Correlation of cytogenetic patterns and clinicobiological features in adult acute myeloid leukemia expressing lymphoid markers [see comments]

Abstract

Cytogenetic, biomolecular, and clinicopathologic features were retrospectively studied in 34 adult patients with acute myelogenous leukemia expressing one or more of the following lymphoid-associated markers (LMs): CD7, CD2, CD10, CD19, CD22, TdT. Six patients showed 11q23 rearrangements (group I); three patients had the classic Ph chromosome (group II); 15 patients had aberrations of the myeloid type (group III), including four patients with structural aberrations of 13q or trisomy 13, three patients with 7q and 1q anomalies, and two patients with trisomy 11q. Ten patients had a normal karyotype (group IV). Anomalies exclusively associated with lymphoid malignancies were not seen. Ig H and/or T-cell receptor genes were found to be rearranged in 50% and 66% of patients in cytogenetic groups I and II, respectively, versus 8% in group III and 12% in group IV. Likewise, more than one LM was more frequently detected in groups I and II. In group III, two of four patients with aberrations of chromosome 13 expressed two or more lymphoid features. Clinically, patients belonging to cytogenetic groups I and II were generally young, presented with a high white blood cell (WBC) count, and had a low complete remission rate. Survival in Ph chromosome-positive cases was uniformly short. We conclude that although there is no cytogenetic anomaly specifically associated with acute myelogenous leukemia expressing LM, a Morphologic, Immunologic, and Cytogenetic classification may constitute a working basis for further studies aimed at a better definition of clinicopathologic features and optimal treatment strategies for these leukemias.

Adult biphenotypic acute leukaemia: an entity with poor prognosis which is related to unfavourable cytogenetics and P‐glycoprotein over‐expression

“…Abnormalities of chromosome 11q23 and t(9;22) are associated with both lymphoid and myeloid leukaemias, suggesting a stem cell transformation. This high percentage of these two cytogenetic abnormalities in BAL was suggested in other studies (Carbonell et al, 1996;Hanson et al, 1993;Hayashi et al, 1990;Cuneo et al, 1992). On the other hand, Pgp phenotype is often correlated with treatment outcome (CR and overall survival) in acute leukaemia patients .…”

“…But the different conclusions remain controversial because they used different scoring systems and the majority of these studies did not report the data separately for children and adults (Curtis et al, 1993), even though the prognosis of BAL children has been reported to be identical to other acute leukaemias (Dinndorf et al, 1986;Pui et al, 1989). In other studies, only the patients which demonstrated expression of myeloid antigens in ALL, or lymphoid antigens in AML were analysed (Boldt et al, 1994;Pui et al, 1989;Cuneo et al, 1992). In our study, comparing adult BAL patients with AML patients, we found that percentage of CD34 þ patients, Ph1 þ patients or unfavourable karyotypes and Pgp expression were significantly higher in BAL than in AML.…”

Adult T‐biphenotypic acute leukaemia: clinical and biological features and outcome

“…However, several reports have shown that in some patients (approximately 20-30%), blast cells simultaneously express both myeloid and lymphoid markers (Drexler et al, 1991(Drexler et al, , 1993Buccheri et al, 1993). These cases were first called mixed-lineage leukaemias, with myeloid-antigen-positive acute lymphoblastic leukaemias (My+ ALL) (Sobol et al, 1987;Davey et al, 1988;Childs et al, 1989;Guyotat et al, 1990;Monpoux et al, 1990;Urbano-Ispizua et al, 1990;Hsu et al, 1991;Kurec et al, 1991;Pui et al, 1991;Kawamura & Tobinai, 1992;Kuerbitz et al, 1992;Hoelzer, 1994) being distinguished from lymphoid-antigen-positive acute myeloblastic leukaemias (Ly+ AML) (Das Gupta et al, 1987;Cross et al, 1988;Cuneo et al, 1992;Smith et al, 1992;Chen et al, 1993;Tien et al, 1993;Kawai et al, 1995;Lauria et al, 1995). They are now known as biphenotypic acute leukaemias (BAL) (Buccheri et al, 1993;Matutes et al, 1997;Uckun et al, 1997;Khalidi et al, 1998;Killick et al, 1999;Mi et al, 1999).…”

DNA aneuploidy in acute myeloblastic leukemia is associated with a high expression of lymphoid markers

“…It could be speculated that the increased expression of lymphoid-related antigens in DNA aneuploid AML patients could be related to the immature myeloblastic phenotype of these cases; however, in our series there was not an overall correlation between immature phenotypes and the expression of lymphoidrelated antigens. Although to the best of our knowledge the immunologic phenotype of AML cases displaying DNA aneuploidy has not been reported, these findings could be due to the higher incidence of chromosomal abnormalities reported in AML cases expressing lymphoid-associated markers (22)(23)(24).…”