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JNCI Journal of the National Cancer Institute 2005 97(17):1302-1306; doi:10.1093/jnci/dji254
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© 2005 Oxford University Press

BRIEF COMMUNICATION

Genomic Instability of Human Mammary Epithelial Cells Overexpressing a Truncated Form of EMSY

Afshin Raouf, Lindsay Brown, Nikoleta Vrcelj, Karen To, Winnie Kwok, David Huntsman, Connie J. Eaves

Affiliations of authors: Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada (AR, KT, WK, CJE); Genetic Pathology Evaluation Center, Department of Pathology and Laboratory Medicine, British Columbia Cancer Agency, Vancouver General Hospital, and the University of British Columbia, Vancouver, British Columbia, Canada (LB, NV, DH); Prostate Center, Vancouver General Hospital, Vancouver, British Columbia, Canada (LB, NV, DH); Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada (CJE)

Correspondence to: Connie J. Eaves, PhD, Terry Fox Laboratory, 675 West 10th Ave., Vancouver, BC V5Z 1L3, Canada (e-mail: ceaves{at}bccrc.ca) or David Huntsman, MD, Department of Pathology, British Columbia Cancer Agency, 600 West 10th Ave., Vancouver, BC V5Z 4E6, Canada (e-mail: dhhuntsman{at}bccancer.bc.ca).

The EMSY gene encodes a protein that interacts with Brca2 and is amplified in some sporadic cases of human breast cancer. To examine whether overexpression of EMSY would mimic the chromosome instability phenotype that is associated with the loss of Brca2 function, we constructed a lentiviral vector (Lenti-EMSY/GFP) that encodes a truncated form of the Emsy protein, including its Brca2-interacting domain, and green fluorescent protein (GFP) and used it to transduce human telomerase-immortalized human breast epithelial (184-hTert) cells, which have a nearly normal karyotype. At passage 5 after transduction, 39 (26%) of 150 EMSY/GFP-transduced metaphase cells contained at least one structural chromosomal abnormality compared with 19 (13%) of 150 GFP-transduced metaphase cells (P = .003, chi-square test); at passage 10, the corresponding frequencies were 42% and 15%, respectively (P<.001). Mitomycin C also produced a severalfold higher frequency of chromosome breaks in the EMSY/GFP-transduced cells than in the control cells. These results support the hypothesis that EMSY overexpression can play a role in the genesis of human breast cancer.


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