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Clonal development and karyotype evolution during leukemogenesis of BCR/ABL
transgenic mice
JW Voncken, C Morris, P Pattengale, G Dennert, C Kikly, J Groffen and N Heisterkamp
Department of Pathology, Childrens Hospital of Los Angeles 90027.
The Philadelphia (Ph) translocation is responsible for the generation of
the chimeric BCR/ABL oncogene. The Ph chromosome constitutes the earliest
detectable chromosome abnormality in chronic myelogenous leukemia and is
also found in acute lymphoblastic leukemia. Mice transgenic for a P190
BCR/ABL-producing DNA construct develop lymphoblastic leukemia/lymphoma and
provide an opportunity to study early stages of the disease as well as
progression. In this study, we have karyotyped the bone marrow of 10
19-day-old BCR/ABL P190 transgenic mice from a line that reproducibly
develops leukemia/lymphoma. Leukemic cells from 17 terminally ill
transgenic founders and progeny were also karyotyped as well as bone marrow
transplant recipients of leukemic donor marrow. Karyotypically visible
aberrations were absent from the early stages of BCR/ABL P190-generated
leukemia and normal metaphases could be found even in the terminal stages
of the disease. A high frequency of aneuploidy was found in advanced
leukemia, with a marked preference for the gain of mouse chromosomes 12,
14, or 17. These results point to a primary role for BCR/ABL in
leukemogenesis and suggest a destabilizing effect of the BCR/ABL gene on
the regulation of cell division.
Volume 79,
Issue 4,
pp. 1029-1036,
02/15/1992
Copyright © 1992 by The American Society of Hematology
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