Their research, published in the British Journal of Cancer, underlines the growing interest in the medical use of active chemicals called cannabinoids, which are found in marijuana.
Experts, however, stressed that the research was still exploratory and many more years of testing would be needed to work out how to apply the findings to the treatment of cancer in humans.
“This is interesting research which opens a new avenue to explore potential drug targets but it is at a very early stage,” said Lesley Walker, director of cancer information at Cancer Research UK, which owns the journal.
“It absolutely isn’t the case that men might be able to fight prostate cancer by smoking cannabis,” she added
The cannabinoids tested by the Spanish team are thought to work against prostate cancer because they block a receptor, or molecular doorway, on the surface of tumour cells. This stops them from dividing.
In effect, the cancer cell receptors can recognize and “talk to” chemicals found in cannabis, said Diaz-Laviada.
“These chemicals can stop the division and growth of prostate cancer cells and could become a target for new research into potential drugs to treat prostate cancer,” she said.
Her team’s work with two cannabinoids — called methanandamide and JWH-015 — is the first demonstration that such cannabis chemicals prevent cancer cells from multiplying.
Some drug companies are already exploring the possibilities of cannabinoids in cancer, including British-based cannabis medicine specialist GW Pharmaceuticals.
It is collaborating with Japan’s Otsuka on early-stage research into using cannabis extracts to tackle prostate cancer — the most commonly diagnosed cancer in men — as well as breast and brain cancer.
GW has already developed an under-the-tongue spray called Sativex for the relief of some of the symptoms of multiple sclerosis, which it plans to market in Europe with Bayer and Almirall.
Other attempts to exploit the cannibinoid system have met with mixed success. Sanofi-Aventis was forced to withdraw its weight-loss drug Acomplia from the market last year because of links to mental disorders.
By Ben Hirschler (Reuters)
What Is Parkinson’s Disease
Parkinson’s disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. The four primary symptoms of PD are tremor, or trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks.
Parkinson’s Disease Foundation
The Parkinson’s Disease Foundation (PDF) is a leading national presence in Parkinson’s disease research, education and public advocacy. We are working for the nearly one million people in the US living with Parkinson’s by funding promising scientific research and supporting people with Parkinson’s, their families and caregivers through educational programs and support services.
Causes of Parkinson’s Disease
Heredity. Having one or more close relatives with Parkinson’s increases the chances that you’ll also develop the disease, although your risk is still less than 5 percent. Exposure to toxins. Ongoing exposure to herbicides and pesticides puts you at slightly increased risk of Parkinson’s.
The body’s ability to produce smooth, controlled, muscular activity is a product of many complex, interrelated functions. Few, however, are as critical as the functioning of the nerve cells, or neurons, in the part of the brain called the substantia nigra.
Treatments of Parkinson’s Disease
Medical Treatment
There is no cure for Parkinson’s disease. Treatment centers on the administration of medication to relieve symptoms. The Food and Drug Administration (FDA) also has approved a surgically implanted device that lessens tremors.
Medication
Medication selection and dosage is tailored to the individual. The physician considers factors such as severity of symptoms, age, and presence of other medical conditions.
Dopamine agonists. Unlike levodopa, these drugs aren’t changed into dopamine. Instead, they mimic the effects of dopamine in the brain and cause neurons to react as though dopamine is present.
Source: healthanddiseases.org
The drug, Velcade (bortezomib), which is a proteasome inhibitor, worked against the disease and prolonged survival in mice with lupus. The finding could one day offer treatment options for other antibody-associated diseases, too, the researchers said.
“Autoantibody-mediated diseases such as autoimmune hemolytic anemia, immune thrombocytopenia, myasthenia gravis and systemic lupus erythematosus are often difficult to treat,” said lead researcher Dr. Reinhard Voll, of the University of Erlangen-Nuremberg.
A big problem is that plasma cells, which are the predominant producers of the disease-causing autoantibodies, can’t be efficiently attacked with current treatments, Voll said.
Lupus is a so-called autoimmune disease in which the immune system attacks healthy cells and tissues by mistake, leading to damage to joints, skin, blood vessels and organs. There are many kinds of lupus, with the most common type being systemic lupus erythematosus, which affects many parts of the body. There’s no one test to diagnose lupus, and it may take months or years to make the diagnosis. There’s also no cure, but medicines and lifestyle changes can help control the disease, according to the U.S. National Institutes of Health
For the new study, Voll’s team found that bortezomib efficiently eliminated the plasma cells in the mice, leading to a drastic decrease in autoantibodies and prolonged survival. And, the drug had no effect on other cells, he said.
“Proteasome inhibitors may be beneficial in refractory human diseases caused predominantly by autoantibodies,” Voll said. “Proteasome inhibitors can selectively deplete plasma cells, which are resistant to current treatments.”
Outside experts were divided on the findings, published in the June 8 online edition of Nature Medicine. “This is a very exciting study that explores a novel mechanism for treating lupus erythematosus,” said Dr. Jennifer Grossman, an assistant professor of medicine at the University of California, Los Angeles. “The fact that antibodies almost completely disappeared is encouraging. I look forward to hearing more about this treatment in the future,” she said.
But, another expert expressed concern that the treatment could adversely affect other cells in the human body.
“I think they’re onto something important, it looks as if it has a remarkable therapeutic effect,” said Dr. Noel Rose, director of the Autoimmune Disease Research Center at Johns Hopkins University. “The downside is that this is a proteasome inhibitor, and there is no reason to think that it would be specific for plasma cells. It does affect other rapidly proliferating cells.”
Rose noted that many drugs may appear safe during an initial trial. “I’m still really suspicious that if this is used clinically, there are going to be side effects like effects on intestinal or other rapidly dividing cells,” he said. “The question is, are the side effects going to be severe enough to prevent the use of this drug?”
More information
To learn more about lupus, the U.S. National Library of Medicine.
LONDON — Doctors have long suspected that people with herpes are more likely to catch HIV. So they thought that by treating herpes, they could also cut a person’s HIV risk. But a new study that tested this strategy found the assumption may have been wrong.
“It’s a significant, disappointing finding,” Francis Ndowa, coordinator of the sexually transmitted infections control team at the World Health Organization, said in an interview.
Ndowa was not connected to the research, published Friday in the medical journal The Lancet.
The finding may spark a rethinking of HIV prevention strategies in Africa, where controlling sexually transmitted diseases such as herpes is usually part of general AIDS prevention plans.
Researchers tracked more than 3,000 men and women infected with herpes in Africa, Peru and the United States. Roughly half were treated with aciclovir, an antiviral that stops herpes ulcers.
After a year and a half, the scientists found that 75 people out of the 1,581 who had been receiving aciclovir were later infected with HIV. Of the 1,591 people who received placebo pills, 64 contracted HIV.
In the trial, researchers chose participants who had herpes and who faced similar risks of getting AIDS. The study also questioned the participants during monthly visits about risky sexual behavior with their recent partners.
The study was paid for by the United States’ National Institute of Allergy and Infectious Diseases, other U.S. government institutes, and by GlaxoSmithKline PLC, which sells aciclovir as Zovirax.
A small study in Tanzania last year also suggested that treating herpes didn’t help reducing HIV susceptibility.
But that doesn’t necessarily mean that the theory of treating herpes to avoid HIV is incorrect, experts said.
“It’s probably likely that we need considerably more potent interventions than we have,” Connie Celum, a professor of global health and medicine at the University of Washington who led the Lancet study, told The Associated Press.
Experts said there was a complex relationship between the two viruses that is still not entirely understood.
When herpes ulcers erupt, that draws white blood cells to the skin to fight the virus. Unfortunately, those white blood cells also have receptors for HIV.
Ndowa said it was possible that even without the telltale ulcers, herpes might have lingered while patients were taking the aciclovir, allowing HIV to gain a foothold.
In an accompanying commentary in the Lancet, Ronald H. Gray and Maria J. Wawer of Johns Hopkins University said it was questionable whether controlling sexually transmitted infectious could work to prevent HIV.
“It is time to reassess the hypothesis and to adjust prevention policy accordingly,” they wrote.
But Ndowa and Celum said the strategy of fighting herpes to prevent AIDS might work, if a different dosage or more powerful drug was tried.
“We don’t exactly know why this didn’t work, but this approach still has potential,” Ndowa said. “Maybe it was just too much to expect from a tablet taken twice a day that it could be effective against HIV.”
The Associated Press