Predicting the outcome of therapy in patients with acute myeloid leukemia (AML) is currently necessary for making treatment decisions. Pretreatment covariates, such as clinical and molecular predictors, have helped identify which patients are more or less likely to survive their disease using the currently available regimens. Progress in establishing optimized flow cytometry and quantitative polymerase chain reaction assays for detecting minimal residual leukemia has provided new potential tools for predicting outcome. However, the most important next step in using these techniques toward personalized treatment of AML would be developing effective and safe strategies for eradicating the residual leukemic cells that are likely chemoresistant. With further refinement and standardization of the assays, and the development of novel, effective, and molecularly targeted agents, monitoring of minimal residual disease is likely to be incorporated into AML guidelines.
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Farhad Ravandi and Jeffrey L. Jorgensen
C. Cameron Yin, Nitin Jain, Meenakshi Mehrotra, Jianhua Zhagn, Alexei Protopopov, Zhuang Zuo, Naveen Pemmaraju, Courtney DiNardo, Cheryl Hirsch-Ginsberg, Sa A. Wang, L. Jeffrey Medeiros, Lynda Chin, Keyur P. Patel, Farhad Ravandi, Andrew Futreal, and Carlos E. Bueso-Ramos
Acute promyelocytic leukemia (APL) is characterized by the fusion of retinoic acid receptor alpha (RARA) with promyelocytic leukemia (PML) or, rarely, other gene partners. This report presents a patient with APL with a novel fusion between RARA and the interferon regulatory factor 2 binding protein 2 (IRF2BP2) genes. A bone marrow examination in a 19-year-old woman who presented with ecchymoses and epistaxis showed morphologic and immunophenotypic features consistent with APL. PML oncogenic domain antibody was positive. Results of fluorescence in situ hybridization, conventional cytogenetics, reverse transcription–polymerase chain reaction (RT-PCR), and oligonucleotide microarray for PML-RARA and common APL variant translocations were negative. Next-generation RNA-sequencing analysis followed by RT-PCR and direct sequencing revealed distinct breakpoints within IRF2BP2 exon 2 and RARA intron 2. The patient received all-trans retinoic acid, arsenic, and gemtuzumab ozogamicin, and achieved complete remission. However, the disease relapsed 10 months later, 2 months after consolidation therapy. This is the first report showing involvement of IRF2BP2 in APL, and it expands the list of novel RARA partners identified in APL.
