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Blood, Vol. 94 No. 7 (October 1), 1999:
pp. 2208-2216
Risk of Lymphoproliferative Disorders After Bone Marrow
Transplantation: A Multi-Institutional Study
Rochelle E. Curtis,
Lois B. Travis,
Philip A. Rowlings,
Gérard Socié,
Douglas W. Kingma,
Peter M. Banks,
Elaine S. Jaffe,
George E. Sale,
Mary M. Horowitz,
Robert P. Witherspoon,
Donna
A. Shriner,
Daniel J. Weisdorf,
Hans-Jochem Kolb,
Keith M. Sullivan,
Kathleen A. Sobocinski,
Robert Peter Gale,
Robert N. Hoover,
Joseph
F. Fraumeni Jr, and
H. Joachim Deeg
From the Division of Cancer Epidemiology and Genetics, and the
Division of Cancer Biology and Diagnosis, Laboratory of Pathology,
National Cancer Institute, Bethesda, MD; International Bone Marrow
Transplant Registry, Medical College of Wisconsin, Milwaukee, WI; Fred
Hutchinson Cancer Research Center, Seattle, WA; Hôpital Saint
Louis, Hématologie-Greffe de Moelle, Paris, France; Carolinas
Medical Center, Charlotte, NC; University of Minnesota Medical School,
Minneapolis, MN; Universität München, Munich, Germany; and
Salick Health Care, Inc, Los Angeles, CA.
We evaluated 18,014 patients who underwent allogeneic bone marrow
transplantation (BMT) at 235 centers worldwide to examine the incidence
of and risk factors for posttransplant lymphoproliferative disorders
(PTLD). PTLD developed in 78 recipients, with 64 cases occurring less
than 1 year after transplantation. The cumulative incidence of PTLD was
1.0% ± 0.3% at 10 years. Incidence was highest 1 to 5 months
posttransplant (120 cases/10,000 patients/yr) followed by a steep
decline to less than 5/10,000/yr among  1-year survivors. In
multivariate analyses, risk of early-onset PTLD (<1 year) was strongly associated (P < .0001) with unrelated or human
leukocyte antigen (HLA) mismatched related donor (relative risk
[RR] = 4.1), T-cell depletion of donor marrow (RR = 12.7), and use of antithymocyte globulin (RR = 6.4) or anti-CD3
monoclonal antibody (RR = 43.2) for prophylaxis or treatment of acute
graft-versus-host disease (GVHD). There was a weaker association with
the occurrence of acute GVHD grades II to IV (RR = 1.9, P = .02) and with conditioning regimens that included radiation (RR = 2.9, P = .02). Methods of T-cell depletion that selectively
targeted T cells or T plus natural killer (NK) cells were associated
with markedly higher risks of PTLD than methods that removed both T and
B cells, such as the CAMPATH-1 monoclonal antibody or elutriation
(P = .009). The only risk factor identified for late-onset
PTLD was extensive chronic GVHD (RR = 4.0, P = .01). Rates
of PTLD among patients with 2 or 3 major risk factors were 8.0% ± 2.9% and 22% ± 17.9%, respectively. We conclude that factors
associated with altered immunity and T-cell regulatory mechanisms are
predictors of both early- and late-onset PTLD.
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