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Vol. 15, No. 10, pp. 1188-1193, May 15, 2001
1 Department of Anatomy and Cell Biology, and
2 Department of Pathology, Columbia University, New York, New
York 10032 USA; 3 Dana-Farber Cancer Institute, Boston,
Massachusetts 02115 USA; 4 Department of Genetics and
Development, and 5 Institute of Cancer Genetics, Columbia
University, New York, New York, 10032 USA
We generated mouse mutants carrying in the Brca1 locus a
modification (Brca1tr) that eliminates the C-terminal
half of the protein product and obtained results indicating that,
depending on genetic background, the missing BRCT and/or other domains
are dispensable for survival, but essential for tumor suppression. Most
of the apparently hypomorphic Brca1tr/tr mutants
developed various tumors. Lymphomas were detected at all ages, whereas
sarcomas and carcinomas, including breast cancer, appeared after a long
latency. The mammary tumors showed striking variability in
histopathological patterns suggesting stochastic engagement of
tumorigenic pathways in their progression, to which the
Brca1tr/tr mutation was apparently a late participant.
[Key Words: Brca1; mouse mutant; mammary tumors]
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