Journal of Clinical Oncology, Vol 21, Issue 5
(March), 2003: 897-906
© 2003 American Society for Clinical Oncology
Treatment-Related Myelodysplasia and Acute Leukemia in Non-Hodgkin’s Lymphoma Patients
James O. Armitage,
Paul P. Carbone,
Joseph M. Connors,
Alexandra Levine,
John M. Bennett,
Stewart Kroll
From the University of Nebraska College of Medicine, Omaha, NE; University of Wisconsin Medical School, Madison, WI; University of Southern California Norris Cancer Hospital, Los Angeles, CA; University of Rochester Cancer Center, Rochester, NY; Corixa Corporation, Seattle WA; and British Columbia Cancer Agency Vancouver Clinic, Vancouver, British Columbia, Canada.
Address reprint requests to James O. Armitage, MD, University of Nebraska College of Medicine, 600 S 42nd St, Nebraska Medical Center Box 98332, Omaha, NE 68198-3332; email: joarmita{at}unmc.edu.
Purpose: Standard therapies for non-Hodgkin’s lymphoma (NHL) are associated with an increased risk of developing treatment-related myelodysplastic syndrome or acute myelogenous leukemia (tMDS/AML). However, there is considerable debate over the incidence or risk of tMDS/AML in NHL patients treated with any particular modality and the factors that contribute to malignant transformation.
Design: Conclusions were based on thorough analysis of data reported in the peer-reviewed literature and careful examination of the statistical methodology and methods for identifying cases of tMDS/AML. Unless noted, data are reported only for NHL patients, excluding Hodgkin’s disease patients.
Results: Despite differences in methods used to identify cases and to estimate the cumulative incidence over time (actuarial v cumulative calculations), up to 10% of NHL patients treated with either conventional-dose chemotherapy or high-dose therapy and autologous stem-cell transplantation may develop tMDS/AML within 10 years of primary therapy. Kaplan-Meier estimates of the actuarial incidence, which are based on censoring of patients who died without developing tMDS/AML, can lead to artificially high estimates with large confidence intervals at later time points. Although there is much debate about the cause(s) of tMDS/AML, there is compelling evidence that alkylating agents, certain other leukemogenic agents, and total-body irradiation (TBI) cause chromosomal damage that can lead to tMDS/AML.
Conclusion: Limiting exposure to alkylating agents and eliminating TBI from transplantation conditioning regimens may reduce the relative risk of tMDS/AML.
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