Expression of CD7 antigen precludes t(8;21)(q22;q22) chromosome aberration in acute myeloblastic leukemia.

The report by Ball et all showed the significance of the lymphoid markers, CD2 and CD19 antigens, expressed by subsets of acute myeloblastic leukemia (AML) in correlation with chromosomal aberrations and prognosis. The report disregarded CD7 antigen as lymphoid marker, probably because the relatively high incidence of the expression of CD7 antigen in AML cases, compared with CD2 or CD19 antigen, was estimated to hamper the rational subgrouping of their cases. However, the relative high incidence of CD7+ AMLZ3 can make its expression or absence eligible for the correlative analysis with other clinical features. We point out that t(8;21)(q22;q22) AML is characterized by the constant absence of the expression of CD7 antigen. Karyotypic results were available in 36 of the 137 cases that were investigated for phenotypic analysis in our laboratory from January 1987 through December 1990. The expression of CD2, CD7, and CD19 antigens was always evaluated. The chromosomal aberration, t(8;21)(q22;q22), was detected in 5 of the 36 cases. Two of the five t(8;21)(q22;q22) AML cases expressed CD19 antigen, but none of them expressed CD7 or CD2 antigen. We collected 14 cases of t(8;21)(q22;q22) AML from available literature"s in which the expression of CD7 antigen was evaluated. None of the 14 reported cases of t(8;21)(q22;q22) AML expressed CD7 or CD2 antigen, but 8 of the 14 cases expressed CD19 antigen. On the contrary, CD7 antigen was expressed by 19 (French-American-British [FAB] M1, 17 cases; M2,2 cases) of our 137 AML cases. Cytogenetical results were obtained from 3 of the 19 cases, showing normal karyotype in two cases and karyotype with lp+ in one. None of the four reported CD7+ AML cases3*' showed t(8;21)(q22;q22). Therefore, it is very likely that CD7 antigen, if expressed in a given case of AML, is a predicting marker on which t(8;21)(q22;q22) can be excluded. This prediction is useful because t(8;21)(q22;q22) AML, usually M2 (FAB), is occasionally M1 (FAB)? and because both M1 and M2 blasts can express CD7 antigen. Ball et all did not clearly show which of the two lymphoid markers, CD2 or CD19 antigen, was expressed by their t(8;21)(q22; q22) AML cases, while they pointed out the high incidence of the expression of the lymphoid markers in the AML cells with t(8;21)(q22;q22). However, AML cells with t(8;21)(q22;q22) have been reported to express CD19 antigen at a rather high incidence$~~ as was also shown in our laboratory. Furthermore, we could not find CD2+ t(8;21)(q22;q22) AML cases in the literature. Our 137 AML cases included three CD2+ cases, which were two CD7+ (FAB M1) and a CD7(FAB M3) with t(15;17) cases. Thus, some unknown feature of t(8;21)(q22;q22) AML cells inclining to B-lineage may explain the constant absence of CD7 or CD2 antigen and the rather high incidence of the expression of CD19 antigen. The heterogeneity of AML will be further studied based on multiple markers including cell surface antigens, chromosomal aberrations, and prognosis. Future analyses may show that the constant absence of some nonmyeloid antigen, which is expressed at a certain incidence by AML cells, correlates with other clinical features like the constant lack of CD7 antigen by t(8;21)(q22;q22) W L cells.