There has been no substantial change in the number of adult brain tumours since mobile phone usage sharply increased in the mid-1990s, Danish scientists say.

The Danish Cancer Society looked at the rates of brain tumours among 20 to 79 year olds from Denmark, Finland, Norway and Sweden.

They found that trends in cancer rates had not altered from the period before mobiles were introduced. But they say longer follow-up studies are needed.

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Organ transplant drug could treat meningioma
21 Jun 2009
Researchers funded by the National Institute of Neurological Disorders and Stroke (NINDS) have found that an organ transplant drug might one day be used to treat meningioma, a type of brain tumour. The drug also could be used to treat neurofibromatosis type 2, a rare disease associated with meningiomas and other benign tumours of the nervous system.
In a study published in Molecular and Cellular Biology, the researchers show that rapamycin – an immunosuppressant used to prevent organ transplant rejection – can shrink meningioma cells grown in the laboratory.
Meningiomas account for 20–30 percent of all brain and spinal cord tumours. They arise from cells in the thin layers of connective tissue that surround the brain and spinal cord, called the meninges. Although most meningiomas are benign, they can cause neurological problems by compressing brain tissue. Surgery is usually effective, but, in some cases, the tumours are not accessible or may persist despite surgery.
"Pharmacological therapies are desperately needed," says Vijaya Ramesh, PhD, an associate professor of neurology at Harvard Medical School and Massachusetts General Hospital (MGH) in Boston. Dr Ramesh is the senior author on the new study; other key authors include James F. Gusella, PhD, Director of the Center for Human Genetic Research at MGH and a professor of neurogenetics at Harvard, and Marianne F. James, PhD, a neurology instructor at Harvard. The study received additional funding from the National Institute of Mental Health (NIMH), the S. Sydney De Young Foundation and Neurofibromatosis, Inc.
Deficiency of a gene called NF2/merlin is the cause behind most cases of isolated (sporadic) meningioma and all cases of neurofibromatosis type 2. Neurofibromatosis type 2 occurs when a person has only one functional copy of the NF2 gene from birth. Sporadic meningioma occurs when meningeal cells in the brain lose both copies of NF2 during a person's lifetime. These effects make NF2 a "tumour suppressor" gene, but until now, researchers knew little about how NF2 suppresses tumours or how to approach possible drug treatments.
Dr Ramesh and her team made a fortuitous discovery. In a 2008 study, they found that NF2-deficient meningioma cells grow larger than normal cells. They recalled that this is also a feature of tumour cells found in people with tuberous sclerosis complex (TSC), a disease in which benign tumours can grow in nearly any tissue, including the eyes and brain. Recent studies have shown that the tumours in TSC are triggered by abnormal activity of a protein called mTOR, which promotes cell growth and is inhibited by rapamycin. Dr Ramesh's team thought that mTOR might also play a pivotal role in meningioma.
In their new study, they found that mTOR is abnormally active in NF2-deficient cells derived from patients with meningioma. When they used a technique called RNA interference (RNAi) to block the activity of NF2 in normal meningeal cells, they observed an increase in mTOR activity and an increase in cell growth. Treatment with rapamycin slowed this growth and reversed it over the course of several days.
The researchers also found that when rapamycin shuts down mTOR, it indirectly activates a signalling pathway called PI3K-Akt, which has been associated with malignancy. They propose that rapamycin in combination with PI3K-Akt inhibitors might safely reduce the growth of meningioma cells.
Preparations are underway to create a mouse model of benign meningioma that will be used to test these treatments, Dr Ramesh says. As in humans, mice that lack the NF2 gene from birth have a risk of meningioma, but the number of mice that actually develop meningoima is small and the tumours themselves are microscopic. Dr Ramesh and her colleagues will use their RNAi technique to suppress NF2 in human meningeal cells, and then implant the cells into the mouse brain.
(Source: National Institute of Neurological Disorders and Stroke: Molecular and Cellular Biology: June 2009)
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Brain tumour gene link found

Thursday 21 February 2008

Cancer Research UK Press Release

Cancer Research UK funded scientists have discovered a mutation in a DNA repair gene which may increase the risk of developing meningioma, a rare type of brain tumour, according to new research published in the latest edition of the Journal of the National Cancer Institute.

The researchers, based at The Institute of Cancer Research, explored 136 DNA repair genes before they homed in on a mutation in the gene BRIP1 - a gene also associated with increased breast cancer risk. This mutation may account for 16 per cent of meningiomas.

More than 7,500 people are diagnosed with malignant or benign brain tumours in the UK each year. Meninigiomas account for over 30 per cent of these, yet little is known about the cause of the disease which tends to affect older people, and women.

The vast majority of meningiomas are benign. They grow slowly in the tissues of the brain or spinal cord and as a result do not respond well to chemotherapy and cannot always be safely removed by surgery.

The new study examined genetic differences in the brains of 1,268 people from four European countries. Data from 631 patients with meningiomas was compared with 637 healthy individuals. Previous US research had analysed a small sample of just 200 people, making this is the largest study of gene involvement in meningioma risk.

Lead researcher, Professor Richard Houlston, based at The Institute of Cancer Research, said: "Using a large sample, we have identified a new region associated with meningioma risk. However, further investigation into the functions of BRIP1, could shed more light on the relationship between the gene and brain tumour growth.

"Currently, the only sure way to diagnose many brain tumours is by biopsy. Research like ours, which examines gene changes may offer the hope of non-invasive ways to diagnose the disease and new tailored treatments for brain cancer patients."

Dr Lesley Walker, Cancer Research UK's director of cancer information, said: "Although meningioma is a rare condition, we welcome any insight that helps us to understand it further. This study has shown some very interesting results. However, further studies are needed to explain how additional changes in the BRIP1 gene may also contribute to the growth of these tumours."