Co‐expression of myeloid antigens in childhood acute lymphoblastic leukaemia: relationship with the stage of differentiation and clinical significance

Abstract

Co-expression of myeloid antigens on the leukaemic blast cells was evaluated in 532 children with a diagnosis of acute lymphoblastic leukaemia (ALL). Using a panel of monoclonal antibodies belonging to CD11b, CD13, CD14, CD15 and CD33 an overall incidence of 4.3% was found, with values ranging between 1.8% for CD14 and 6.1% for CD15. When the data were further dissected, a significantly higher incidence of co-expression was noted in null-ALL (15/70 cases = 21.4%), compared to cases expressing a more mature immunophenotype, i.e. common-ALL (7/394 cases = 1.7%) and T-ALL (1/68 cases = 1.4%) (P less than 0.001). In null-ALL, 9/15 patients were infants, five of whom with the t(4;11); two further children also had a t(4;11). The clinical outcome of the 23 cases which co-expressed myeloid antigens was unfavourable. Only two of the 15 null-ALL, two of the seven common-ALL and the unique case with T-ALL are in fact in persistent first remission between 19 and 93 months from diagnosis. Though the overall incidence of childhood ALL expressing myeloid antigens is low, the evidence that this co-expression may be related to an unfavourable clinical course and that it more frequently occurs in null-ALL, particularly in the first year of life, suggests that the routine assessment of myeloid antigens may allow to identify a subgroup of childhood ALL with a poor clinical outcome.

Myeloid antigen co‐expression in childhood acute lymphoblastic leukaemia: relationship with in vitro drug resistance

“…In the present study 60/167 ALL patients (36%) co‐expressed the CD13 and/or CD33 antigen. In other reports the percentage of My + cases varied between 4% and 32% but the majority of studies reported a frequency of about 15% in childhood ALL (Basso et al , 1992; Cantú‐Rajnoldi et al , 1991; Fink et al , 1993; Kaspers et al , 1994a; Kurec et al , 1991; Pui et al , 1990, 1991; Putti et al , 1997; Reiter et al , 1994; Uckun et al , 1997; Wiersma et al , 1991). Differences in the percentage of My + ALL children can be explained by the definition of My + which depends on the cut‐off percentage of positively stained cells used, the number of markers (one or more) that should be positive and the choice of myeloid markers such as CD11b, CD13, CD14, CD15, CD33, CDw65 or myeloid peroxidase.…”

“…My + ALL may originate from progenitor cells which had not (yet) committed to generate either myeloid or lymphoid cells (lineage promiscuity) or from progenitor cells which have both myeloid and lymphoid features (lineage infidelity) (Drexler et al , 1991; Greaves et al , 1986; Smith et al , 1983). Several studies demonstrated that My + ALL children had a poorer long‐term clinical outcome compared with My − ALL patients (Basso et al , 1992; Cantú‐Rajnoldi et al , 1991; Fink et al , 1993; Kurec et al , 1991; Wiersma et al , 1991). In contrast, other studies could not confirm this result (Pui et al , 1990, 1991; Putti et al , 1997; Reiter et al , 1994; Uckun et al , 1997).…”

Leukemic blasts with markers of four cell lineages in Down's syndrome (“megakaryoblastic leukemia”)

“…Based on MoAb studies in children with ALL and AML diagnosed by standard criteria, coexpression of lymphoid and myeloid markers are reported in 4.3-12.6% [17,18,19] and 16.8-18.9% [18,19], respectively. In a study on adult patients with AML, San Miguel et a1 .…”

Rapid mitogen-induced aminopeptidase N surface expression in human T cells is dominated by mechanisms independent of de novo protein biosynthesis

“…With respect to the haematopoietic system, aminopeptidase N has been accepted to be exclusively expressed on cells of the myelo-monocytic lineage (11,12). Subsequently APN was shown, however, to be expressed on the surface of malignant B cells as well (13)(14)(15)(16)(17)(18). The expression of the CD13 antigen on the surface of T cells stimulated by concanavalin A has been reported earlier by ANSORGE et al (19) and KUNZ et al (20).…”