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5 December 2013 11:26 am ,
Vol. 342 ,
At age 30, Dutch biologist Freek Vonk has built up a respectable career as a snake scientist. But in his home country,...
Since arriving on the island of Guam in the 1940s, the brown tree snake ( Boiga irregularis ) has extirpated native...
An animal rights group known as the Nonhuman Rights Project filed lawsuits in three New York courts this week in an...
Researchers have been hot on the trail of the elusive Denisovans, a type of ancient human known only by their DNA and...
Thousands of scientists in the Russian Academy of Sciences (RAS) are about to lose their jobs as a result of the...
Dyslexia, a learning disability that hinders reading, hasn't been associated with deficits in vision, hearing, or...
Exotic, elusive, and dangerous, snakes have fascinated humankind for millennia. They can be hard to find, yet their...
Researchers have sequenced and analyzed the first two snake genomes, which represent two evolutionary extremes. The...
- 5 December 2013 11:26 am , Vol. 342 , #6163
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Popping Cancer's Bubble
13 April 2005 (All day)
Two teams of researchers have identified a new cellular target that may be key to preventing and treating some forms of breast cancer.
Up to 5% of breast cancer in women is due to mutations in the BRCA1 or BRCA2 genes. These genes normally fix errors in a cell's DNA by swapping out whole sections of damaged DNA for fresh. Mutations in BRCA1 or BRCA2 can cause breast cells to become cancerous. Cancer cells might be unstoppable, but as long as they grow, they still need to repair their DNA.
Five years ago, molecular biologist Thomas Helleday of Stockholm University, Sweden, noticed that sick cells that couldn't swap out entire sections of damaged DNA could be killed by chemicals that interfered with another DNA fixer: a protein called PARP that patches up problems at single bases of DNA. Further work showed that PARP could be deleted without causing additional tumors, suggesting that interfering with PARP would not compromise normal cells. Helleday's team and another group of researchers led by Alan Ashworth of the Institute of Cancer Research, London, wondered what would happen if they could inhibit PARP in BRCA-deficient cancer cells.
To do so, Ashworth's team added PARP inhibitor to mouse cells in culture that lacked both copies of either BRCA1 or BRCA2. After 48 hours, the treated cells had stopped growing, and their chromosomes looked mangled. Cells that had at least one functioning copy of each BRCA grew normally when mixed with the PARP inhibitor, suggesting healthy cells tolerate the chemical well. Helleday's group got similar results with human breast cancer cells growing in culture. Both teams also showed that the PARP inhibitor prevented the formation of BRCA-2-deficient tumors in mice or was able to shrink them once they appeared.
PARP inhibitors are already being tested for safety in people for diseases other than breast cancer, so both groups believe human trials for breast cancer can begin within the year. Both teams report their results 14 April in Nature.
Cell biologist Keith Caldecott at the University of Sussex in Brighton, United Kingdom, says the result is "extremely promising" but cautions that "there's a long way to go with this" to show that it works against human breast cancer. Most anticancer drugs take advantage of the fact that cancer cells grow faster than normal, he says, and they also kill normal cells. Because this method leaves normal cells virtually untouched, it has no precedent, making it impossible to predict how well the cultured cells and mice data will translate to humans.