The karyotype of leukemic cells of 78 acute leukemia patients (37 ANLL, 34ALL, and 7 of unknown type) was studied by means of G-banding. Chromosomal abnormalities were found in 50 patients (72%). Chromosomes 8,21,5,7,11, and 19 were preferentially involved in the abnormalities, both in ANLL and in ALL. A high incidence of the characteristic rearrangement t(8;21) was noted in AML: (in 6 of 22 AMP patients). An identical reciprocal translocation--t(4;11)--was seen in 4 out of 34 ALL patients.

Results of chromosome studies of blood and bone marrow cells from 101 patients with Ph1 positive chronic myeloid leukemia (CML) confirm the assumptions that clinical and morphologic manifestations of the disease correlate with karyotype peculiarities of leukemia cells. Several variants of the clinical course of CML may be distinguished. One is the variant with a short chronic phase and a comparatively long terminal phase. In blastic crisis the blast cells are peroxidase negative and do not possess cytoplasmic inclusions. Acute transformation occurs without any additional chromosome damage. The second, more common form is less severe because of longer chronic phase but it has a short and grave acute stage. The blast cells present definite signs of myeloid differentiation, they have basophilic or neutrophilic cytoplasmic granules and are peroxidase positive. Marker i(17q) often combined with trisomy 8 is a characteristic chromosome abnormality in the terminal stage of this variant. The third type has an extremely long chronic phase but ends in a rapidly progressing severe and resistant to therapy "lymphoid" blastic crisis. Blast cells have typical "lymphoid" morphology, they are peroxidase negative and contain granular PAS positive substance. Various additional chromosome changes appear in the terminal stage. Future studies of a larger series of patients may possibly reveal more CML variants.

Forty cases of chronic myeloid leukemia (CML) were studied and subgroups of cases with similar chromosomal abnormalities in terminal stage were defined. Certain correlations were observed between the type of chromosomal changes, and clinical and morphologic manifestations of the disease: (1) It seems that, in cases without any karyotype changes other than translocation (9;22), the terminal stage is longer and milder than in cases with additional chromosomal abnormalities; (2) cases with marker i(17q) are clinically and morphologically rather uniform and are characterized by distinct signs of myeloid differentiation of blast cells, absent in other cases; (3) in cases with various atypical chromosomal abnormalities, the course of the terminal stage is the most rapid and grave. The blast cells differ from myeloblasts and resemble lymphoid elements.

Karyotypes of 30 malignant lymphomas were studied with the aid of G-banding. Frequent occurrence of rearranged chromosomes 14 and 11 was noted. In several tumors, identical acrocentric markers, appearing after translocation of the long arm of chromosome 11 on the long arm of chromosome 14, were revealed. Other common karyotype abnormalities in lymphomas were trisomy 3 and trisomy 18. The chromosomes preferentially involved in karyotype abnormalities of the malignant lymphomas are mostly not altered in other hemoblastoses.

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