Prognostic impact of CD56 in pediatric AML

Sir, CD56 is a 200–220 kD glycoprotein expressed predominantly on human natural killer (NK) cells and a minor subset of T cells [1, 2]. It is detected in a broad spectrum of lymphoproliferative diseases, predominantly of large granular lymphocytes, acute myeloid leukemia (AML), and other tumors such as EBV-associated nasal lymphomas and multiple myeloma. Also, CD56 antigenic expression represents an important adverse prognostic factor in both adult AML and acute promyelocytic leukemia as has been observed in majority of the studies [3– 5]. However, despite several reports of the poor prognostic impact of CD56 in various tumors, the study of its impact in pediatric AML is lacking. The aim of our study was to evaluate the impact of CD56 expression on the clinical outcome in pediatric AML patients. One hundred consecutive pediatric patients (68 male/ 32 female) diagnosed on morphology, cytochemistry, and flow cytometry as de novo AML (excluding acute promyelocytic leukemia) were studied retrospectively for CD56 expression by flow cytometry in All India Institute of Medical Sciences during the period of April 2011 to January 2014. Myeloblasts were considered as CD56 positive when >20% blasts expressed CD56 beyond the unstained cell population [6]. The study protocol was approved by the institute ethics committee. All the patients were uniformly given induction therapy with 3 + 7 course of 60 mg/m daunorubicin and 100 mg/m cytosine arabinoside, followed by consolidation with high dose cytarabine. The patients were followed up for a minimum period of 1 year, and survival data were calculated. Event-free survival (EFS) was defined as the time period between the start of induction therapy and relapse, death, or last follow-up. Disease-free survival (DFS) was defined as the time period between complete remission attainment and relapse, death, or last followup. Overall survival (OS) was defined as the interval between the date of diagnosis and the date of death, or last follow-up. Relapse rate (RR) was defined as the number of patients relapsing after achievement of complete remission (CR). Complete remission rate was defined as the percentage of patients achieving morphological remission after induction therapy. Actuarial Kaplan–Meier curves were plotted for EFS, DFS, and OS and compared by the log-rank test. All statistical tests were performed using the SPSS statistical software (Version 17.0, SPSS Inc., Chicago, IL, USA). The level of significance was set at P < 0.05. The age of the study population ranged from 1 to 18 years (median = 9 years). Mean hemoglobin, absolute neutrophil count, platelet count, and conventional cytogenetic findings of the study population are shown in Table 1. Cytogenetic abnormalities were favorable if t (8;21), inv(16), or t(16;16) were found; unfavorable in the case of 7/7q , 5/5q , del(11)(q23), del(3), t(9;22) or in the case of more than three chromosomal anomalies (complex karyotypes). All other karyotypic abnormalities were defined as intermediate [7]. CD56 expression was seen in 39 of 100 (26 male/13 female) patients. Sixty-one of 100 patients (42 male/19 female) did not express CD56. The EFS was 47.3% in the CD56 positive patients cohort (n = 39) and 48.84% in the CD56 negative patients (n = 61). DFS was 57.3% and 69.7% in CD56 positive and negative group, respectively. RR was 35.9% and 27.9% in CD56 positive and negative group, respectively. Complete remission rate was 94.87% and 98.36% in CD56 positive and negative group, respectively. OS was 58.3% and 57% in CD56 positive and negative group, respectively. No statistically significant difference was found in between the CD56 positive and negative groups with respect to EFS, DFS, RR, and OS (P = 0.65, 0.23, 0.40, and 0.97, respectively) (Figure 1). Cytogenetics was performed in all the cases. However, results were available only for 69 patients. Among these, 21, 43, and five patients belonged to the good, intermediate, and poor prognosis groups, respectively (Table 1). In the remaining, cytogenetics was noncontributory due to absence of metaphases/inadequate sample. In the good prognosis group (n = 21), 14 patients had t(8;21). Out of these, myeloblasts in nine patients expressed CD56 while five patients were negative for CD56. No statistically significant difference was found in between the CD56