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Altered myeloid development and acute leukemia in transgenic mice
expressing PML-RAR alpha under control of cathepsin G regulatory sequences
JL Grisolano, RL Wesselschmidt, PG Pelicci and TJ Ley
Department of Internal Medicine, Washington University Medical School, St
Louis, MO 63110, USA.
Acute promyelocytic leukemia (APML) is characterized by abnormal myeloid
development, resulting an accumulation of leukemic promyelocytes that are
often highly sensitive to retinoic acid. A balanced t(15;17) (q22;q21)
reciprocal chromosomal translocation is found in approximately 90% of APML
patients; this translocation fuses the PML gene on chromosome 15 to the
retinoic acid receptor alpha (RAR alpha) gene on chromosome 17, creating
two novel fusion genes, PML-RAR alpha and RAR alpha-PML. The PML-RAR alpha
fusion gene product, which is expressed in virtually all patients with
t(15;17), is thought to play a direct role in the pathogenesis of APML. To
determine whether PML-RAR alpha is sufficient to cause APML in an animal
model, we used the promyelocyte-specific targeting sequences of the human
cathepsin G (hCG) gene to direct the expression of a PML-RAR alpha cDNA to
the early myeloid cells of transgenic mice. Mice expressing the hCG-PML-RAR
alpha transgene were found to have altered myeloid development that was
characterized by increased percentages of immature and mature myeloid cells
in the peripheral blood, bone marrow, and spleen. In addition,
approximately 30% of transgene-expressing mice eventually developed acute
myeloid leukemia after a long latent period. The splenic promyelocytes of
mice with both the nonleukemic and leukemic phenotypes responded to
all-trans retinoic acid (ATRA) treatment, which caused apoptosis of myeloid
precursors. Although low-level expression of the hCG-PML-RAR alpha
transgene is not sufficient to directly cause acute myeloid leukemia in
mice, its expression alters myeloid development, resulting in an
accumulation of myeloid precursors that may be susceptible to cooperative
transforming events.
Volume 89,
Issue 2,
pp. 376-387,
01/15/1997
Copyright © 1997 by The American Society of Hematology
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