CASE REPORT Therapy related CMML: a case report and review of the literature Faheem Ahmed Æ Nadia Osman Æ Fred Lucas Æ Guy Neff Æ Teresa Smolarek Æ John M. Bennett Æ Rami S. Komrokji Received: 16 February 2009 / Revised: 6 April 2009 / Accepted: 6 April 2009 / Published online: 9 May 2009 Ó The Japanese Society of Hematology 2009 Abstract Therapy related chronic myelomonocytic leu- kemia (t-CMML) is rare. We report a 23-year-old female who developed acute fulminant hepatic failure after drug overdose. She underwent ABO incompatible orthotopic liver transplant. She received cyclophosphamide along with other immunosuppressants. Seven years later, she was diagnosed with t-CMML-2 with 45XX,-7 karyotype. She received 4 cycles of azacitidine and proceeded with allo- geneic bone marrow transplant. This is the first a case of t-CMML reported in a liver transplant recipient. In this article, we also summarize all reported cases of t-CMML, and we review therapy related MDS in recipients of solid organ transplant. Keywords CMML Á Therapy related MDS Á Liver transplantation 1 Introduction Myelodysplastic syndromes (MDS) are a group of neo- plastic stem cell disorder. MDS are characterized by bone marrow failure with a tendency to progress to acute mye- loid leukemia (AML) [1]. Therapy related myelodysplastic syndrome (t-MDS) is well-described entity [2]. The new World Health Organization (WHO) classification recog- nizes t-MDS/AML as separate category with worse out- come [3]. Sporadic reports of t-MDS/AML after solid organ transplantation have been published. Chronic myelomonocytic leukemia (CMML) is a rare disease. Previously CMML was classified as a myelodys- plastic syndrome subtype in the French–American–British (FAB) classification [4, 5]. By the new WHO classification, CMML is moved to a new category called myelodysplas- tic/myeloproliferative disorders (MDS/MPD) [3, 6, 7]. This new classification is recognition of the different prolifera- tive behavior of CMML compared to other MDS subtypes. F. Ahmed Á N. Osman Hematology and Medical Oncology Division, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH, USA F. Lucas Department of Pathology, University of Cincinnati, Cincinnati, OH, USA G. Neff Digestive Disease Division, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH, USA T. Smolarek Division of Human Genetics, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA J. M. Bennett Department of Medicine, The James P. Wilmot Cancer Center, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA R. S. Komrokji Department of Oncologic Sciences, University of South Florida, Tampa, FL 33612, USA R. S. Komrokji (&) Department of Hematologic Malignancies, Moffitt Cancer Center and Research Institute, FOB 3rd floor, 12902 Magnolia Drive, Tampa, FL 33612, USA e-mail: Rami.komrokji@moffitt.org 123 Int J Hematol (2009) 89:699–703 DOI 10.1007/s12185-009-0318-1