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.

Prostate cancer patient anger at huge bills despite paying insurance

MEN with prostate cancer are being slugged with out-of-pocket expenses of up to $23,000 because Medicare and health funds don’t cover the full cost of their treatment.

A study of more than 900 men by Griffith University’s Health Institute found men were “left shocked and angry when they received huge bills even after paying insurance for 20 years”.

Even though around 70 per cent of the men in the study were private health fund members they were forced to raid their savings, ask family members for money and cut back mortgage payments to fund their treatment.

Around 20,000 men are diagnosed with prostate cancer each year and at the same time as they face hefty medical bills they need to take around a month off work while they are treated. Senior researcher Dr Louisa Gordon said failure to index the Medicare rebate to health care inflation was the reason for growing out-of-pocket expenses.

Medicare rebates no longer represented the realistic cost of professional medical care and treatment, and some doctors failed to warn patients of the costs they faced, she said. “The medical system, whether public or private, needs to become a lot more transparent and informative so people can make informed choices during a stressful time,” Dr Gordon said. Health Minister Tanya Plibersek dismissed concerns about rising out-of-pocket health expenses during the election health debate claiming bulk billing figures were high.

Government data showed many out-of-pocket expenses related to band aids and condoms, she told the National Press Club. The study, however, found doctors and specialist fees for prostate treatment average $13,000 but Medicare refunded just $8,664. An online study of 289 men who received prostate treatment in the last five years found those diagnosed after January 2012 had average out-of-pocket costs of $11,077.

Labor yesterday slammed Tony Abbott’s promise to abolish the means test on private health insurance subsidies within a decade claiming it would cost $1 billion a year to restore the payments. This would mean he’d have to cut funding to the states equivalent to the cost of more than 2700 hospital beds to restore a subsidy to very high income earners, Labor claims.

Prostate cancer treatment praised

Australia and New Zealand are among the best places in the world to be diagnosed with prostate cancer, according to a visiting US professor who says aggressive treatment is being avoided in many cases.

In many countries, a diagnosis of prostate cancer almost always leads to removal or radiation therapy. In Australia and New Zealand, however, many low-risk patients are being managed by active surveillance.This means they are monitored with regular blood tests, biopsies and MRIs and aggressive action is taken only if the disease becomes life-threatening. Visiting American professor James Eastham, who will address urologists at a conference in Melbourne on Monday, is full of praise for his colleagues in Australia and New Zealand. He says about one in three men who are newly diagnosed with prostate cancer are candidates for active surveillance. In Australia and New Zealand, about half of these are managed with active surveillance. This is well ahead of the US, where only about 10 per cent of eligible patients are managed by active surveillance. This leads to over-treatment. ‘I’m impressed. This is not the traditional way of treating cancer,’ said Prof Eastham, from the Memorial Sloan Kettering Cancer Centre in New York. He will reassure the annual scientific meeting of the Urological Society of Australia and New Zealand that the latest research from around the world suggests active surveillance is a safe and effective way to manage patients. ‘It maximises quality of life without compromising quantity of life.’ Prof Eastham also agrees with the society’s position on screening men at the age of 40. ‘We know testing saves lives,’ he says.

Chemotherapy can boost cancer – study

Cancer-busting chemotherapy can cause damage to healthy cells that triggers them to secrete a protein that sustains tumour growth and resistance to further treatment, a study says. Researchers in the US made the ‘completely unexpected’ finding while seeking to explain why cancer cells are so resilient inside the human body when they are easy to kill in the lab. They tested the effects of a type of chemotherapy on tissue collected from men with prostate cancer, and found ‘evidence of DNA damage’ in healthy cells after treatment, the scientists wrote in Nature Medicine. Chemotherapy works by inhibiting reproduction of fast-dividing cells such as those found in tumours.

The scientists found that healthy cells damaged by chemotherapy secreted more of a protein called WNT16B, which boosts cancer cell survival. ‘The increase in WNT16B was completely unexpected,’ study co-author Peter Nelson of the Fred Hutchinson Cancer Research Center in Seattle told AFP. The protein was taken up by tumour cells neighbouring the damaged cells. ‘WNT16B, when secreted, would interact with nearby tumour cells and cause them to grow, invade, and importantly, resist subsequent therapy,’ said Nelson.

In cancer treatment, tumours often respond well initially, followed by rapid regrowth and then resistance to further chemotherapy. Rates of tumour cell reproduction have been shown to accelerate between treatments. ‘Our results indicate that damage responses in benign cells… may directly contribute to enhanced tumour growth kinetics,’ wrote the team. The researchers said they confirmed their findings with breast and ovarian cancer tumours.

The result paves the way for research into new, improved treatment, said Nelson. ‘For example, an antibody to WNT16B, given with chemotherapy, may improve responses (kill more tumour cells),’ he said in an email exchange. ‘Alternatively, it may be possible to use smaller, less toxic doses of therapy.’

5th Annual Men’s Health Conference

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