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BCR/ABL P210 and P190 cause distinct leukemia in transgenic mice
JW Voncken, V Kaartinen, PK Pattengale, WT Germeraad, J Groffen and N Heisterkamp
Department of Pathology Research and Laboratory Medicine, Childrens
Hospital of Los Angeles, CA 90027, USA.
DNA constructs encoding BCR/ABL P210 have been introduced into the mouse
germ line using microinjection of one-cell fertilized eggs. Kinetics of
BCR/ABL P210 expression in transgenic mice were very similar to those of
BCR/ABL P190 constructs in transgenic mice. mRNA transcripts were
detectable early in embryonic development and also in hematopoietic tissue
of adult animals. Expression of BCR/ABL in peripheral blood preceded
development of overt disease. P210 founder and progeny transgenic animals,
when becoming ill, developed leukemia of B, T-lymphoid, or myeloid origin
after a relatively long latency period. In contrast, P190-transgenic mice
exclusively developed leukemia of B-cell origin, with a relatively short
period of latency. The observed dissimilarities are most likely due to
intrinsically different properties of the P190 and P210 oncoproteins and
may also involve sequences that control transgene expression. The delayed
progression of BCR/ABL P210-associated disease in the transgenic mice is
consistent with the apparent indolence of human chronic myeloid leukemia
during the chronic phase. We conclude that, in transgenic models,
comparable expression of BCR/ABL P210 and BCR/ABL P190 results in
clinically distinct conditions.
Volume 86,
Issue 12,
pp. 4603-4611,
12/15/1995
Copyright © 1995 by The American Society of Hematology
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