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.
The research, published in the Journal of the National Cancer Institute, says radio frequency electromagnetic fields emitted from mobile phones have been proposed as a risk factor for brain tumours, but a biological mechanism that could explain the potential effects has not been identified.
Cancer incidence
The study was based on 59,684 brain tumour cases diagnosed over 30 years from 1974 to 2003 among 16 million adults.
During this time, the incidence rate of cancers known as gliomas increased gradually by 0.5% per year among men and by 0.2% per year among women.
For cancers known as meningioma, the incidence rate increased by 0.8% among men and, after the early 1990's, by 3.8% among women.This more rapid change for women was driven, the researchers say, by the 60-79 year age group.
Isabelle Deltour, of the Danish Cancer Society in Copenhagen who led the study said the lack of a detectable increase in tumour rates up to 2003 may suggest that the time it takes for cancer to develop from mobile phone use is longer than 10 years of exposure or that the number of tumours it promotes is too small to be detected.
She said: "Our results extend those of previous studies of time trends up to 1998 by adding five years of follow-up.
"Because of the high prevalence of mobile phone exposure in this population and worldwide, longer follow-up of time trends in brain tumour incidence is warranted."
Christopher Jennings was very excited when he spotted this recent press release from the US :[ Latest News Articles ]
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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