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1129 Outcome after Allogeneic Stem Cell Transplantation for Adult Acute Myeloid Leukaemia Patients Exhibiting Isolated or Associated Trisomy 8 Chromosomal Abnormality: A Survey on Behalf of the Acute Leukemia Working Party (ALWP) of the EBMT

Saturday, December 6, 2008, 5:30 PM-7:30 PM
Hall A (Moscone Center)
Poster Board I-234

Patrice Chevallier1*, Myriam Labopin2*, Arnon Nagler3, Per T. Ljungman, MD, PhD4, Leo Verdonck5*, Liisa Volin6*, Axel Zander7*, J.ürgen Finke8, Gerard Socie9*, Catherine Cordonnier, MD10, Jean-Luc Harousseau11, Mohamad Mohty, MD, PhD12 and Vanderson Rocha13

1Hematology, CHU Hotel-Dieu, Nantes, France
2EBMT Paris Office, Paris, France
3Division of Hematology and Bone Marrow Transplantation, Chaim Sheba Medical Center, Tel Hashomer, Israel
4Karolinska University Hospital, Stockholm, Sweden
5Haematology, University Medical Centre, Utrecht, Netherlands
6Helsinki University Central Hospital, Helsinki, Finland
7Haematology, University Hospital Eppendorf, Hamburg, Germany
8Hematology/Oncology, University Medical Center Freiburg, Freiburg, Germany
9Haematology, Hopital Saint-Louis
10Hematologie Clinique, Hopital Henri Mondor, Creteil, France
11Hôpital Hôtel Dieu, Nantes, France
12Hematology Dept., CHU de Nantes, Nantes, France
13BMT unit, Hopital Saint Louis APHP and Université Paris VII, Paris, France

Trisomy 8 (+8) is one of the most common chromosomal abnormality encountered in acute myeloid leukemia (AML), occurring in about 10 to 15% of cases. Currently, data assessing specifically the role of allogeneic hematopoietic stem cell transplantation (allogeneic-HSCT) in the setting of AML with +8 are still relatively sparse. The aim of this multicenter retrospective analysis was to perform a survey on overall outcomes after allogeneic-HSCT of AML patients harboring +8 as a sole chromosomal abnormality or associated with other abnormalities.
We have identified 182 de novo AML patients who underwent allogeneic-HSCT between 1990 and 2007 exhibiting isolated +8 (n=136) or +8 associated to other favorable (n=8), intermediate (n=30), high-risk (n=7) or unknown (n=1) group cytogenetics reported to the EBMT. Median age was 37 years. At transplant 108 (59%) patients were in first complete remission (CR). The donor was HLA identical sibling in 115 (63%) and peripheral blood HSCT was used in 54% (n=98). Conditioning regimen was myeloablative in 82%.
With a median follow-up of 48 months, 5-year non-relapse mortality (NRM), relapse rate (RR), LFS and OS were 25%, 30%, 45% and 47%, respectively. Five-years OS and LFS was not significantly different between AML patients with isolated or associated +8 (44% vs. 56% P=0.14 and 41% vs. 55%, P=0.11). In a multivariate analysis, LFS rate was improved when patients were female and transplanted in CR with an HLA identical sibling donor. LFS rate were 62% and 64% when using an HLA identical sibling donor in patients in CR1 and CR2/CR3, respectively. Isolated or associated +8 were not a risk factor for any outcomes (OS, LFS, RR, NRM).
We conclude that allo-HSCT, from an HLA identical sibling donor, appears to be the treatment of choice  for AML patients in CR at transplant with isolated or associated +8.

Disclosures: No relevant conflicts of interest to declare.

*signifies non-member of ASH