Courtesy of Beth A. Weaver
The paper:
B.A. Weaver et al., "Aneuploidy acts both oncogenically and as a tumor
suppressor," Cancer Cell, 11:25–36. (Cited in 70 papers)
The finding:
Beth Ann Weaver, a cell biologist at the University of
Wisconsin–Madison, showed that mice with lower levels of centromere
protein E (CENP-E), a motor protein that sorts chromosomes during mitosis, had
higher rates of abnormal chromosome numbers, or aneuploidy.
CENP-E–deficient mice also had more spleen and lung tumors but,
surprisingly, had fewer liver tumors.
The controversy:
Weaver's group claimed that aneuploidy was the sole culprit in altered tumor
formation rates, but CENP-E might have other effects, too, says Robert Benezra of
Memorial Sloan-Kettering Cancer Center. "You can never be sure that you are only
inducing aneuploidy," he says. The Mayo Clinic's Jan van Deursen agrees: "The claim
that this is the best model for aneuploidy is a little bit overblown."
The look back:
The findings spurred van Deursen and others to reanalyze older studies for a
link between tumor suppression and aneuploidy. For example, data from New York
Medical College's Wei Dai indicated that aneuploidy also suppressed cancer of the
small intestine (PNAS, 102:4365–70, 2005).
The step forward:
Weaver's lab is currently testing the hypothesis that lower rates of
aneuploidy drive cancer, while higher rates cause cell death and therefore suppress
cancer.
| Percentage of mice with cancer |
| Cocktail |
Spleen tumor |
Liver tumor |
| Wild type: |
0% |
14% |
| CENP-E deficient: |
10% |
7% |