there is a single platform to allow us to look at everything in 1 sitting. We are a ways away from that, but that may be on the horizon: Something like RNA sequencing would give us a lot of the information that we could get from other disparate forms of genetic assays. For the moment, we are stuck with the different technologies, which are great technologies. Each has advantages and disadvantages, so it is important for the user to be cognizant of the advantages and disadvantages of the respective assays, their turnaround times, what they are testing for, and what their sensitivities are in terms of tracking minimal residual disease [MRD]. As a hematopathologist, it is a wonderful area to be involved in, and we do our best to tell you what is going on with your patient so you can treat them appropriately. Stay in touch with your hematopathologist; they are your friend.

Harry P. Erba, MD, PhD: Thank you, Adam.Sasha?

Alexander E. Perl, MD, MS: There is continual advancement in AML. It is exciting to see that the flurry of drugs that were approved in 2017 was not the end of the line, but it was actually the start of a lot of interesting studies that have happened since then, primarily in the area of combinations. It is exciting to see all these things come together and new avenues taking off.

Harry P. Erba, MD, PhD: Eunice?

Eunice S. Wang, MD: I agree with Sasha. We are seeing a lot of novel combinations building on the new backbone of venetoclax-azacitidine or venetoclax as opposed to 7+3 chemotherapy-based regimens, which have been our backbone. I am excited about the immunotherapeutic approaches for both primary and refractory AML, as well as MRD-positive or low-burden disease. I am also excited by the potential that we may be able to, in a precision medicine way, target and have better therapies for patients with TP53-mutant disease or MLL [mixed lineage leukemia] rearranged disease, for whom we had no therapeutic avenues available to us prior to this year.

Harry P. Erba, MD, PhD: What I find most exciting, having been in this field for 25 years—and not as a transplanter—is that there is a real focus on the majority of patients we see, the older patients at the end of their lives, who are facing a disease that can be catastrophic and obviously life-ending. What has troubled us all this time is that our approach has been always that this is a curable disease, yet when you think about it, even with what we have had until recently, the number of patients cured is quite low. Of course, that needs to be our focus, and what I have enjoyed about the last 3 years and the development that we see ongoing is that there will be patients who will not be eligible for curative therapies based on their biology or the disease biology, but we are evaluating new therapies that appear to be not only extending life but also improving quality of life. Those are important end points for our studies: improving quality of life, decreasing hospitalization, decreasing transfusions, and bringing meaningful responses to our patients. This has been an exciting time for all of us in caring for our patients with acute myeloid leukemia.

I want to thank you again, our viewing audience. We hope you found this OncLive® Peer Exchange® discussion to be useful and informative. Thank you.

Transcripted Edited for Clarity