(Healthday News) -- A U.S. Food and Drug Administration advisory panel voted Thursday to support approval of Provenge, a vaccine aimed at extending survival for patients with deadly metastatic prostate cancer.
The FDA panel voted unanimously that the vaccine was "reasonably safe," noting that while it failed to meet some study endpoints, it did extend patient survival, according to published reports.
The panel then voted 13-to-4 to say there was substantial evidence to show the vaccine was effective for treating advanced prostate cancer that no longer responds to standard hormone treatment.
The FDA does not have to follow the advice of its advisory panels, but it typically does. The agency is expected to make its final decision by May 15.
Hopes have been high for the vaccine, which researchers said was the first ever shown to have an impact on cancer patients' survival. Those claims were based on a three-year study, released early in 2005, of 127 men with advanced, metastatic prostate cancer.
The trial found that patients infused with Provenge experienced an average 18 percent increase in survival, compared to those on a placebo. That worked out to 4.5 months of extra survival -- 25.9 months for those receiving Provenge vs. 22 months for those not taking the vaccine.
Provenge was developed by Seattle-based Dendreon.
"The concept behind the vaccine is to try to stimulate the patient's own immune system to recognize the prostate cancer cells and keeps them in check," said Dr. Simon Hall, a prostate cancer specialist at Mount Sinai Medical Center in New York City who worked on the trials for the vaccine.
In one phase III trial, men who had metastatic prostate cancer were three to four times more likely to be alive three years after vaccination, Hall said.
"However, the intent of that trial was not to show survival," Hall said. "The intent was to see if you could get patients to delay pain or new lesions in their bones. But they found it had no effect on that."
Before the panel met Thursday, FDA officials had expressed some reservations about the data submitted by Dendreon.
"The submitted data tend to support a finding of clinically meaningful increased survival, but doubts remain about the persuasiveness of the efficacy data," agency officials stated in documents released ahead of the meeting.
The advisory panel also noted that neither of the two studies submitted by Dendreon convincingly showed that Provenge met the primary goal of delaying progression of prostate cancer.
As reported by UPI, an increase in the frequency of "cerebrovascular accidents," such as stroke in men treated with Provenge, also "constitutes a potential safety concern," the FDA said. Stroke risk was 3.9 percent in treated patients compared to 2.6 percent in patients receiving a placebo.
Besides promising a potential benefit to men with prostate cancer, the therapy gives "proof of principle" to the idea that immune-based treatments can have a real impact on prostate cancer and other malignancies, experts said.
"There have been many failures with this kind of approach, and many have wondered if we shouldn't set the bar lower, somehow lower our expectations, and not hope for extended survival," Dr. Bruce Roth, a prostate cancer researcher at Vanderbilt University, told HealthDay when the 2005 study was released.
"But these findings are saying, 'No, looking for a survival advantage is a valid endpoint to look at for these agents,'" he said.
If caught early, prostate cancer remains very curable. However, despite advances in early detection, the disease remains the second leading cancer killer of U.S. men, according to the American Cancer Society. Even among men who develop the disease while it is still confined to the prostate, between 30 percent to 40 percent will experience a recurrence in years to come.
Because prostate cells depend heavily on testosterone to grow, therapies that reduce levels of circulating testosterone are often the first course of action in men who experience a recurrence. However, prostate cancer cells gradually grow resistant to hormonal therapy, and until very recently, doctors could only offer patients palliative therapies once that relapse occurred.
Hall said there was a new trial underway that was starting to confirm the survival results from the first study.
One advantage of the vaccine is that it has fewer side effects than chemotherapy, Hall added.
"The vaccine doesn't cure the disease, but it controls the disease for a period of time," he said. "And it is much less toxic than chemotherapy."
More information
For more on prostate cancer, head to the American Cancer Society.
Jumat, 30 Maret 2007
Protein May Be Key to Rheumatoid Arthritis
(HealthDay News) -- In the quest for the causes of and potential treatments for rheumatoid arthritis, Japanese researchers have identified a protein that could be a target for future therapy.
Rheumatoid arthritis (RA) is a chronic and disabling autoimmune disease that first attacks the fluid that surrounds the joints, causing it to thicken and grow abnormally, damaging the joints and surrounding cartilage rather than protecting them. More than 2 million Americans suffer from the illness, according to the Arthritis Foundation.
By identifying a protein that appears to be one of the culprits in the unhealthy buildup of this fluid, which is called synovial fluid, Dr. Yasushi Miura and his colleagues at Kobe University School of Medicine hope that a new, targeted medication can be developed to treat the disease.
"The protein Decoy receptor 3 (DcR3) is one of the pathological factors of RA and can be a new therapeutic target for treatment," said Miura, an associate professor in the division of orthopedic sciences at the medical school.
His findings are published in the April issue of Arthritis & Rheumatism, the journal of the American College of Rheumatology.
DcR3 is a member of the large tumor necrosis factor receptor (TNFR) "super family," which has been identified in the last decade as important in the regulation of cell growth and cell death, fundamental processes in biology, said Dr. Robert Hoffman, director of the division of rheumatology and immunology at the University of Miami Miller School of Medicine in Florida.
"We have known of the importance of cell growth and cell death in studying cancer but more recently have found that it is also important in autoimmune diseases like RA and lupus," he said.
It was the similarity between the growth of malignant tumors and the abnormal growth of synovial tissue, called hyperplasia, that sparked Miura's research into DcR3 and rheumatoid arthritis. DcR3 is known to be produced in tumor cells, including lung and colon cancers.
What Miura and his colleagues found was that DcR3 works with another member of the TNFR family to slow the normal cell death of synovial fluid cells, resulting in the hyperplasia that causes some of the inflammation characteristic of rheumatoid arthritis.
Hoffman said: "This is a novel application of the connection between this specific member of the TNFR super family and RA, and studies like this are how we advance science. But it is currently a giant leap to suggest that this could be a therapy for RA."
For their study, Miura and his colleagues isolated and cultured cells from synovial fluid from19 patients with rheumatoid arthritis, obtained during total knee replacement surgery. For comparison, they also extracted synovial fluid cells in the same manner from 14 patients with osteoarthritis.
The researchers then exposed the synovial fluid cells to another TNFR protein called Fas, which induces cell death, called apoptosis. Finally, the cells were incubated with a pro-inflammatory member of the TNFR family, called TNFa. The TNFR family includes proteins that both induce and retard cell death, Miura explained.
While DcR3 was present in the same amounts in the synovial fluid cells of both the rheumatoid arthritis and osteoarthritis patients, when the TNFa was introduced, DcR3 production increased in the cells of the RA patients, slowing down the Fas-induced cell death. The rate of cell death did not change in the fluid of the osteoarthritis patients, perhaps, Miura suggested, because the TNFa levels were higher in the fluid of RA patients to begin with.
Miura said the results show that DcR3 acts in conjunction with TNFa to suppress the cell death necessary to keep synovial fluid healthy, and research aimed at reducing the amount of DcR3 in the synovial fluid in rheumatoid arthritis patients could be productive.
Dr. Stephen Lindsey, head of rheumatology at the Ochsner Clinic Foundation in Baton Rouge, La., said, "We are always looking for better and more specific targets to control immune response, and this study is very intriguing."
Lindsey said there are drugs available that inhibit those proteins that suppress cell death, but because they are "global," rather than targeted to particular proteins, there are many side effects, including infection.
More information
The Arthritis Foundation offers more information on rheumatoid arthritis.
Rheumatoid arthritis (RA) is a chronic and disabling autoimmune disease that first attacks the fluid that surrounds the joints, causing it to thicken and grow abnormally, damaging the joints and surrounding cartilage rather than protecting them. More than 2 million Americans suffer from the illness, according to the Arthritis Foundation.
By identifying a protein that appears to be one of the culprits in the unhealthy buildup of this fluid, which is called synovial fluid, Dr. Yasushi Miura and his colleagues at Kobe University School of Medicine hope that a new, targeted medication can be developed to treat the disease.
"The protein Decoy receptor 3 (DcR3) is one of the pathological factors of RA and can be a new therapeutic target for treatment," said Miura, an associate professor in the division of orthopedic sciences at the medical school.
His findings are published in the April issue of Arthritis & Rheumatism, the journal of the American College of Rheumatology.
DcR3 is a member of the large tumor necrosis factor receptor (TNFR) "super family," which has been identified in the last decade as important in the regulation of cell growth and cell death, fundamental processes in biology, said Dr. Robert Hoffman, director of the division of rheumatology and immunology at the University of Miami Miller School of Medicine in Florida.
"We have known of the importance of cell growth and cell death in studying cancer but more recently have found that it is also important in autoimmune diseases like RA and lupus," he said.
It was the similarity between the growth of malignant tumors and the abnormal growth of synovial tissue, called hyperplasia, that sparked Miura's research into DcR3 and rheumatoid arthritis. DcR3 is known to be produced in tumor cells, including lung and colon cancers.
What Miura and his colleagues found was that DcR3 works with another member of the TNFR family to slow the normal cell death of synovial fluid cells, resulting in the hyperplasia that causes some of the inflammation characteristic of rheumatoid arthritis.
Hoffman said: "This is a novel application of the connection between this specific member of the TNFR super family and RA, and studies like this are how we advance science. But it is currently a giant leap to suggest that this could be a therapy for RA."
For their study, Miura and his colleagues isolated and cultured cells from synovial fluid from19 patients with rheumatoid arthritis, obtained during total knee replacement surgery. For comparison, they also extracted synovial fluid cells in the same manner from 14 patients with osteoarthritis.
The researchers then exposed the synovial fluid cells to another TNFR protein called Fas, which induces cell death, called apoptosis. Finally, the cells were incubated with a pro-inflammatory member of the TNFR family, called TNFa. The TNFR family includes proteins that both induce and retard cell death, Miura explained.
While DcR3 was present in the same amounts in the synovial fluid cells of both the rheumatoid arthritis and osteoarthritis patients, when the TNFa was introduced, DcR3 production increased in the cells of the RA patients, slowing down the Fas-induced cell death. The rate of cell death did not change in the fluid of the osteoarthritis patients, perhaps, Miura suggested, because the TNFa levels were higher in the fluid of RA patients to begin with.
Miura said the results show that DcR3 acts in conjunction with TNFa to suppress the cell death necessary to keep synovial fluid healthy, and research aimed at reducing the amount of DcR3 in the synovial fluid in rheumatoid arthritis patients could be productive.
Dr. Stephen Lindsey, head of rheumatology at the Ochsner Clinic Foundation in Baton Rouge, La., said, "We are always looking for better and more specific targets to control immune response, and this study is very intriguing."
Lindsey said there are drugs available that inhibit those proteins that suppress cell death, but because they are "global," rather than targeted to particular proteins, there are many side effects, including infection.
More information
The Arthritis Foundation offers more information on rheumatoid arthritis.
Health Tip: Symptoms of Dyslexia
(HealthDay News) -- Dyslexia is a learning disability that affects the way a child reads and writes.
The Nemours Foundation says an inability to perform the following functions are common warning signs of dyslexia among preschool and elementary school children:
Learning to read and speak.
Rhyming.
Understanding and identifying things like colors, shapes, numbers, letters and days of the week.
Reading and writing one's own name.
Correlating letters and sounds.
Mixing up letter sequences and reading incorrectly, such as reading "top" as "pot."
Poor handwriting and difficulty with other fine-motor skills.
The Nemours Foundation says an inability to perform the following functions are common warning signs of dyslexia among preschool and elementary school children:
Learning to read and speak.
Rhyming.
Understanding and identifying things like colors, shapes, numbers, letters and days of the week.
Reading and writing one's own name.
Correlating letters and sounds.
Mixing up letter sequences and reading incorrectly, such as reading "top" as "pot."
Poor handwriting and difficulty with other fine-motor skills.
Health Tip: Toilet Training Your Child
(HealthDay News) -- Toilet training should begin only when the child is able to recognize and communicate when a diaper is soiled.
According to the American Academy of Family Physicians, this most often occurs between 18 and 24 months of age. But some children may remain in diapers as late as 2 1/2 to 3 years old, the academy says.
Before training begins, introduce your child to her potty chair by keeping it in her play area, the physician's group advises. Let her sit in the chair any time she wants to -- fully clothed -- but never force her to sit in it.
Finally, encourage her to sit on her potty chair without a diaper on. Show her how you place waste from her diaper into the potty chair, then transfer to the toilet. Allow her to flush the toilet and watch the waste disappear.
According to the American Academy of Family Physicians, this most often occurs between 18 and 24 months of age. But some children may remain in diapers as late as 2 1/2 to 3 years old, the academy says.
Before training begins, introduce your child to her potty chair by keeping it in her play area, the physician's group advises. Let her sit in the chair any time she wants to -- fully clothed -- but never force her to sit in it.
Finally, encourage her to sit on her potty chair without a diaper on. Show her how you place waste from her diaper into the potty chair, then transfer to the toilet. Allow her to flush the toilet and watch the waste disappear.
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