Universal cancer marker shows new treatment options

A single screening method that can force a wide range of cancers to reveal themselves has been discovered. The universal cancer marker could help doctors find and treat tumours, and provide surgeons with a "dotted line" to cut them out.

The key to the technique is the receptor for follicle-stimulating hormone (FSH). This receptor – typically involved in controlling women's reproductive cycles – appears in unusually large amounts in prostate tumours. So Aurelian Radu at Mount Sinai School of Medicine in New York and colleagues looked for it in 1336 human tumour samples, including prostate, breast, lung and liver cancers.

The group applied colour-labelled antibodies for the FSH receptor to the samples. They found that in every sample, the antibodies bound to blood vessels around the periphery of the tumour.

Radu doesn't yet know why tumour blood vessels express the receptor, though he thinks it might play a role in the formation of new vessels.

 

One-stop screening

 

The marker could be useful in pinpointing and treating tumours, says Radu. Currently, different imaging techniques are used to identify different types of tumour. "Using this marker, we can use one imaging technique for the whole body," says Radu. He hopes broader screening will enable earlier detection of secondary tumours.

Kairbaan Hodivala-Dilke at Barts and The London School of Medicine and Dentistry's Institute of Cancer agrees: "It's certainly a good marker, and could be especially useful in surgery, which is a bit hit-and-miss at the moment," she says. Using colour-labelled antibodies to highlight the edges of a tumour could enable surgeons to "cut along the dotted line".

Additionally, by attaching a cancer drug to an FSH receptor antibody, "we have the potential to target therapy exclusively to the tumour", says Radu.

Drugs that inhibit the FSH receptor are already in development as potential contraceptives, says Radu. He hopes that some might be trialled as anti-cancer drugs in the future.

Gene therapy proposed to treat depression

A NOVEL treatment for depression may soon get the go ahead: injecting genes directly into the brain. It would be the first attempt to treat a psychiatric illness with gene therapy.

A gene called p11 is vital for enabling neurons to respond to the neurotransmitter serotonin. A lack of p11 has been shown to lead to depression in humans.

To test whether gene therapy could help, Michael Kaplitt of the Weill Cornell Medical College in New York City and colleagues first demonstrated that mice lacking p11 showed symptoms of depression, failing to respond with the same vitality as healthy mice when exposed to challenges, such as showing decreased effort when having to swim to an island.

Next they injected viruses containing p11 directly into the nucleus accumbens of the mice lacking p11. This part of the brain is where a lack of p11 manifests itself as depression in humans. The team found this reversed the depression in the mice (Science Translational Medicine, DOI: 10.1126/scitranslmed.3001079).

Although the proposal to do the same in humans sounds drastic, Kaplitt points out that a similar procedure has already been used to deliver genes to the brain's of people with Parkinson's disease.

"We're already doing a primate study to support a potential human trial, so this is moving ahead very rapidly," says Kaplitt.

 

“Injecting a virus containing the missing gene into a mouse's brain reversed its depression”

Low levels of vitamin B12 linked to Alzheimer's

People with low levels of vitamin B₁₂ may be at greater risk of developing Alzheimer's disease. The finding supports previous research showing large doses of B vitamins might halve the rate of brain shrinkage.

Babak Hooshmand and colleagues at the Karolinska Institute in Stockholm, Sweden, followed 271 healthy people aged 65 to 79 for seven years. The researchers measured the blood concentration of the amino acid homocysteine, high levels of which have been linked to negative effects on the brain, such as stroke. They also measured levels of active vitamin B₁₂, which can decrease homocysteine levels.

By the end of the study, 17 people had developed Alzheimer's. A level of homocysteine moderately above average corresponded to a 16 per cent higher risk of developing Alzheimer's, while a level of active B₁₂ slightly above average meant a 2 per cent lower risk.

"This is a very convincing study," says David Smith of the University of Oxford, who has investigated the effect of B-vitamin supplements on brain shrinkage. He says it is the first to show that low levels of active vitamin B₁₂ are a risk factor for developing dementia several years later.

Although B₁₂ deficiency is common among elderly people, more evidence is needed before recommending B₁₂ supplements to stave off dementia, says Hooshmand.