Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Stem Cells. Aug 26, 2016; 8(8): 231-242
Published online Aug 26, 2016. doi: 10.4252/wjsc.v8.i8.231
Therapy-related myeloid neoplasms - what have we learned so far?
Mohammad Faizan Zahid, Aric Parnes, Bipin N Savani, Mark R Litzow, Shahrukh K Hashmi
Mohammad Faizan Zahid, Medical College, Aga Khan University, Karachi 74800, Pakistan
Aric Parnes, Division of Hematology, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, United States
Bipin N Savani, Hematology and Stem Cell Transplantation Section, Division of Hematology/Oncology, Department of Medicine, Vanderbilt University Medical Center and Veterans Affairs Medical Center, Nashville, TN 37232, United States
Mark R Litzow, Shahrukh K Hashmi, Mayo Clinic Transplant Center, Blood and Marrow Transplant Program, Mayo Clinic, Rochester, MN 55905, United States
Author contributions: Zahid MF conceptualized the topic of the review; Zahid MF and Hashmi SK wrote the manuscript; Parnes A, Savani BN, Litzow MR and Hashmi SK critically revised the manuscript for important intellectual content; all authors approved the final version of the manuscript submitted.
Conflict-of-interest statement: The authors declared no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Mohammad Faizan Zahid, MBBS, Medical College, Aga Khan University, P.O. Box 3500, Stadium road, Karachi 74800, Pakistan.
Telephone: +92-323-4407740
Received: May 27, 2016
Peer-review started: May 28, 2016
First decision: July 6, 2016
Revised: July 21, 2016
Accepted: August 6, 2016
Article in press: August 8, 2016
Published online: August 26, 2016

Therapy-related myeloid neoplasms are neoplastic processes arising as a result of chemotherapy, radiation therapy, or a combination of these modalities given for a primary condition. The disease biology varies based on the etiology and treatment modalities patients receive for their primary condition. Topoisomerase II inhibitor therapy results in balanced translocations. Alkylating agents, characteristically, give rise to more complex karyotypes and mutations in p53. Other etiologies include radiation therapy, high-dose chemotherapy with autologous stem cell transplantation and telomere dysfunction. Poor-risk cytogenetic abnormalities are more prevalent than they are in de novo leukemias and the prognosis of these patients is uniformly dismal. Outcome varies according to cytogenetic risk group. Treatment recommendations should be based on performance status and karyotype. An in-depth understanding of risk factors that lead to the development of therapy-related myeloid neoplasms would help developing risk-adapted treatment protocols and monitoring patients after treatment for the primary condition, translating into reduced incidence, early detection and timely treatment.

Keywords: Therapy-related acute myeloid leukemia, Therapy-related myelodysplastic syndromes, Ionizing radiation, Alkylating agents, Allogeneic hematopoietic stem cell transplantation, Topoisomerase II inhibitors, Therapy-related myeloid neoplasms

Core tip: Therapy-related myeloid neoplasms are becoming an increasing problem as the survival of cancer patients lengthens. The etiology has an important influence on the biological characteristics, time to onset and prognosis of the resultant disease. Although treatment of therapy-related myeloid neoplasms represents a substantial challenge due to prior treatment and comorbidities, cure is possible, especially with allogeneic stem cell transplantation, particularly in those with good-risk karyotype. Ultimately, individual assessment of risk factors may lead to developing risk-adapted therapies to reduce the incidence of this serious complication without affecting therapy for the underlying disorders.