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JCI early table of contents for Nov. 26, 2012


Tumor cells frequently have an irregular number of chromosomes, a condition known as aneuploidy. During cell division, checkpoint proteins stop the process of division to ensure that each daughter cell receives the appropriate number of chromosomes; defects in these checkpoints can cause aneuploidy. In this issue of the Journal of Clinical Investigation, researchers led by Paul Galardy at the Mayo Clinic in Rochester, MN, investigated the role of the checkpoint protein USP44. Using a mouse that lacks Usp44, they found that loss of USP44 prevents chromosomes from splitting evenly between daughter cells. Usp44-deficient mice were prone to spontaneous tumors, particularly in the lungs. Interestingly, low USP44 expression was correlated with poor prognosis in human lung cancer. In a companion commentary, Andrew Holland and Don Cleveland of the University of California, San Diego, discuss how theses findings impact our understanding of aneuploidy in cancer.

USP44 regulates centrosome positioning to prevent aneuploidy and suppress tumorigenesis

Paul Galardy
Mayo Clinic, Rochester, MN, USA
Phone: 507-284-2695; E-mail:

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The deubiquitinase USP44 is a tumor suppressor that protects against chromosome missegregation

Andrew Holland
Ludwig Inst. Cancer Research & UCSD, La Jolla, CA, USA
Phone: 858-534-7899; E-mail:

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Contact: Jillian Hurst
Journal of Clinical Investigation

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