Aziz Nazha, MD, hematologist and medical oncologist, director, Center for Clinical Artificial Intelligence, Cleveland Clinic, discusses the potential role of ropeginterferon alfa-2b in polycythemia vera (PV).

FDA accepted a Biologics License Application

 for ropeginterferon alfa-2b for use as a treatment for patients with PV in the absence of symptomatic splenomegaly. 

According to Nazha, ropeginterferon alfa-2b is a promising agent. However, the agent may not be suitable for all-comers. The agent will likely be reserved for younger patients with PV who do not respond to hydroxyurea or ruxolitinib (Jakafi), Nazha explains. Additionally, the agent may have utility as an up-front treatment for younger patients. 

Ropeginterferon alfa-2b may be used in older patients with PV as well since the safety profile appears to be manageable, says Nazha. 

Notably, the approval of ropeginterferon alfa-2b would provide a treatment option to pregnant women, a population of which are not eligible for hydroxyurea and ruxolitinib, concludes Nazha.

Videos

Aziz Nazha, MD, discusses the potential role of ropeginterferon alfa-2b in polycythemia vera.  



Dr. Nazha on the Potential Role of Ropeginterferon Alfa-2b in Polycythemia Vera 

Aziz Nazha, MD, hematologist and medical oncologist, director, Center for Clinical Artificial Intelligence, Cleveland Clinic, discusses the risk of progression to myelofibrosis in patients with polycythemia vera (PV).

About 15% to 20% of patients with PV will experience progression to myelofibrosis within 7 to 15 years of their initial diagnosis of PV, Nazha says. Moreover, it is important to discuss potential signs of progression with patients. 

PV is associated with an increased level of red blood cells, Nazha explains. Although anemia may be a result of treatment, patients who become anemic may be experiencing progression to myelofibrosis.

Additional signs of progression include significantly elevated lactate dehydrogenase, erythroleukoplastic changes, or severe splenomegaly of 20 cm to 30 cm, Nazha says. 

Additionally, more fibrosis inside the bone marrow should be observed when patients with PV undergo a bone marrow biopsy, concludes Nazha.

Aziz Nazha, MD, discusses the risk of progression to myelofibrosis in patients with polycythemia vera.  



Dr. Nazha on the Risk of Progression to Myelofibrosis in Polycythemia Vera 

Aziz Nazha, MD, hematologist, Leukemia Program at the Cleveland Clinic, Taussig Cancer Institute, discusses results of a mutational model to predict response to hypomethylating agents in myelodysplastic syndromes (MDS).

In a recent study, 122 patients with MDS and myeloid malignancies treated at the Taussig Cancer Institute between 2000 and 2012 received four cycles of azacitidine or decitabine. Using a gene mutation panel, patients were then divided into those who had complete responses, partial responses, or hematologic improvements, and those who demonstrated no response, Nazha explains. Certain mutations, such as IDH1 and IDH2, were found to be most prevalent among those who responded, as well as TET2 and RAD21. However, patients with ASXL1 were less likely to respond to these treatments.

A multi-variant analysis used these data to determine important prognostic factors that impact response in patients with MDS. In a new mutational model, patients who harbor the IDH1, IDH2, or TET2 mutation have a score of 1, while patients with STAG2 or RAD21 have a score of 2. For patients with the ASXL1 mutation, the score is —1.5. If a patient’s score is 2 to 3, the response rate for hypomethylating agents is 85%. If a score is –1.5, the response rate is 15% to 18%, Nazha says.

Aziz Nazha, MD,  hematologist, Leukemia Program at the Cleveland Clinic, Taussig Cancer Institute, discusses results of a mutational model to predict response to hypomethylating agents in myelodysplastic syndromes (MDS).


Aziz Nazha, MD

Articles

Dr. Nazha on the Potential Role of Ropeginterferon Alfa-2b in Polycythemia Vera

Dr. Nazha on the Risk of Progression to Myelofibrosis in Polycythemia Vera

Dr. Nazha on Mutational Model to Predict Response to Hypomethylating Agents in MDS