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Graft-versus-leukemia reactions after bone marrow transplantation
MM Horowitz, RP Gale, PM Sondel, JM Goldman, J Kersey, HJ Kolb, AA Rimm, O Ringden, C Rozman and B Speck
Division of Hematology/Oncology, Medical College of Wisconsin, Milwaukee
53226.
To determine whether graft-versus-leukemia (GVL) reactions are important in
preventing leukemia recurrence after bone marrow transplantation, we
studied 2,254 persons receiving HLA-identical sibling bone marrow
transplants for acute myelogenous leukemia (AML) in first remission, acute
lymphoblastic leukemia (ALL) in first remission, and chronic myelogenous
leukemia (CML) in first chronic phase. Four groups were investigated in
detail: recipients of non--T-cell depleted allografts without
graft-versus-host disease (GVHD), recipients of non-- T-cell depleted
allografts with GVHD, recipients of T-cell depleted allografts, and
recipients of genetically identical twin transplants. Decreased relapse was
observed in recipients of non--T-cell depleted allografts with acute
(relative risk 0.68, P = .03), chronic (relative risk 0.43, P = .01), and
both acute and chronic GVDH (relative risk 0.33, P = .0001) as compared
with recipients of non--T-cell depleted allografts without GVHD. These data
support an antileukemia effect of GVHD. AML patients who received identical
twin transplants had an increased probability of relapse (relative risk
2.58, P = .008) compared with allograft recipients without GVHD. These data
support an antileukemia effect of allogeneic grafts independent of GVHD.
CML patients who received T-cell depleted transplants with or without GVHD
had higher probabilities of relapse (relative risks 4.45 and 6.91,
respectively, P = .0001) than recipients of non--T-cell depleted allografts
without GVHD. These data support an antileukemia effect independent of GVHD
that is altered by T-cell depletion. These results explain the efficacy of
allogeneic bone marrow transplantation in eradicating leukemia, provide
evidence for a role of the immune system in controlling human cancers, and
suggest future directions to improve leukemia therapy.
Volume 75,
Issue 3,
pp. 555-562,
02/01/1990
Copyright © 1990 by The American Society of Hematology

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E. S. Morris, K. P. A. MacDonald, and G. R. Hill
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C. Berger, M. E. Flowers, E. H. Warren, and S. R. Riddell
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S. Lee, Y.-J. Kim, C.-K. Min, H.-J. Kim, K.-S. Eom, D.-W. Kim, J.-W. Lee, W.-S. Min, and C.-C. Kim
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R. W. Schrier and C. R. Parikh
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B. W. Blaser, S. Roychowdhury, D. J. Kim, N. R. Schwind, D. Bhatt, W. Yuan, D. F. Kusewitt, A. K. Ferketich, M. A. Caligiuri, and M. Guimond
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D. S. Krause and R. A. Van Etten
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M. Kami, A. Makimoto, Y. Heike, and Y. Takaue
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D. H. Kaplan, B. E. Anderson, J. M. McNiff, D. Jain, M. J. Shlomchik, and W. D. Shlomchik
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T. Crough, M. Nieda, and A. J. Nicol
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