Shark blood could fight breast cancer

Antibodies in shark blood may be able to prevent growth of breast cancer

A TYPE of antibody found only in the blood of sharks could help tackle breast cancer, scientists have said.

It is thought that the unique IgNAR antibodies in sharks could be used to prevent the growth of cancer cells.

It is thought that the unique IgNAR antibodies could be used to prevent the growth of cancer cells and research into them could lead to the development of new drugs to fight one of the most common form of the disease. Biologists from the University of Aberdeen have been awarded 200,000 pounds ($345,660) by Scottish cancer research charity the Association for International Cancer Research (AICR) to carry out a three-year study. Their work will focus on two molecules, HER2 and HER3, found on the surface of cancer cells which, when they pair-up, are responsible for signalling cancer cells to grow and divide.
Potentially, IgNAR antibodies could be used to stop these molecules from working and sending the signal. “IgNAR antibodies are interesting because they bind to targets, such as viruses or parasites, in a very different way to the antibodies found in humans,” said Dr Helen Dooley who is from the university’s School of Biological Sciences and will lead the study. “They can do this because their attachment region is very small and so can fit into spaces that human antibodies cannot. “We believe we can exploit the novel binding of IgNAR and use it to stop HER2 and HER3 molecules from working, and prompting cancer cells to grow and divide.” Very high levels of HER2 are found on the surface of cancer cells in women who have HER2-positive breast cancer, this affects around a quarter of women with breast cancer. While HER2-positive breast cancer can be treated with drugs but resistance to this successful treatment is a growing problem. “With the funding from AICR we can begin to explore the potential of IgNAR as a future treatment for breast cancer,” Dooley said. “This is only the first step in a very long process but if our hypothesis holds true we hope to develop new anti-cancer drugs based upon these unique shark antibodies.”

New study shows link between stress gene and spread of breast cancer

WE ALL know stress is bad for our health. But a new study shows that a “master-switch” stress gene enables the spread of cancer. In an unexpected finding, scientists have linked the activation of a stress gene in immune-system cells to the spread of breast cancer to other parts of the body.

Researchers at Ohio State University found this gene, called ATF3, may be the crucial link between stress and cancer. Previous public health studies have shown that stress is a risk factor for cancer. Researchers already know that ATF3 is activated, or expressed, in response to stressful conditions in all types of cells. Under typical circumstances, turning on ATF3 can actually cause normal and benign cells to commit suicide if the cells decide that the stressors, such as irradiation and a lack of oxygen, have irrevocably damaged the cells.

This research suggests, however, that cancer cells somehow coax immune-system cells that have been recruited to the site of a tumour to express ATF3. Though it’s still unclear how, ATF3 promotes the immune cells to act erratically and give cancer an escape route from a tumour to other areas of the body. The senior author of the study said this gene is the enemy. “It’s like what Pogo said: ‘We have met the enemy, and he is us’,” professor of molecular and cellular biochemistry Tsonwin Hai said. “If your body does not help cancer cells, they cannot spread as far. So really, the rest of the cells in the body help cancer cells to move, to set up shop at distant sites. And one of the unifying themes here is stress.”

Hai and colleagues first linked the expression of the ATF3 gene in immune-system cells to worse outcomes among a sample of almost 300 breast-cancer patients. When she examined human samples from the 300 patients, she was stunned to find that the expression of ATF3 gene in certain immune-system cells was associated with worse cancer outcomes in this group of patients. ATF3 in cancer cells showed no such association.

They followed with animal studies and found that mice lacking the ATF3 gene had less extensive metastasis of breast cancer to their lungs than did normal mice that could activate ATF3. Hai, has studied ATF3 in cancer cells for years, said this stress gene could one day function as a drug target to combat cancer metastasis if additional studies bear out these results.

In the meantime, she said the results provide important insights into how cells in a tumour use their signalling power to co-opt the rest of the body into aiding cancer’s survival and movement to distant organs.

The research is published in a recent issue of the Journal of Clinical Investigation.