Phenotypic and clinical heterogeneity of CD56-positive acute nonlymphoblastic leukemia

Abstract

The precise phenotype and clinical course are described of a subgroup of acute nonlymphoblastic leukemias (ANLL) expressing the NK-cell differentiation antigen CD56. As previously reported, CD56+ leukemias occurred in a frequency of about 20% of ANLL cases showing clinical and immunophenotypical heterogeneity. Carrying various myelomonocytic markers, all cases were diagnosed to be of nonlymphoid origin. Positive or negative expression of CD34 allowed us to distinguish two major subtypes of CD56+ leukemias representing immature and more differentiated cells carrying further differentiation antigens (CD14 and/or CD15) of the myelomonocytic lineages. These phenotypes correlated with the M0, M2, M4, and M5 leukemias of the FAB classification.

CD56 antigenic expression in acute myeloid leukemia identifies patients with poor clinical prognosis

“…In fact, this antigen, an isoform of the neural adhesion molecules (NCAM), has been recorded not only in aggressive non-Hodgkin's T cell lymphomas, 15,16 but also in malignant plasma cells 33 and in several myeloproliferative disorders including acute leukemias. [18][19][20][21][22][23][24][25] In this latter setting, CD56 expression was frequently associated with a poorer outcome, 23 as documented in AML patients with t(8;21) (q22;q22) and in APL cases, in which, the presence of CD56 antigen on the membrane of leukemic blasts led to a significant reduction of CR and overall survival duration. [23][24][25] In this study, conducted in a large series of AML patients, the presence of CD56 antigen was documented in 37/152 (24%), 33 of whom were also evaluable for response.…”

“…[6][7][8][9][10][11] More recently, CD56 antigen, a 200-220 kDa cell surface glycoprotein, identified as an isoform of the neural adhesion molecules (NCAM) [12][13][14] was firstly described as a marker of natural killer cells and subsequently, has also been found expressed in several lympho-hematopoietic neoplasms including acute myeloid leukemias (AML). [15][16][17][18][19][20][21][22] In fact, it has been previously reported that in AML patients with t(8;21) (q22;q22), generally considered at lower risk of relapse, the presence of CD56 antigen on blast cells may influence complete remission (CR) duration and survival, 23 suggesting that CD56 expression could be useful in stratifying therapeutic approaches for this subtype of AML. 23,24 Similar data have also been reported in patients with acute promyelocytic leukemias (APL) where the presence of CD56 antigen on APL blasts seems to identify a poorer risk prognostic group.…”

AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: Implication in stepwise leukemogenesis and response to Gleevec

“…A number of observations also suggest a role for C-KIT, another member of type III RTK family that is important for the development of a range of cells including hematopoietic cells (2), in leukaemogenesis. High expression of C-KIT in AML (60-80%) has been reported (21,22), and point mutations of C-KIT have been identified in 33.3-45% of AML with inv (16) and 12.8-46.8% of AML M2 with t(8;21) (23-25). However, many of these studies screened for C-KIT mutations only in a proportion of C-KIT coding sequence, and others were limited by the small case number studied.…”

Neural Cell Adhesion Molecule (CD56)–Positive Acute Myelogenous Leukemia and Myelodysplastic and Myeloproliferative Syndromes

“…This included patients with AML, MDS, and CML in blast crisis. Although anomalous expression of CD56 has been reported in AML 8,[19][20][21][22][23][24][25][26][27] 23,27 A l t h o u g h 8 of 23 p a t i e n t s in our s t u d y had hepatomegaly at diagnosis, no biopsy was performed. None of our patients had documented soft-tissue involvement.…”

“…This includes clinically aggressive lymphomas, 1 1 -1 4 plasma cell myelomas, 1 5 -1 7 and a recently described myeloid/NK cell acute leukemia with morphologic features similar to acute promyelocytic leukemia. 18 CD56 also has been reported to be expressed in a subset of AML 8,[19][20][21][22][23][24][25][26][27] and CML. 8 ' 33 We found anomalous expression of CD56 in 20% of patients with increased myeloblasts.…”