Expression of CD56 in Acute Myeloid Leukemia (AML) Is Associated with Poor Outcome When Patients Treated with Stem Cell Transplant in Second Remission but Not in the First Remission

Author:

Chaudhri Naeem A.1,Almhareb Fahed1,Walter Claudia Ulrike2,Nounou Randa2,Khalil Salem2,Bakshi Nasir2,Owaidah Tarek2,Al Zahrani Hazzaa1,Mohamed Said1,Rasheed Walid1,Alsharif Fahad1,Aljurf Mahmoud1,Albitar Maher2

Affiliation:

1. Oncology Center, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia,

2. Pathology and Laboratory Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia

Abstract

Abstract Abstract 4880 Background: The CD56 is a neural cell adhesion molecule (N-CAM) expressed in natural killer cells. CD56 expression on the surface of leukemic cells in acute myeloid leukemia (AML) has been reported to correlate with higher rate of relapse and to be associated with poor outcome when patients are treated with conventional intensive chemotherapy. The role of allogeneic hematopoietic stem cell transplantation (HSCT) in improving outcome in this subgroup of AML patients is not known. We investigated whether the outcome of CD56-positive AML patients differ from average AML patients when treated with allogeneic HSCT after intensive chemotherapy and its prognostic relevance in patients transplanted in the first (CR1) or second complete remission (CR2). Methods: Immunophenotyping data of 106 patients with AML who were treated with allogeneic HSCT was reviewed. The expression of the CD56 on the blast population as determined by flow cytometry was correlated with clinical data and outcome. The median age of patients was 24 (range: 14–57) and included 72 patients in the intermediate cytogenetic group and 30 in the adverse cytogenetic group. Of the 106 patients, 71 (67%) were treated with HSCT in their first remission (CR1) and the remaining patients were treated in CR2. Results: Twenty nine (28%) of all studied patients expressed CD56 on the surface of the blasts at diagnosis. When we consider only patients treated with HSCT in CR1, 17 (24%) were CD56 positive. The overall survival (OS) and event free survival (EFS) for patients who were positive for CD56 were not significantly different from the rest of the patients in the CR1 group. In contrast, in the group of patients who were treated with HSCT after relapsing (CR2), patients with CD56 positivity had significantly shorter OS (P=0.03) and DFS (P=0.006). In this group, 11 of the 35 (31%) were CD56+ and their median survival was 8.85 months while the median has not been reached in the CD56 negative patients. Conclusion: Our data suggests that the expression of CD56 in AML is a significant poor prognostic factor if patients are treated with HSCT after relapsing in their second remission. Although this should be confirmed in larger studies, the CD56 expression in AML should be considered as an adverse risk factor and favors treatment with allogeneic HSCT in the first remission and not after relapse in second remission. AML patients with CD56 positive blasts have higher incidence of relapse after chemotherapy and they might lose their opportunity of good outcome if HSCT is delayed and performed only in the second remission. Disclosures: No relevant conflicts of interest to declare.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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