The clinical, hematological, and cytogenetic characteristics of a male patient with AMMoL are described. Before treatment a clone with the complex karyotype 45,X,de1(7)(q32), t(8;21)(q22;q22) was present in the bone marrow. During partial remission induced by cytostatics, the percentage of normal cells increased, and a cell line having a 46,XY,de1(7)(q32) karyotype was found. After four therapy courses. when remission was complete, only chromosomally normal cells were seen. The cytogenetic data suggest that in this case the 8/21 translocation and loss of the Y chromosome were only secondary events.
Cancer 45285-288. 1980. HROMOSOMAL ABERRATIONS occur in the bone C marrow cells of 40-60% of the patients with acute myeloid leukemia and appear to be nonrandom.2,G.7*1i Trisomies for the chromosomes Nos. 8, 9, or 21 and monosomy for chromosome No. 7 are the most often found numerical karyotypic changes. Also, certain structural chromosome rearrangements are seen relatively often, such as a translocation between the chromosomes Nos. 8 and 21,2,49" and a translocation between the chromosomes Nos. 15 a n d 17. The latter translocation has, until now, only been found in the bone marrow of patients with acute promyelocytic le~kemia.'.'~~.''
The translocation 8/21 might b e rather specific for "classical" AML.2,8,15 It is often accompanied by t h e loss of a sex chromosome, resulting in 45,X,t(8;21) cells.' Progression of t h e 45,X,t(8;21) karyotype to more complex aberrations has also been 0 b ~e r v e d . I ~
In the present article, we wish t o describe the clinical and cytogenetic characteristics of a male AMMoL patient whose bone marrow contained 45,X,t(8;21) cells and showed a deletion of the long arm of a chromosome No. 7. Our data may suggest that in this patient the 7q-deletion arose as the primary karyotypic change and that the 8/21 transiocation and loss of the Y chromosome were only secondary.