Chronic Myelomonocytic Leukemia Is Associated with More Frequent and More Rapid Progression to Acute Myeloid Leukemia and Shorter Survival Than Myelodysplastic Syndrome, but Is Less Frequently Treated: Analysis of Surveillance Epidemiology and End Results Data Linked to Medicare Enrollment Claims

Abstract 2784

Chronic myelomonocytic leukemia (CMML) is a clonal stem cell disorder that displays features of both a myelodysplastic syndrome (MDS) and a myeloproliferative neoplasm (MPN). Originally classified as an MDS subtype in the French-American-British (FAB) classification system, it was reclassified as an MDS/MPN in the World Health Organization (WHO) system. Based on SEER and NAACCR data, CMML is associated with shorter survival than MDS and MPN, but no other population-based data have been available to date. We used the Surveillance Epidemiology and End Results (SEER) dataset linked to Medicare enrollment and claims data to compare patient demographics, baseline characteristics, treatments received, progression to acute myeloid leukemia (AML) and survival between CMML and MDS. The sample included 792 CMML and 6,588 MDS patients diagnosed from 2001 through 2005. MDS cases were 34.6% low-risk [RA, RARS, RCMD, del (5q)], 13.7% high-risk (RAEB), 1.4% therapy-related and 50.4% not otherwise specified. CMML and MDS patients did not differ in age (peak proportion at 80–84 years in both) or race distribution (90% and 88% white non-Hispanic, respectively). Male predominance was greater in CMML than in MDS (59.2% vs. 53.8%; p =.004). Baseline renal disease was more common among CMML patients (13.0% vs. 7.4%; p <.0001), while CHF/ischemic heart disease (37.4% vs. 44.6%; p =.000) and liver disease (2.8% vs.4.3%; p=.041) were more common in MDS. There was no difference in the proportion with poor performance status, diagnosis of other cancers within 5 years of CMML/MDS diagnosis, health care use prior to diagnosis or median household income. More CMML than MDS patients received no treatment (25.25% vs. 15.7%; p <.0001). Among patients who were treated, fewer CMML patients received blood transfusions (59.5% vs. 70.4%; p <.0001), erythropoiesis-stimulating agents (46.3% vs. 62.4; p <.0001) and granulocyte colony-stimulating factor (7.32% vs. 16.9%; p <.0001), while more CMML patients were treated with cytarabine (2.02 vs. 0.87; p =.002), etoposide (1.01 vs. 0.36%; p = 0.009) and bone marrow transplantation (1.14% vs. 0.47%; p =.016). There was no difference in treatment with hypomethylating agents between CMML and MDS patients (5.81% vs. 7.64%; p =.064). A higher percentage of CMML patients progressed to AML (42.6% vs. 16.3%; p < .0001) and progression occurred earlier (median 8 vs. 33 weeks; p < .0001). CMML patients had a lower survival probability at 1 year (51% vs. 66%; p <.0001) and at 3 years (19% vs. 37%; p <.0001), and a shorter median survival (13.3 vs. 24 months; p <.0001). Survival remained significantly lower across gender, age and race groups. In this population-based study, we have demonstrated that CMML patients less frequently receive therapeutic interventions, in relation to MDS patients, but in fact have a higher rate of progression to AML, more rapid progression to AML and shorter survival. The percentages of patients receiving hypomethylating agents for both diseases was low in our dataset and has likely increased following FDA approval of azacitidine in 2004 and decitabine in 2006. Our data support early application of disease-modifying therapies in CMML, and also support the need for clinical trials focused on this disease entity.