Is there a role for autologous stem cell transplantation for patients with acute myelogenous leukemia? A retrospective analysis.
For patients with acute myelogenous leukemia (AML) who are unable to secure an acceptable HLA donor, the role of autologous stem cell transplantation (auto-SCT) has remained controversial. Its effectiveness remains unclear as, when analyzed on intention-to-treat strategies, a significant number do not undergo the procedure, whereas others seem to fail therapy from pretransplant recurrences. To improve our counseling to our patients on these 2 therapeutic options, we compared the outcome of patients in first remission of AML who actually underwent autologous or allogeneic transplantation. The choice for the type of graft was based on availability of HLA identical siblings. Patients received myeloablative conditioning followed by allogeneic or autologous cytokine mobilized peripheral blood stem cell transplantation. For prophylaxis of graft-versus-host disease (GVHD), grafts were incubated ex vivo with anti-CD52 antibodies and patients were prescribed cyclosporin until day 90. Patients were stratified by clinical and laboratory factors as well as cytogenetic risk. The endpoints were treatment-related mortality (TRM), disease-free survival (DFS), and overall survival (OS). The median presentation age for both transplant groups was 35 (14-60) years. Of the 112 consecutive patients achieving remission, autologous or allogeneic grafts were transplanted to 43 and 32 patients, respectively. There was no significant difference in the presentation clinical features, laboratory parameters, marrow morphology, or proportion of low and intermediate cytogenetic risk for both transplant options. Treatment mortality as well as relapse rate was similar (14% and 15%; 39% and 27%, respectively). At a median of 1609 and 1819 posttransplant days, 56% and 63% in each group survived. In univariate analysis performance status, cytogenetic risk, morphologic features of dysplasia, blast count, and lactate dehydrogenase (LDH) were significant factors for survival. Although for the entire group there was no difference in survival between both modalities, all patients with unfavorable cytogenetics receiving an autologous graft died of disease recurrence (3-year survival 35% versus 0%; P = .05). We conclude that patients with AML who have low or intermediate cytogenetic risk undergoing myeloablative conditioning followed by autologous or allogeneic T cell-depleted stem cell transplantation appeared to have similar outcome. However, those with unfavorable karyotype are unlikely to be cured with autologous grafts and are candidates for experimental modalities.
Novitzky
Nicolas
N
The University of Cape Town Leukaemia Centre and the Division of Haematology, Department of Medicine, Faculty of Health Sciences, University of Cape Town, Groote Schuur Hospital, Observatory, Cape Town, South Africa. nicolas.novitzky@uct.ac.za
Thomas
Valda
V
du Toit
Cecile
C
McDonald
Andrew
A
D000328:Adult; D000911:Antibodies, Monoclonal / Q000276:immunology; D015703:Antigens, CD / Q000276:immunology; D000951:Antigens, Neoplasm / Q000276:immunology; D000074301:CD52 Antigen; D002869:Chromosome Aberrations; D016572:Cyclosporine / Q000494:pharmacology; D018572:Disease-Free Survival; D005260:Female; D006023:Glycoproteins / Q000276:immunology; D006086:Graft vs Host Disease / Q000401:mortality / Q000517:prevention & control*; D006680:HLA Antigens / Q000032:analysis; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D007621:Karyotyping; D015470:Leukemia, Myeloid, Acute / Q000235:genetics / Q000276:immunology* / Q000401:mortality / Q000473:pathology* / Q000628:therapy; D008297:Male; D012008:Recurrence; D012189:Retrospective Studies; D012307:Risk Factors; D035781:Siblings; D013019:South Africa; D019172:Transplantation Conditioning / Q000379:methods; D014182:Transplantation, Autologous; D014184:Transplantation, Homologous; D016896:Treatment Outcome
D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D000951:Antigens, Neoplasm; D000074301:CD52 Antigen; C000613862:CD52 protein, human; D006023:Glycoproteins; D006680:HLA Antigens; D016572:Cyclosporine