Recorded at the first “HemOnc Pulse” Live meeting, this podcast episode features a panel discussion on unanswered questions in myelodysplastic syndromes (MDS) with Rami Komrokji, MD, Vice-Chair of the Malignant Hematology Department at Moffitt Cancer Center; Sanam Loghavi, MD, an Associate Professor of Pathology at the University of Texas MD Anderson Cancer Center; Jamile Shammo, MD, FACP, FASCP, a Professor at the Northwestern University Feinberg School of Medicine; Sangeetha Venugopal, MD, MS, an Assistant Professor of Medicine at the University of Miami Sylvester Comprehensive Cancer Center; and Amer Zeidan, MBBS, MHS, an Associate Professor of Medicine at Yale University.
The panel mainly focused on how to define and classify MDS and clonal hematopoiesis of indeterminate potential (CHIP), a precursor to MDS.
“Diseases happen on a spectrum,” said Dr. Zeidan. “The way we define things is boxing them into categories, but that does not always happen in reality.”
“The best way to describe MDS is to put it into simple categories that are biologically relevant,” Dr. Shammo said, adding that mutation type plays a role in classifying the disease as MDS or CHIP.
“We get a lot of CHIP that is clinically insignificant,” Dr. Loghavi said. “However, I think the context of which we are detecting CHIP is very important. There are high-risk genes and low-risk genes, so there are a lot of things that go into play. As a field, we are learning how to deal with these patients.”
Dr. Komrokji classifies MDS into three categories: chronic phase MDS, accelerated phase MDS, and blast phase MDS.
“Classification is really a common language we use to communicate to reflect on the biology and the phenotype,” he said. “It’s not always the prognostic tool that you’re going to use in practice to decide the treatment.”
How do clinicians decide treatment? For low-risk MDS, a patient’s serum erythropoietin (EPO) levels predict which erythropoietin stimulating agent is best suited for them, Dr. Shammo explained.
Dr. Venugopal outlined frontline treatment for high-risk MDS, including oral hypomethylating agents such as cedazuridine and decitabine, while Dr. Ziedan discussed the VERONA trial and venetoclax in high-risk MDS.
“The VERONA study is likely to expand the label and make [venetoclax] easier to get, but most places don’t have a big problem getting the drug,” he said. “In patients with less than 10% blast or TP53 mutations, I’m not 100% sure it’s being used as a chronic treatment other than a bridge to transplant. Venetoclax is quite myelosuppressive. Those patients will become heavily transfusion-dependent, and there will be a risk of infections. Drug adjustment is very important.”
Finally, the panel addressed unanswered questions regarding transplant for high-risk MDS, including timing of transplant, the best bridges to transplant, and maintenance therapy post-transplant.