(HealthDay News) -- Nurses, printers and woodworkers are more likely than the average population to develop work-related asthma, according to a European research team that is calling for more monitoring of workers' exposure to chemicals that could cause the illness.
Workplace conditions may be responsible for one out of four new asthma cases in industrialized countries, the team found. They analyzed health information and workplace exposure details from more than 6,800 people who participated in the European Community Respiratory Health Survey between 1990 and 1995.
None of the participants had asthma at the beginning of the nine-year study. Exposure to possible asthma-causing substances was calculated using an "asthma-specific job exposure matrix" with additional insight from asthma experts.
Writing in the July 27 issue of The Lancet, the researchers reported that exposure to substances known to cause occupational asthma increased the risk of asthma by an average of 60 percent. The occupations with the greatest excess risk were printing (137 percent), nursing (122 percent), woodworking (122 percent), agriculture/forestry (85 percent), and cleaning (71 percent).
The risk of asthma tripled after certain incidents, such as fires, mixed cleaning products or chemical spills, leading the researchers to highlight the importance of following up with workers after similar events.
The increased risk for nurses was of particular interest to the researchers, who theorized that the high rate of asthma in that profession could be attributed to sensitizing substances, respiratory allergens, and irritants including sterilizers and disinfectants such as glutaraldehyde or bleach, as well as latex in the early 1990s.
More information
To learn more about asthma, visit the Asthma and Allergy Foundation of America.
Friday, July 27, 2007
Saturday, July 21, 2007
Research Points to Single Origin of Humans
(HealthDay News) -- All humans originated from a single point in Africa and migrated across the world, say British researchers at the University of Cambridge.
Previously, there were two theories on the origin of humans. One theory said that all humans originated in Africa. The second theory said that different populations of humans evolved from different areas of the world.
But in a new study published in the July 19 issue of Nature, researchers say they have proven the single origin of humans theory by combining studies of global genetic variations in humans with skull measurements across the world.
The researchers studied genetic diversity of human populations around the world and measured more than 6,000 skulls from across the globe, kept in academic collections.
They found that losses in genetic diversity the farther a population is from Africa are mirrored by losses in variation in physical attributes.
Variation in the physical attributes of the skulls was highest among the sample from southeastern Africa, and it decreased at the same rate as the genetic data the farther the skull was away from Africa.
"The origin of anatomically modern humans has been the focus of much heated debate. Our genetic research shows the further modern humans have migrated from Africa, the more genetic diversity has been lost within a population," lead researcher Andrea Manica, from the university's department of zoology, said in a prepared statement.
"However, some have used skull data to argue that modern humans originated in multiple spots around the world. We have combined our genetic data with new measurements of a large sample of skulls to show definitively that modern humans originated from a single area in sub-Saharan Africa," Manica said.
The decrease in genetic diversity in populations farther from Africa was likely a result of "bottlenecks" -- events that temporarily reduced populations during human migration.
The researchers attempted to use their data to find non-African origins for modern humans, testing the theory of multiple origins.
"To test the alternative theory for the origin of modern humans, we tried to find an additional, non-African origin. We found this just did not work. Our findings show that humans originated in a single area in Sub-Saharan Africa," co-researcher Francois Balloux said in a prepared statement.
More information
The U.S. National Human Genome Research Institute has more about genetic variation.
Previously, there were two theories on the origin of humans. One theory said that all humans originated in Africa. The second theory said that different populations of humans evolved from different areas of the world.
But in a new study published in the July 19 issue of Nature, researchers say they have proven the single origin of humans theory by combining studies of global genetic variations in humans with skull measurements across the world.
The researchers studied genetic diversity of human populations around the world and measured more than 6,000 skulls from across the globe, kept in academic collections.
They found that losses in genetic diversity the farther a population is from Africa are mirrored by losses in variation in physical attributes.
Variation in the physical attributes of the skulls was highest among the sample from southeastern Africa, and it decreased at the same rate as the genetic data the farther the skull was away from Africa.
"The origin of anatomically modern humans has been the focus of much heated debate. Our genetic research shows the further modern humans have migrated from Africa, the more genetic diversity has been lost within a population," lead researcher Andrea Manica, from the university's department of zoology, said in a prepared statement.
"However, some have used skull data to argue that modern humans originated in multiple spots around the world. We have combined our genetic data with new measurements of a large sample of skulls to show definitively that modern humans originated from a single area in sub-Saharan Africa," Manica said.
The decrease in genetic diversity in populations farther from Africa was likely a result of "bottlenecks" -- events that temporarily reduced populations during human migration.
The researchers attempted to use their data to find non-African origins for modern humans, testing the theory of multiple origins.
"To test the alternative theory for the origin of modern humans, we tried to find an additional, non-African origin. We found this just did not work. Our findings show that humans originated in a single area in Sub-Saharan Africa," co-researcher Francois Balloux said in a prepared statement.
More information
The U.S. National Human Genome Research Institute has more about genetic variation.
Thursday, July 19, 2007
Scientists Spot Genes Behind Heart Disease
(HealthDay News) -- A number of common genes can boost carriers' risk of heart trouble, an international team of researchers report.
"We found that there are several common gene variants, occurring at frequencies of 20 to 50 percent in the population, each of which increases your risk of having coronary artery disease or heart attack by between 20 and 40 percent," said lead researcher Dr. Nilesh Samani, a professor of genetics at the Institute of Genetics at University of Leicester, in the United Kingdom.
It has been known for a long time that a family history of heart disease is one of the most potent risk factors for someone developing the disease themselves, Samani noted.
Now, he said, "we have identified some of the individual components of this genetic risk. All the genes we have identified have not previously been recognized as being involved in causing heart attacks."
Specifically, the researchers found several new genetic variations that increase the risk of developing heart disease by as much as 40 percent. "Particularly, variants in our DNA on chromosomes 2, 6, 9, 10 and 15, and two on chromosome 1, were associated with increased risk of developing coronary artery disease and heart attacks," said co-researcher Dr. Heribert Schunkert, from the University of Lubeck, Germany.
The study is one of the largest efforts to screen the entire genome, since it combines two independent samples from many thousands of patients (and even more healthy controls) in order to identify minute differences spurring heart disease, Schunkert said.
Still, studies in an even wider set of people are needed before these findings can be applied in a clinical setting, Samani said. However, gene tests might ultimately play a role in predicting the risk of heart disease.
"This, in turn, could allow us to target preventative measures more specifically to those at highest risk," Samani said. "Working out how they affect risk may open up fresh biochemical targets to develop effective drugs against," he said.
The report is published in the July 18 online edition of the New England Journal of Medicine.
One expert believes much more needs to be done to understand which gene does what when it comes to heart disease.
"These genes are just markers for heart disease -- we have no idea what they do functionally," noted Peter Kraft, an assistant professor of epidemiology at the Harvard School of Public Health and co-author of an accompanying journal perspective article.
This is just a first step in understanding how genes affect heart disease, Kraft said. In addition, there are probably other, as yet unidentified, genes that also play a role in heart disease, he said.
Kraft cautioned that the findings should not be taken to mean that genes are destiny and that heart trouble is inevitable for certain people. "That's not the message to take home," he said. "The increase in risk is small on an individual level," he said.
Moreover, the risk for heart disease is more responsive to other factors, such as smoking and obesity, Kraft said.
These findings will lead to a better understanding of the biological causes of heart disease, Kraft said. "These studies offer the opportunity for startling new discoveries," he added.
Another expert agreed that the findings are a long way from being used by doctors to screen for heart disease or even in the development of heart drugs.
The study is part of ongoing research to identify genes associated with common diseases, and it will be five to 10 years before these discoveries will have any practical impact on treating heart disease, said Anne M. Bowcock, a professor of genetics at Washington University School of Medicine in St. Louis.
"These are relatively low-risk effects," she said. "How much of the disease they contribute to is not clear right now."
More information
For more on genes and disease, visit the U.S. National Center for Biotechnology Information.
"We found that there are several common gene variants, occurring at frequencies of 20 to 50 percent in the population, each of which increases your risk of having coronary artery disease or heart attack by between 20 and 40 percent," said lead researcher Dr. Nilesh Samani, a professor of genetics at the Institute of Genetics at University of Leicester, in the United Kingdom.
It has been known for a long time that a family history of heart disease is one of the most potent risk factors for someone developing the disease themselves, Samani noted.
Now, he said, "we have identified some of the individual components of this genetic risk. All the genes we have identified have not previously been recognized as being involved in causing heart attacks."
Specifically, the researchers found several new genetic variations that increase the risk of developing heart disease by as much as 40 percent. "Particularly, variants in our DNA on chromosomes 2, 6, 9, 10 and 15, and two on chromosome 1, were associated with increased risk of developing coronary artery disease and heart attacks," said co-researcher Dr. Heribert Schunkert, from the University of Lubeck, Germany.
The study is one of the largest efforts to screen the entire genome, since it combines two independent samples from many thousands of patients (and even more healthy controls) in order to identify minute differences spurring heart disease, Schunkert said.
Still, studies in an even wider set of people are needed before these findings can be applied in a clinical setting, Samani said. However, gene tests might ultimately play a role in predicting the risk of heart disease.
"This, in turn, could allow us to target preventative measures more specifically to those at highest risk," Samani said. "Working out how they affect risk may open up fresh biochemical targets to develop effective drugs against," he said.
The report is published in the July 18 online edition of the New England Journal of Medicine.
One expert believes much more needs to be done to understand which gene does what when it comes to heart disease.
"These genes are just markers for heart disease -- we have no idea what they do functionally," noted Peter Kraft, an assistant professor of epidemiology at the Harvard School of Public Health and co-author of an accompanying journal perspective article.
This is just a first step in understanding how genes affect heart disease, Kraft said. In addition, there are probably other, as yet unidentified, genes that also play a role in heart disease, he said.
Kraft cautioned that the findings should not be taken to mean that genes are destiny and that heart trouble is inevitable for certain people. "That's not the message to take home," he said. "The increase in risk is small on an individual level," he said.
Moreover, the risk for heart disease is more responsive to other factors, such as smoking and obesity, Kraft said.
These findings will lead to a better understanding of the biological causes of heart disease, Kraft said. "These studies offer the opportunity for startling new discoveries," he added.
Another expert agreed that the findings are a long way from being used by doctors to screen for heart disease or even in the development of heart drugs.
The study is part of ongoing research to identify genes associated with common diseases, and it will be five to 10 years before these discoveries will have any practical impact on treating heart disease, said Anne M. Bowcock, a professor of genetics at Washington University School of Medicine in St. Louis.
"These are relatively low-risk effects," she said. "How much of the disease they contribute to is not clear right now."
More information
For more on genes and disease, visit the U.S. National Center for Biotechnology Information.
Tuesday, July 17, 2007
New Test Helps Detect Spreading Breast Cancer
(HealthDay News) -- The first molecular laboratory test to help doctors detect whether breast cancer has spread to nearby lymph nodes has been approved by the U.S. Food and Drug Administration, the agency said Monday.
The GeneSearch BLN Assay detects molecules that are abundant in breast tissue but are normally rare in lymph nodes. The body's lymphatic system helps protect against infection.
The first lymph node that filters fluid from the breast is called the "sentinel node," which is commonly removed during a lumpectomy or mastectomy because it's where breast cancer cells are most likely to spread first, the agency said. The GeneSearch test offers an additional way to evaluate the sentinel node.
In clinical testing involving 416 women, the test accurately predicted that breast cancer had spread 88 percent of the time. Among women in whom cancer hadn't spread, the test was 94 percent accurate, the FDA said.
The test is manufactured by a New Jersey-based Johnson & Johnson subsidiary, Veridex, LLC.
More information
To learn more about metastatic breast cancer, visit the U.S. National Cancer Institute.
The GeneSearch BLN Assay detects molecules that are abundant in breast tissue but are normally rare in lymph nodes. The body's lymphatic system helps protect against infection.
The first lymph node that filters fluid from the breast is called the "sentinel node," which is commonly removed during a lumpectomy or mastectomy because it's where breast cancer cells are most likely to spread first, the agency said. The GeneSearch test offers an additional way to evaluate the sentinel node.
In clinical testing involving 416 women, the test accurately predicted that breast cancer had spread 88 percent of the time. Among women in whom cancer hadn't spread, the test was 94 percent accurate, the FDA said.
The test is manufactured by a New Jersey-based Johnson & Johnson subsidiary, Veridex, LLC.
More information
To learn more about metastatic breast cancer, visit the U.S. National Cancer Institute.
Friday, July 13, 2007
Brain May Be Able to Suppress Memories
(HealthDay News) -- Unwanted memories might be willfully banished from human consciousness, according to a new study that also outlines just how the brain might accomplish this feat.
The research, published in the July 13 issue of Science, may help end the debate as to how much control people have over their memories, scientists say.
It might also lead to treatments for individuals battling psychological ills tied to past traumatic events -- illnesses such as Post-traumatic stress disorder (PTSD), chronic anxiety, depression, phobias and Obsessive-compulsive disorder.
"These are people who have problems in clearing their consciousness -- at that moment in time -- of these reoccurring traumatic events," explained lead researcher Brendan Depue, a graduate student in the department of psychology at the University of Colorado, Boulder.
Depue stressed that the idea of suppressed memory does not include the controversial notion of "repressed memory," where the mind suddenly recalls a past trauma after a period of years or even decades.
Instead, his team looked at the ability of humans to consciously erase a memory they've only just made.
To do so, they presented healthy adults with 40 pairs of pictures. One picture in each pair depicted a person's face and was the "cue" photo. It was matched with a "target" image -- usually a picture of a disturbing, emotion-laden scene, such as a wounded soldier, an empty electric chair, or a grisly car crash.
Participants were shown these cue-target picture pairs until they appeared to know them all by heart.
In the second phase of the experiment, participants were hooked up to a functional MRI (fMRI) brain scanner and then presented with only the "cue" photos of people's faces. They were instructed that if the photo was contained within a green border, this meant that they should try and think of the matched target picture. However, if it was presented inside a red border, that meant they should try not to think of the matched picture.
Participants performed this "think/don't think" exercise 12 times for each picture.
Finally, at the end of the experiment, they were tested on whether they could still remember all the matched pairs -- something they had been able to do with ease before.
The result: Participants had much more trouble remembering paired photos they had tried not to think of in the second phase of the experiment. They had no trouble recalling the other photo match-ups, however.
"So, when individuals invoke this suppressive control, the items are recalled less frequently," Depue concluded. "It looks like individuals have gained some control over the [memories], and they actually are suppressed," he said.
How might the brain do this? According to fMRI brain images recorded during the think/don't think task, "what seems to occur is that the prefrontal cortex -- what neuroscientists consider the center of cognitive control -- becomes more active in the case of suppression," Depue said.
At the same time, "you see deactivation in areas of the visual cortex, which is normally active when someone is remembering a picture," he said.
Two other brain areas central to memory and emotion -- the hippocampus and the amygdala -- were also quieted down during the "don't think" test. "Those two areas are interconnected greatly and have to do with memorizing and retrieving emotional memories," Depue explained.
He said decisions made in the prefrontal cortex appear to be "modulating" the more primitive areas of the brain, regions that would normally leap to retrieve a memory.
"I liken it to meditation," Depue said. "If you meditate, you continually practice to clear your mind from thoughts. It could be that when you are meditating, you are using part of this specific mechanism to do that."
Another brain expert was intrigued by the findings.
"It looks like they are confirming that humans can actively suppress memory," said Paul Sanberg, director of the Center for Excellence for Aging and Brain Repair at the University of South Florida College of Medicine, in Tampa.
It makes sense that the prefrontal cortex would take the lead in this type of activity, Sanberg said. "In our prefrontal cortex, we've evolved mechanisms to control older parts of the brain," he explained.
According to Depue, if people could harness the power of the mind to suppress traumatic, unwanted memories, it could pave the way to treatments against a range of psychiatric illnesses.
"The next step is to actually try and do this with clinical populations, looking specifically at whether they show some dysfunction in the neural mechanisms that we've outlined in this article," the researcher said. "Then we'd try and pinpoint just what in the brain is going wrong."
More information
Find out about PTSD at the U.S. National Institute of Mental Health.
The research, published in the July 13 issue of Science, may help end the debate as to how much control people have over their memories, scientists say.
It might also lead to treatments for individuals battling psychological ills tied to past traumatic events -- illnesses such as Post-traumatic stress disorder (PTSD), chronic anxiety, depression, phobias and Obsessive-compulsive disorder.
"These are people who have problems in clearing their consciousness -- at that moment in time -- of these reoccurring traumatic events," explained lead researcher Brendan Depue, a graduate student in the department of psychology at the University of Colorado, Boulder.
Depue stressed that the idea of suppressed memory does not include the controversial notion of "repressed memory," where the mind suddenly recalls a past trauma after a period of years or even decades.
Instead, his team looked at the ability of humans to consciously erase a memory they've only just made.
To do so, they presented healthy adults with 40 pairs of pictures. One picture in each pair depicted a person's face and was the "cue" photo. It was matched with a "target" image -- usually a picture of a disturbing, emotion-laden scene, such as a wounded soldier, an empty electric chair, or a grisly car crash.
Participants were shown these cue-target picture pairs until they appeared to know them all by heart.
In the second phase of the experiment, participants were hooked up to a functional MRI (fMRI) brain scanner and then presented with only the "cue" photos of people's faces. They were instructed that if the photo was contained within a green border, this meant that they should try and think of the matched target picture. However, if it was presented inside a red border, that meant they should try not to think of the matched picture.
Participants performed this "think/don't think" exercise 12 times for each picture.
Finally, at the end of the experiment, they were tested on whether they could still remember all the matched pairs -- something they had been able to do with ease before.
The result: Participants had much more trouble remembering paired photos they had tried not to think of in the second phase of the experiment. They had no trouble recalling the other photo match-ups, however.
"So, when individuals invoke this suppressive control, the items are recalled less frequently," Depue concluded. "It looks like individuals have gained some control over the [memories], and they actually are suppressed," he said.
How might the brain do this? According to fMRI brain images recorded during the think/don't think task, "what seems to occur is that the prefrontal cortex -- what neuroscientists consider the center of cognitive control -- becomes more active in the case of suppression," Depue said.
At the same time, "you see deactivation in areas of the visual cortex, which is normally active when someone is remembering a picture," he said.
Two other brain areas central to memory and emotion -- the hippocampus and the amygdala -- were also quieted down during the "don't think" test. "Those two areas are interconnected greatly and have to do with memorizing and retrieving emotional memories," Depue explained.
He said decisions made in the prefrontal cortex appear to be "modulating" the more primitive areas of the brain, regions that would normally leap to retrieve a memory.
"I liken it to meditation," Depue said. "If you meditate, you continually practice to clear your mind from thoughts. It could be that when you are meditating, you are using part of this specific mechanism to do that."
Another brain expert was intrigued by the findings.
"It looks like they are confirming that humans can actively suppress memory," said Paul Sanberg, director of the Center for Excellence for Aging and Brain Repair at the University of South Florida College of Medicine, in Tampa.
It makes sense that the prefrontal cortex would take the lead in this type of activity, Sanberg said. "In our prefrontal cortex, we've evolved mechanisms to control older parts of the brain," he explained.
According to Depue, if people could harness the power of the mind to suppress traumatic, unwanted memories, it could pave the way to treatments against a range of psychiatric illnesses.
"The next step is to actually try and do this with clinical populations, looking specifically at whether they show some dysfunction in the neural mechanisms that we've outlined in this article," the researcher said. "Then we'd try and pinpoint just what in the brain is going wrong."
More information
Find out about PTSD at the U.S. National Institute of Mental Health.
Tuesday, July 10, 2007
Prostate Cancer Gene Also Raises Colon Cancer Risk
(HealthDay News) -- Compelling evidence from four studies confirms that a key change in DNA previously linked to prostate cancer cancer also raises colon cancer risk, scientists report.
They stress that the risk to any individual carrier of the rs6983267 variant gene -- which is located on a region of chromosome 8 called 8q24 -- are relatively slight. Overall, carriers of this variant have about a 20 percent higher risk of developing a colorectal malignancy compared to non-carriers, the researchers said.
The gene's real power comes in its prevalence.
According to scientists, the number of people who carry the variant on region 8q24 includes about half of the populations studied, researchers say.
"In other words, it is very common in the general population," said Dr. Malcolm Dunlop, of Cancer Research UK and the University of Edinburgh, Scotland.
Dunlop, the lead investigator on one of three studies published in the July 8 online edition of Nature Genetics, told reporters at a Friday news conference that "between 4 to 9 percent of all bowel cancers" may be traced to this particular chromosomal locus.
His team honed in on the 8q24 region after comparing the genomes of almost 7,500 colon cancer patients against those of almost 7,800 unaffected controls.
Similar results were found in a U.S. study that was led by Christopher Haiman of the University of Southern California, Los Angeles. His team combed through the DNA of more than 1,800 people from a variety of racial and ethnic backgrounds; comparing key differences in DNA against genes from more than 5,500 healthy controls.
Again, the rs6983267 variant conferred about a 22 percent increase in colorectal cancer risk, Haiman's team reported. Prior studies had already tied this variant to an increased risk for prostate cancer.
"This is the first common genetic risk factor that has been reproducibly associated with risks in multiple cancers," Haiman told reporters. "The association observed with this variant in both prostate and colorectal cancer provides very strong support for the hypothesis that there may be a common biological mechanism underlying cancer risk in this region of the genome."
The California team stressed that the level of risk to an individual conferred by the gene did not change, regardless of the person's sex, race, site of tumor, tumor stage or the presence of colon cancer risk factors such as family history, smoking or drinking.
However, rs6983267 was found more frequently in some ethnicities than in others. "The frequency of this specific genetic variation varies widely in the population -- from about 85 percent of African-Americans to as low as 30 percent of Japanese," Haiman said.
Carrying rs6983267 does not place any individual black American at an extraordinarily higher risk for colon cancer, Haiman explained. However, due to its relative high prevalence among blacks, it probably accounts for about 40 percent of all cases of colorectal cancers among this minority, he said.
Another researcher noted that genes like the one in region 8q24 are often more dangerous when they clump together in the same person.
"Although individually these markers may only contribute small amounts of risk, collectively, in certain individuals, they may actually have composite risks which are comparable to that of known, high-risk [mutations]," explained Dr. Richard Houlston, of the Institute of Cancer Research in Sutton, U.K.
Comparing genomic differences among 930 people with colorectal cancer and 960 controls, his team also zeroed in on rs6983267 as boosting tumor risk. Given the genes' link to prostate cancer, "it does tend to suggest that some of these things may actually have a generic effect on more than one malignancy," Houlston said at the press conference.
A fourth study -- this time led by a consortium from Israel, Spain and the United States -- uncovered a similar connection between genetic variations on 8q24 and a rise in colon cancer risk. That research was published in the July issue of Cancer Biology and Therapy.
While intriguing, experts agreed that the finding does not have immediate implications for the detection, prevention and treatment of colorectal cancer, which kills more than 51,000 Americans each year, according to the American Cancer Society.
"These are encouraging findings, but obviously we need a lot more information about the genetic implications," said Dr. Durado Brooks, the society's director of prostate and colorectal cancer.
Genetic tests that might assess people's risk or help in cancer diagnosis are still years away, and, for now, the new finding "will not in any way significantly alter clinical practice," he said.
Still, the assembled experts agreed that clinical application remains the ultimate goal of their research efforts.
Ideally, Dunlop said, tests might someday be developed to spot genes like rs6983267, "such that you could tailor interventions such as more intensive [patient] surveillance and even prevention," he said. "This is big step forward, but there is more to come."
More information
Find out more about colorectal cancer at the American Cancer Society.
They stress that the risk to any individual carrier of the rs6983267 variant gene -- which is located on a region of chromosome 8 called 8q24 -- are relatively slight. Overall, carriers of this variant have about a 20 percent higher risk of developing a colorectal malignancy compared to non-carriers, the researchers said.
The gene's real power comes in its prevalence.
According to scientists, the number of people who carry the variant on region 8q24 includes about half of the populations studied, researchers say.
"In other words, it is very common in the general population," said Dr. Malcolm Dunlop, of Cancer Research UK and the University of Edinburgh, Scotland.
Dunlop, the lead investigator on one of three studies published in the July 8 online edition of Nature Genetics, told reporters at a Friday news conference that "between 4 to 9 percent of all bowel cancers" may be traced to this particular chromosomal locus.
His team honed in on the 8q24 region after comparing the genomes of almost 7,500 colon cancer patients against those of almost 7,800 unaffected controls.
Similar results were found in a U.S. study that was led by Christopher Haiman of the University of Southern California, Los Angeles. His team combed through the DNA of more than 1,800 people from a variety of racial and ethnic backgrounds; comparing key differences in DNA against genes from more than 5,500 healthy controls.
Again, the rs6983267 variant conferred about a 22 percent increase in colorectal cancer risk, Haiman's team reported. Prior studies had already tied this variant to an increased risk for prostate cancer.
"This is the first common genetic risk factor that has been reproducibly associated with risks in multiple cancers," Haiman told reporters. "The association observed with this variant in both prostate and colorectal cancer provides very strong support for the hypothesis that there may be a common biological mechanism underlying cancer risk in this region of the genome."
The California team stressed that the level of risk to an individual conferred by the gene did not change, regardless of the person's sex, race, site of tumor, tumor stage or the presence of colon cancer risk factors such as family history, smoking or drinking.
However, rs6983267 was found more frequently in some ethnicities than in others. "The frequency of this specific genetic variation varies widely in the population -- from about 85 percent of African-Americans to as low as 30 percent of Japanese," Haiman said.
Carrying rs6983267 does not place any individual black American at an extraordinarily higher risk for colon cancer, Haiman explained. However, due to its relative high prevalence among blacks, it probably accounts for about 40 percent of all cases of colorectal cancers among this minority, he said.
Another researcher noted that genes like the one in region 8q24 are often more dangerous when they clump together in the same person.
"Although individually these markers may only contribute small amounts of risk, collectively, in certain individuals, they may actually have composite risks which are comparable to that of known, high-risk [mutations]," explained Dr. Richard Houlston, of the Institute of Cancer Research in Sutton, U.K.
Comparing genomic differences among 930 people with colorectal cancer and 960 controls, his team also zeroed in on rs6983267 as boosting tumor risk. Given the genes' link to prostate cancer, "it does tend to suggest that some of these things may actually have a generic effect on more than one malignancy," Houlston said at the press conference.
A fourth study -- this time led by a consortium from Israel, Spain and the United States -- uncovered a similar connection between genetic variations on 8q24 and a rise in colon cancer risk. That research was published in the July issue of Cancer Biology and Therapy.
While intriguing, experts agreed that the finding does not have immediate implications for the detection, prevention and treatment of colorectal cancer, which kills more than 51,000 Americans each year, according to the American Cancer Society.
"These are encouraging findings, but obviously we need a lot more information about the genetic implications," said Dr. Durado Brooks, the society's director of prostate and colorectal cancer.
Genetic tests that might assess people's risk or help in cancer diagnosis are still years away, and, for now, the new finding "will not in any way significantly alter clinical practice," he said.
Still, the assembled experts agreed that clinical application remains the ultimate goal of their research efforts.
Ideally, Dunlop said, tests might someday be developed to spot genes like rs6983267, "such that you could tailor interventions such as more intensive [patient] surveillance and even prevention," he said. "This is big step forward, but there is more to come."
More information
Find out more about colorectal cancer at the American Cancer Society.
Tuesday, July 03, 2007
Molecule Signals Heart Disease in Early Stages
(HealthDay News) -- A molecule that could be a powerful new marker for heart disease and stroke has passed its first real-world test, researchers report.
In an eight-year study, high blood levels of myeloperoxidase (MPO) were closely associated with the early development of heart disease, and its predictive abilities were independent of classic risk factors such as high cholesterol, high blood pressure and diabetes. The finding is detailed in the July 10 issue of the Journal of the American College of Cardiology.
"This is the first time this particular marker has been looked at in an apparently healthy population," said Dr. Stanley L. Hazen, head of the section of preventive cardiology and cardiac rehabilitation at the Cleveland Clinic. His group has been working on MPO for more than a decade.
Hazen has filed for patents on MPO as a biomarker for cardiovascular disease. MPO tests now are available commercially and "at least five pharmaceutical companies are working to develop inhibitors of MPO," Hazen said.
MPO is a protein secreted by white blood cells. It signals inflammation and releases a bleach-like substance that damages the cardiovascular system. "Over a decade ago, our group showed that it is involved in tissue damage," Hazen said. "There are very large research and genetic studies that link MPO to the development of heart disease."
The new report describes use of MPO levels as a screening tool in a healthy population living in Norfolk, England. MPO readings were taken from thousands of residents at the start of the study. Eight years later, the researchers compared those readings in the 1,138 people who had developed coronary artery disease and 2,237 people, matched for age and sex, who had not.
The incidence of heart disease was 49 percent higher in people ranked among the top 25 percent of MPO levels, compared to those in the lowest quarter. Their risk was 36 percent higher when traditional risk factors including cholesterol levels, high blood pressure, smoking and diabetes were taken into account.
"Even if your other biomarkers were normal, if MPO levels were high, you were at higher risk," Hazen said. "The magnitude of the risk is roughly comparable to the risk of elevated LDL cholesterol."
LDL cholesterol collects in fatty plaques that eventually block arteries. It is a major target of medications aimed at reducing risk of heart attack and stroke, most notably statins.
The first commercially available test for MPO levels was approved by the U.S. Food and Drug Administration a year ago, Hazen said. "Its first intended use is for evaluating people with a history of chest pain, people who go to the emergency room or cardiologist," he said. His hope is that it eventually will become a standard screening tool.
"We believe it is potentially of utility for people who you don't know may be at risk," he said.
A high MPO reading now indicates that the physician should concentrate on reducing known risk factors, but MPO itself could eventually become a target of drug treatment, he said.
"One fascinating aspect of this study is that this marker of inflammation precedes by nearly a decade the development of clinical coronary disease," Dr. Christopher Cannon, an associate professor of medicine at Harvard Medical School, said in a statement. "This suggests MPO could be used to catch the disease in a very early stage and help in true prevention of coronary artery disease."
MPO might also be a marker for unstable plaque, deposits that can erupt to emit artery-blocking fragments, Cannon added. "More study is needed, but among hundreds of markers tested to date, MPO looks like a keeper that will one day become part of clinical care," he said.
More information
The known risk factors for cardiovascular disease are described by the American Heart Association.
In an eight-year study, high blood levels of myeloperoxidase (MPO) were closely associated with the early development of heart disease, and its predictive abilities were independent of classic risk factors such as high cholesterol, high blood pressure and diabetes. The finding is detailed in the July 10 issue of the Journal of the American College of Cardiology.
"This is the first time this particular marker has been looked at in an apparently healthy population," said Dr. Stanley L. Hazen, head of the section of preventive cardiology and cardiac rehabilitation at the Cleveland Clinic. His group has been working on MPO for more than a decade.
Hazen has filed for patents on MPO as a biomarker for cardiovascular disease. MPO tests now are available commercially and "at least five pharmaceutical companies are working to develop inhibitors of MPO," Hazen said.
MPO is a protein secreted by white blood cells. It signals inflammation and releases a bleach-like substance that damages the cardiovascular system. "Over a decade ago, our group showed that it is involved in tissue damage," Hazen said. "There are very large research and genetic studies that link MPO to the development of heart disease."
The new report describes use of MPO levels as a screening tool in a healthy population living in Norfolk, England. MPO readings were taken from thousands of residents at the start of the study. Eight years later, the researchers compared those readings in the 1,138 people who had developed coronary artery disease and 2,237 people, matched for age and sex, who had not.
The incidence of heart disease was 49 percent higher in people ranked among the top 25 percent of MPO levels, compared to those in the lowest quarter. Their risk was 36 percent higher when traditional risk factors including cholesterol levels, high blood pressure, smoking and diabetes were taken into account.
"Even if your other biomarkers were normal, if MPO levels were high, you were at higher risk," Hazen said. "The magnitude of the risk is roughly comparable to the risk of elevated LDL cholesterol."
LDL cholesterol collects in fatty plaques that eventually block arteries. It is a major target of medications aimed at reducing risk of heart attack and stroke, most notably statins.
The first commercially available test for MPO levels was approved by the U.S. Food and Drug Administration a year ago, Hazen said. "Its first intended use is for evaluating people with a history of chest pain, people who go to the emergency room or cardiologist," he said. His hope is that it eventually will become a standard screening tool.
"We believe it is potentially of utility for people who you don't know may be at risk," he said.
A high MPO reading now indicates that the physician should concentrate on reducing known risk factors, but MPO itself could eventually become a target of drug treatment, he said.
"One fascinating aspect of this study is that this marker of inflammation precedes by nearly a decade the development of clinical coronary disease," Dr. Christopher Cannon, an associate professor of medicine at Harvard Medical School, said in a statement. "This suggests MPO could be used to catch the disease in a very early stage and help in true prevention of coronary artery disease."
MPO might also be a marker for unstable plaque, deposits that can erupt to emit artery-blocking fragments, Cannon added. "More study is needed, but among hundreds of markers tested to date, MPO looks like a keeper that will one day become part of clinical care," he said.
More information
The known risk factors for cardiovascular disease are described by the American Heart Association.
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