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Vol. 14, No. 3, pp. 272-277, February 1, 2000
1 Dana-Farber Cancer Institute, and Harvard Medical
School, Boston, Massachusetts 02115 USA; 2 Department of
Pathology, Tufts University Schools of Medicine and Veterinary
Medicine, Boston, Massachusetts 02111 USA; 3 Departments of
Pharmacology and Cancer Biology, Duke University Medical Center,
Durham, North Carolina 27710 USA
Mice with monoallelic inactivation of the CBP gene develop highly
penetrant, multilineage defects in hematopoietic differentiation and,
with advancing age, an increased incidence of hematologic malignancies.
The latter are characterized, at least in some cases, by loss of
heterozygosity (LOH) at the CBP locus. No such pathology was observed
in wild-type or p300 heterozygous null mice of the same age and genetic
background. Thus, a full complement of CBP, but not p300, is required
for normal hematopoietic differentiation. These results also provide
the first experimental evidence for the hypothesis that CBP has
tumor-suppressing activity.
[Key Words: CBP; p300; hematopoiesis; LoH; tumor suppressor]
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