Impact of Therapy-Related De Novo Acute Myeloid Leukemia on Response and Survival

determined by microarray analysis and validated by qRT-PCR. Future studies will address the mechanism of how PP2A regulates these miRs. Conclusion: Loss of B55 alpha PP2A activity in leukemia can induce diverse survival signaling pathways and allow expression of pro-tumor microRNAs. 207 Impact of Therapy-Related De Novo Acute Myeloid Leukemia on Response and Survival Koji Sasaki, Elias Jabbour, Hagop Kantarjian, Jorge Cortes, Guillermo Garcia-Manero, Gautam Borthakur, Sherry Pierce, Naveen Pemmaraju, Susan O’Brien, Farhad Ravandi Department of Leukemia, The University of Texas MD Anderson Cancer Center Background: The available data on outcome of patients with therapy-related de novo acute myeloid leukemia (t-de novo AML) without antecedent myelodysplastic syndrome (MDS) are limited. Methods: We retrospectively reviewed the records of patients with newly diagnosed AML who presented to MD Anderson Cancer Center between January 2000 and January 2014. T-de novo AML was defined as at least 20% blasts in bone marrow with a history of any previous cytotoxic chemotherapy or radiation therapy and without antecedent MDS. The overall survival (OS) and leukemiaTable 1 Characteristics and Outcomes of Patients with De Novo AM t-de novo AML (n[ 187) de n ( Age at diagnosis, median, years (range) 64 (21-89) 6 Prior radiation therapy, No. (%) 101 (54) Prior chemotherapy, No. (%) 186 (99) WBC count at diagnosis, median, 10/mL (range) 3.2 (0.2-191) 4. Hgb at diagnosis, median, g/dL (range) 9.1 (4.5-12.9) 9. Plt count at diagnosis, median, 10/mL (range) 34 (4-454) 5 LDH at diagnosis, median, IU/L (range) 1359 (210-22090) 118 PB blast percentage at diagnosis, median (range) 8 (0-98) 9. BM blast percentage at diagnosis, median (range) 41 (0-96) 4 Molecular genetic abnormalities at diagnosis, No. (%) FLT3-ITD 17 (9) 9 FLT3-D835 6 (3) 2 NPM1 7 (4) 10 JAK2 3 (2) RAS 17 (9) 5 free survival (LFS) in patients with t-de novo AML were compared to those with de novo AML with normal karyotype (NK) or complex karyotype (CK). Results: Of 1677 patients with newly diagnosed AML, 383 had de novo NK-AML, 218 had de novo CKAML, and 187 had t-de novo AML. The median follow-up was 9.3 months (range, 0.2-161.0). Patient characteristics and outcomes are summarized in Table 1. Of the 187 patients with t-de novo AML, 69 had a history of lymphoma; 63, breast cancer; 10, colon cancer; 10, sarcoma; and 69, another type of cancer. Fifteen of the patients with t-de novo AML (8%) had a favorable-risk karyotype, 53 patients (28%) an intermediate-risk karyotype, and 119 patients (64%) a poor-risk karyotype. The median LFS durations in t-de novo AML, NK-AML, and CK-AML were 7 months (95% confidence interval [CI], 5.1-8.7), 19 months (95%CI, 13.0-25.2), and 6 months (95%CI, 9.0-13.5) (P 100103/mL, platelets <30 0103/mL, nonfavorable cytogenetic abnormalities, positive RAS mutation, and the absence of complete remission or complete remission with incomplete platelet recovery as poor prognostic features related to OS. Conclusion: LFS and OS for patients with t-de novo AML were shorter than those for patients with NK-AML but did not differ significantly from those for patients with CK-AML.