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17 April 2014 12:48 pm ,
Vol. 344 ,
Officials last week revealed that the U.S. contribution to ITER could cost $3.9 billion by 2034—roughly four times the...
An experimental hepatitis B drug that looked safe in animal trials tragically killed five of 15 patients in 1993. Now,...
Using the two high-quality genomes that exist for Neandertals and Denisovans, researchers find clues to gene activity...
A new report from the Intergovernmental Panel on Climate Change (IPCC) concludes that humanity has done little to slow...
Astronomers have discovered an Earth-sized planet in the habitable zone of a red dwarf—a star cooler than the sun—500...
Three years ago, Jennifer Francis of Rutgers University proposed that a warming Arctic was altering the behavior of the...
- 17 April 2014 12:48 pm , Vol. 344 , #6181
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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.