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Health notes: Aspirin ineffective against colon tumor with BRAF mutation

  • June 29, 2013 - 5:04 PM

Aspirin can’t beat certain tumors

Aspirin’s benefit in thwarting colon cancer is driven by a gene mutation that makes tumor cells less sensitive to the drug’s effects, according to a study that may lead to personalized prevention strategies.

Developing colon cancer with a mutation of the gene BRAF was similar for both regular aspirin users and nonusers, according to research published Tuesday in the Journal of the American Medical Association. Regular aspirin users had a 27 percent reduced risk of developing cancer without the mutation compared with those who didn’t regularly take the drug, the study found.

The finding, one of the first to show that aspirin use doesn’t prevent colon tumors with the BRAF defect, may help guide doctors when recommending the drug’s use to prevent the disease, said Andrew Chan, a study author. More studies are needed to better understand the role aspirin plays in cancer prevention, who is most at risk and which polyps may develop into tumors with a BRAF mutation, he said.

“We’ve entered a new era in which we would potentially start to think about personalizing preventive intervention,” said Chan, an associate professor of medicine at Harvard Medical School in Boston, in a telephone interview. “That’s something we haven’t been doing so far. We’ve been really trying to develop one size fits all treatment.”

vaccine promising for diabetes

An experimental vaccine designed to tamp down the abnormal immune response that causes Type 1 diabetes helped preserve patients’ insulin-producing cells in a study that may change the way the disease is treated.

Researchers from Stanford University in California and Leiden University Medical Center in the Netherlands created a vaccine that selectively targets the destructive immune cells and stops their attack. The data were published Wednesday in the journal Science Translational Medicine.

Type 1 diabetes is caused when the body’s immune system destroys insulin-releasing cells in the pancreas, called beta cells, requiring patients to inject themselves with insulin replacement therapy. Scientists have long sought a treatment approach that targets the cause of the disease.

“Although insulin saves people’s lives and was discovered 100 years ago, we need something better than that,” said Lawrence Steinman, a professor at Stanford School of Medicine near Palo Alto, Calif., and an author of the study. “One of the long sought-after goals of immunological therapy is to do just this, antigen-specific modulation.”

Type 1 diabetes, also called juvenile diabetes, affects as many as 3 million people in the U.S., according to JDRF, an organization that funds research for the disease.

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