NASA in final preparations for Nov. 8 asteroid flyby

ScienceDaily (Oct. 28, 2011) — NASA scientists will be tracking asteroid 2005 YU55 with antennas of the agency's Deep Space Network at Goldstone, Calif., as the space rock safely flies past Earth slightly closer than the moon's orbit on Nov. 8. Scientists are treating the flyby of the 1,300-foot-wide (400-meter) asteroid as a science target of opportunity -- allowing instruments on "spacecraft Earth" to scan it during the close pass.

Tracking of the aircraft carrier-sized asteroid will begin at 9:30 a.m. local time (PDT) on Nov. 4, using the massive 70-meter (230-foot) Deep Space Network antenna, and last for about two hours. The asteroid will continue to be tracked by Goldstone for at least four hours each day from Nov. 6 through Nov. 10. Radar observations from the Arecibo Planetary Radar Facility in Puerto Rico will begin on Nov. 8, the same day the asteroid will make its closest approach to Earth at 3:28 p.m. PST.

The trajectory of asteroid 2005 YU55 is well understood. At the point of closest approach, it will be no closer than 201,700 miles (324,600 kilometers) or 0.85 the distance from the moon to Earth. The gravitational influence of the asteroid will have no detectable effect on anything here on Earth, including our planet's tides or tectonic plates. Although 2005 YU55 is in an orbit that regularly brings it to the vicinity of Earth (and Venus and Mars), the 2011 encounter with Earth is the closest this space rock has come for at least the last 200 years.

During tracking, scientists will use the Goldstone and Arecibo antennas to bounce radio waves off the space rock. Radar echoes returned from 2005 YU55 will be collected and analyzed. NASA scientists hope to obtain images of the asteroid from Goldstone as fine as about 7 feet (2 meters) per pixel. This should reveal a wealth of detail about the asteroid's surface features, shape, dimensions and other physical properties (see "Radar Love" -- http://www.jpl.nasa.gov/news/news.cfm?release=2006-00a ).

Arecibo radar observations of asteroid 2005 YU55 made in 2010 show it to be approximately spherical in shape. It is slowly spinning, with a rotation period of about 18 hours. The asteroid's surface is darker than charcoal at optical wavelengths. Amateur astronomers who want to get a glimpse at YU55 will need a telescope with an aperture of 6 inches (15 centimeters) or larger.

The last time a space rock as big came as close to Earth was in 1976, although astronomers did not know about the flyby at the time. The next known approach of an asteroid this large will be in 2028. NASA detects, tracks and characterizes asteroids and comets passing close to Earth using both ground- and space-based telescopes. The Near-Earth Object Observations Program, commonly called "Spaceguard," discovers these objects, characterizes a subset of them, and plots their orbits to determine if any could be potentially hazardous to our planet.

NASA's Jet Propulsion Laboratory manages the Near-Earth Object Program Office for NASA's Science Mission Directorate in Washington. JPL is a division of the California Institute of Technology in Pasadena.

More information about asteroids and near-Earth objects is at: http://www.jpl.nasa.gov/asteroidwatch .

More information about asteroid radar research is at: http://echo.jpl.nasa.gov/ .

More information about the Deep Space Network is at: http://deepspace.jpl.nasa.gov/dsn .

Recommend this story on Facebook, Twitter,
and Google +1:

Other bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by NASA/Jet Propulsion Laboratory.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Read More

High tech detection of breast cancer using nanoprobes and SQUID

ScienceDaily (Oct. 28, 2011) — Mammography saves lives by detecting very small tumors. However, it fails to find 10-25% of tumors and is unable to distinguish between benign and malignant disease. New research published in BioMed Central's open access journal Breast Cancer Research provides a new and potentially more sensitive method using tumor-targeted magnetic nanoprobes and superconducting quantum interference device (SQUID) sensors.

A team of researchers from University of New Mexico School of Medicine and Cancer Research and Treatment Center, Senior Scientific, LLC, and the Center for Integrated Nanotechnologies facility at Sandia National Laboratories created nanoprobes by attaching iron-oxide magnetic particles to antibodies against HER-2, a protein overexpressed in 30% of breast cancer cases. Using these tiny protein-iron particles the team was able to distinguish between cells with HER-2 and those without, and were able to find HER-2 cancer cells in biopsies from mice. In their final test the team used a synthetic breast to determine the potential sensitivity of their system.

Dr Helen Hathaway explained, "We were able to accurately pinpoint 1 million cells at a depth of 4.5 cm. This is about 1000x fewer cells than the size at which a tumor can be felt in the breast and 100x more sensitive than mammographic x-ray imaging. While we do not expect the same level of nanoparticle uptake in the clinic, our system has an advantage in that dense breast tissue, which can mask traditional mammography results, is transparent to the low-frequency magnetic fields detected by the SQUID sensors."

Future refining of the system could allow not only tumor to be found but to be classified according to protein expression (rather than waiting for biopsy results). This in turn could be used to predict disease progression and refine treatment plans and so improve patient survival.

Recommend this story on Facebook, Twitter,
and Google +1:

Other bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by BioMed Central.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Helen J Hathaway, Kimberly S Butler, Natalie L Adolphi, Debbie M Lovato, Robert Belfon, Danielle L Fegan, Todd C Monson, Jason E Trujillo, Trace E Tessier, Howard C Bryant, Dale L Huber, Richard S Larson and Edward R Flynn. Detection of breast cancer cells using targeted magnetic nanoparticles and ultra-sensitive magnetic field sensors. Breast Cancer Research, 2011; 13: R108 DOI: 10.1186/bcr3050

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Read More

Python study may have implications for human heart health

ScienceDaily (Oct. 27, 2011) — A surprising new University of Colorado Boulder study shows that huge amounts of fatty acids circulating in the bloodstreams of feeding pythons promote healthy heart growth, results that may have implications for treating human heart disease.

CU-Boulder Professor Leslie Leinwand and her research team found the amount of triglycerides -- the main constituent of natural fats and oils -- in the blood of Burmese pythons one day after eating increased by more than fiftyfold. Despite the massive amount of fatty acids in the python bloodstream there was no evidence of fat deposition in the heart, and the researchers also saw an increase in the activity of a key enzyme known to protect the heart from damage.

After identifying the chemical make-up of blood plasma in fed pythons, the CU-Boulder researchers injected fasting pythons with either "fed python" blood plasma or a reconstituted fatty acid mixture they developed to mimic such plasma. In both cases, the pythons showed increased heart growth and indicators of cardiac health. The team took the experiments a step further by injecting mice with either fed python plasma or the fatty acid mixture, with the same results.

"We found that a combination of fatty acids can induce beneficial heart growth in living organisms," said CU-Boulder postdoctoral researcher Cecilia Riquelme, first author on the Science paper. "Now we are trying to understand the molecular mechanisms behind the process in hopes that the results might lead to new therapies to improve heart disease conditions in humans."

The paper is being published in the Oct. 28 issue of the journal Science. In addition to Leinwand and Riquelme, the authors include CU postdoctoral researcher Brooke Harrison, CU graduate student Jason Magida, CU undergraduate Christopher Wall, Hiberna Corp. researcher Thomas Marr and University of Alabama Tuscaloosa Professor Stephen Secor.

Previous studies have shown that the hearts of Burmese pythons can grow in mass by 40 percent within 24 to 72 hours after a large meal, and that metabolism immediately after swallowing prey can shoot up by fortyfold. As big around as telephone poles, adult Burmese pythons can swallow prey as large as deer, have been known to reach a length of 27 feet and are able to fast for up to a year with few ill effects.

There are good and bad types of heart growth, said Leinwand, who is an expert in genetic heart diseases including hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes. While cardiac diseases can cause human heart muscle to thicken and decrease the size of heart chambers and heart function because the organ is working harder to pump blood, heart enlargement from exercise is beneficial.

"Well-conditioned athletes like Olympic swimmer Michael Phelps and cyclist Lance Armstrong have huge hearts," said Leinwand, a professor in the molecular, cellular and developmental biology department and chief scientific officer of CU's Biofrontiers Institute. "But there are many people who are unable to exercise because of existing heart disease, so it would be nice to develop some kind of a treatment to promote the beneficial growth of heart cells."

Riquelme said once the CU team confirmed that something in the blood plasma of pythons was inducing positive cardiac growth, they began looking for the right "signal" by analyzing proteins, lipids, nucleic acids and peptides present in the fed plasma. The team used a technique known as gas chromatography to analyze both fasted and fed python plasma blood, eventually identifying a highly complex composition of circulating fatty acids with distinct patterns of abundance over the course of the digestive process.

In the mouse experiments led by Harrison, the animals were hooked up to "mini-pumps" that delivered low doses of the fatty acid mixture over a period of a week. Not only did the mouse hearts show significant growth in the major part of the heart that pumps blood, the heart muscle cell size increased, there was no increase in heart fibrosis -- which makes the heart muscle more stiff and can be a sign of disease -- and there were no alterations in the liver or in the skeletal muscles, he said.

"It was remarkable that the fatty acids identified in the plasma-fed pythons could actually stimulate healthy heart growth in mice," said Harrison. The team also tested the fed python plasma and the fatty acid mixture on cultured rat heart cells, with the same positive results, Harrison said.

The CU-led team also identified the activation of signaling pathways in the cells of fed python plasma, which serve as traffic lights of sorts, said Leinwand. "We are trying to understand how to make those signals tell individual heart cells whether they are going down a road that has pathological consequences, like disease, or beneficial consequences, like exercise," she said.

The prey of Burmese pythons can be up to 100 percent of the constricting snake's body mass, said Leinwand, who holds a Marsico Endowed Chair of Excellence at CU-Boulder. "When a python eats, something extraordinary happens. Its metabolism increases by more than fortyfold and the size of its organs increase significantly in mass by building new tissue, which is broken back down during the digestion process."

The three key fatty acids in the fed python plasma turned out to be myristic acid, palmitic acid and palmitoleic acid. The enzyme that showed increased activity in the python hearts during feeding episodes, known as superoxide dismutase, is a well-known "cardio-protective" enzyme in many organisms, including humans, said Leinwand.

The new Science study grew out of a project Leinwand began in 2006 when she was named a Howard Hughes Medical Institute Professor and awarded a four-year, $1 million undergraduate education grant from the Chevy Chase, Md.-based institute. As part of the award Leinwand initiated the Python Project, an undergraduate laboratory research program designed to focus on the heart biology of constricting snakes like pythons thought to have relevance to human disease.

Undergraduates contributed substantially to the underpinnings of the new python study both by their genetic studies and by caring for the lab pythons, said Leinwand. While scientists know a great deal about the genomes of standard lab animal models like fruit flies, worms and mice, relatively little was known about pythons. "We have had to do a lot of difficult groundwork using molecular genetics tools in order to undertake this research," said Leinwand.

CU-Boulder already had a laboratory snake facility in place, which contributed to the success of the project, she said.

"The fact that the python study involved faculty, postdoctoral researchers, a graduate student and an undergraduate, Christopher Wall, shows the project was a team effort," said Leinwand. "Chris is a good example of how the University of Colorado provides an incredible educational research environment for undergraduates." Wall is now a graduate student at the University of California, San Diego.

Hiberna Corp., a Boulder-based company developing drugs based on natural models of extreme metabolic regulation, signed an exclusive agreement with CU's Technology Transfer Office in 2008, licensing technology developed by Leinwand based on the natural ability of pythons to dramatically increase their heart size and metabolism.

Directed by Nobel laureate and CU Distinguished Professor Tom Cech, the Biofrontiers Institute was formed to advance human health and welfare by exploring critical areas of biology and translating new knowledge into practical applications. The institute is educating a new generation of interdisciplinary scientists to work together on solutions to complex biomedical challenges and to expand Colorado's leadership in biotechnology. For more information on the Biofrontiers Institute visit cimb.colorado.edu .

Recommend this story on Facebook, Twitter,
and Google +1:

Other bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Colorado at Boulder.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Cecilia A. Riquelme, Jason A. Magida, Brooke C. Harrison, Christopher E. Wall, Thomas G. Marr, Stephen M. Secor, Leslie A. Leinwand. Fatty Acids Identified in the Burmese Python Promote Beneficial Cardiac Growth. Science, 2011; 334 (6055): 528-531 DOI: 10.1126/science.1210558

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Read More

Progeria: Promising results from new gene therapy on animals

ScienceDaily (Oct. 27, 2011) — Huge progress has been made over the last few years in scientific research into progeria, a disease that leads to premature aging in children. In 2003, a team directed by Nicolas Lévy discovered the gene, and, in 2008, 12 children were able to begin clinical trials in which two molecules were combined to slow down the characteristic effects of the disease: premature aging. Researchers are continuing their efforts in an attempt to counter the consequences of the genetic defect that causes progeria.

Until now, no model had been able to accurately imitate the effects of the disease in humans. For several years, research has been conducted in close collaboration from teams led by Nicolas Lévy and Annachiara De Sandre-Giovannoli at Inserm/Université de la Méditerranée and from a team led by Carlos López-Otín (University of Oviedo) and has succeeded in making such a model possible. The lifespan of mice treated through gene therapy is significantly extended and several other parameters related to them are improved. The research, published Oct. 26, 2011 in Science Translational Medicine, received backing from the AFM thanks to donations from a Telethon.

Progeria is a rare genetic disease. Children suffering from it seem to experience accelerated aging (chronic hair loss, joint pains, thin and hairless skin, cardiovascular problems). In 2003, Nicolas Lévy and his team identified the cause of the disease when they discovered the involvement of the LMNA (nuclear protein-coding) gene, lamin A/C. The mutation causes the production of a truncated protein, progerin, which accumulates in the nuclei of cells and its toxic effects cause their deformation and various other malfunctions. It has since been proven that progerin progressively accumulates in normal cells, thus establishing a link between the disease and physiological aging.

In 2008, European clinical trials began on twelve children suffering from progeria. The treatment is based on a combination of two existing molecules: statins (prescribed in the treatment and prevention of atherosclerosis and cardiovascular risks) and aminobisphosphonates (prescribed in to treat osteoporosis and to prevent complications in some forms of cancer). The use of both these molecules aims to chemically alter progerin to reduce its toxicity. However, although this treatment aimed to slow down the development of the disease, it did not reduce the quantities of progerin. To study this aspect, researchers needed to obtain a relevant animal model.

An "authentic" progeria model…

To generate a model of this kind, Spanish and French researchers decided to introduce a gene mutation (G609G), equivalent to that identified in humans (G608G), in mice to reproduce the exact pathological mechanism found in the children, with a view to then blocking it. The mice models were created under the supervision of Bernard Malissen using the IBISA platform located at the Marseille-Luminy Centre of Immunology. This approach made it possible to obtain young mice that produced progerin, characteristic of the disease in humans. After three weeks alive, the mutated mice displayed growth defects, weight loss caused by bone deformation and cardiovascular and metabolic anomalies mirroring the human phenotype and considerably reducing their lifespan (an average of 103 days compared with two years for wild mice). The progerin thus produced accumulates in mouse cells via genetic mechanisms (abnormal splicing) identical to those observed in humans, i.e. the source of anomalies characteristic of the disease.

… for a targeted gene therapy

Using this unique progeria animal model, the researchers focussed their efforts on implementing a mutation-targeted treatment, with a view to reducing, and, if possible, preventing the production of progerin. To this end, they used "vivo-morpholino" antisense oligonucleotide technology. "This technology, explains Nicolas Lévy, is based on introducing a synthetic antisense aglionecleotide into mice. As is the case with progeria, this sequence is applied to block (or facilitate) the production of a functional protein using a gene. In this case, the production of progerin, as well as lamin A from the gene, were reduced."

There was a highly significant increase in life expectancy of mice treated using this new technology, from an average of 155 days to a maximum of 190 days.

Nicolas Levy's team, with continued collaboration with Carlos López-Otín, now intend to translate this preclinical research into a new therapeutic trial for children, possibly combined with other pharmacological molecules. Other research is being conducted in parallel to find alternative administration channels for antisense oligonucleotides.

Recommend this story on Facebook, Twitter,
and Google +1:

Other bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by INSERM (Institut national de la santé et de la recherche médicale).

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Fernando G. Osorio, Claire L. Navarro, Juan Cadiñanos, Isabel C. López-Mejía, Pedro M. Quirós, Catherine Bartoli, José Rivera, Jamal Tazi, Gabriela Guzmán, Ignacio Varela, Danielle Depetris, Félix De Carlos, Juan Cobo, Vicente Andrés, Annachiara De Sandre-Giovannoli, José M. P. Freije, Nicolas Lévy, Carlos López-Otín. Splicing-Directed Therapy in a New Mouse Model of Human Accelerated Aging. Science Translational Medicine, 2011; 3 (106): 106ra107 DOI: 10.1126/scitranslmed.3002847

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Read More

Insects are scared to death of fish

ScienceDaily (Oct. 27, 2011) — The mere presence of a predator causes enough stress to kill a dragonfly, even when the predator cannot actually get at its prey to eat it, say biologists at the University of Toronto.

"How prey respond to the fear of being eaten is an important topic in ecology, and we've learned a great deal about how these responses affect predator and prey interactions," says Professor Locke Rowe, chair of the Department of Ecology and Evolutionary Biology (EEB) and co-principal investigator of a study conducted at U of T's Koffler Scientific Reserve.

"As we learn more about how animals respond to stressful conditions -- whether it's the presence of predators or stresses from other natural or human-caused disruptions -- we increasingly find that stress brings a greater risk of death, presumably from things such as infections that normally wouldn't kill them," says Rowe.

Shannon McCauley, a post-doctoral fellow, and EEB professors Marie-Josée Fortin and Rowe raised juvenile dragonfly larvae (Leucorrhinia intacta) in aquariums or tanks along with their predators. The two groups were separated so that while the dragonflies could see and smell their predators, the predators could not actually eat them.

"What we found was unexpected -- more of the dragonflies died when predators shared their habitat," says Rowe. Larvae exposed to predatory fish or aquatic insects had survival rates 2.5 to 4.3 times less than those not exposed.

In a second experiment, 11 per cent of larvae exposed to fish died as they attempted to metamorphose into their adult stage, compared to only two per cent of those growing in a fish-free environment. "We allowed the juvenile dragonflies to go through metamorphosis to become adult dragonflies, and found those that had grown up around predators were more likely to fail to complete metamorphosis successfully, more often dying in the process," says Rowe.

The scientists suggest that their findings could apply to all organisms facing any amount of stress, and that the experiment could be used as a model for future studies on the lethal effects of stress.

The research is described in a paper titled "The deadly effects of 'nonlethal' predators," published in Ecology and highlighted in Nature this week. It was supported by grants to Fortin and Rowe from the Canada Research Chairs program and the Natural Sciences and Engineering Research Council of Canada, and a post-doctoral fellowship awarded to McCauley.

Recommend this story on Facebook, Twitter,
and Google +1:

Other bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Toronto.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Shannon J. McCauley, Locke Rowe, Marie-Josée Fortin. The deadly effects of “nonlethal” predators. Ecology, 2011; 92 (11): 2043 DOI: 10.1890/11-0455.1

Note: If no author is given, the source is cited instead.

Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Read More

More clues to causes of breast cancer: Hyperactivation of Akt and overexpression of IKBKE observed in 50 percent of human cancers

ScienceDaily (Oct. 27, 2011) — Publishing in the current issue of The Journal of Biological Chemistry, researchers at Moffitt Cancer Center in Tampa, Fla., have discovered additional mechanisms of "Akt" activation and suggest a component of that activation mechanism -- inhibitor of nuclear factor kappa-B kinase subunit epsilon (IKBKE) -- could be targeted as a therapeutic intervention for treating cancer.

Akt, also known as protein kinase B, is one of about 500 protein kinases in the human genome. Kinases are known to regulate the majority of cellular pathways. Akt modifies other proteins chemically and regulates cell proliferation.

"Recent evidence suggests that IKBKE is an oncogenic kinase that participates in malignant transformation and tumor development," said Moffitt senior researcher and lead author Jin Q. Cheng, Ph.D., M.D. "Our study identified Akt as a bona fide substrate of IKBKE and IKBKE direct activation of Akt independent PI3K and revealed a functional link between IKBKE and Akt activation in breast cancer."

Cheng's lab studies a variety of genetic alterations and their molecular mechanisms in both ovarian and breast cancer, particularly on their effect on the molecules that are regulated by Akt and the small molecule inhibitors of Akt.

"We found that inhibition of Akt suppresses IKBKE's oncogenic transformation," said Cheng. "This is significant because overexpression of IKBKE and activation of Akt has been observed in more than 50 percent of human cancers. Akt inhibitors targeting PH domain do not have inhibitory effect on IKBKE-induced Akt."

The researchers experimented with a variety of inhibitors currently being used in clinical trials.

The laboratory study utilized breast cancer cell lines from received from patient donors at Moffitt and cell lines received from Harvard University and Johns Hopkins University. The work was supported by a National Institutes of Health grant and a grant from the James and Esther King Biomedical Research Program.

Recommend this story on Facebook, Twitter,
and Google +1:

Other bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by H. Lee Moffitt Cancer Center & Research Institute.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

J.-P. Guo, D. Coppola, J. Q. Cheng. IKBKE Protein Activates Akt Independent of Phosphatidylinositol 3-Kinase/PDK1/mTORC2 and the Pleckstrin Homology Domain to Sustain Malignant Transformation. Journal of Biological Chemistry, 2011; 286 (43): 37389 DOI: 10.1074/jbc.M111.287433

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Read More

Regular aspirin intake halves cancer risk, study finds

ScienceDaily (Oct. 28, 2011) — Scientists including those from Queen's University have discovered that taking regular aspirin halves the risk of developing hereditary cancers.

Hereditary cancers are those which develop as a result of a gene fault inherited from a parent. Bowel and womb cancers are the most common forms of hereditary cancers. Fifty thousand people in the UK are diagnosed with bowel and womb cancers every year; 10 per cent of these cancers are thought to be hereditary.

The decade-long study, which involved scientists and clinicians from 43 centres in 16 countries and was funded by Cancer Research UK, followed nearly 1,000 patients, in some cases for over 10 years. The study found that those who had been taking a regular dose of aspirin had 50 per cent fewer incidents of hereditary cancer compared with those who were not taking aspirin.

The research focused on people with Lynch syndrome which is an inherited genetic disorder that causes cancer by affecting genes responsible for detecting and repairing damage in the DNA. Around 50 per cent of those with Lynch syndrome develop cancer, mainly in the bowel and womb. The study looked at all cancers related to the syndrome, and found that almost 30 per cent of the patients not taking aspirin had developed a cancer compared to around 15 per cent of those taking the aspirin.

Those who had taken aspirin still developed the same number of polyps, which are thought to be precursors of cancer, as those who did not take aspirin but they did not go on to develop cancer. It suggests that aspirin could possibly be causing these cells to destruct before they turn cancerous.

Over 1,000 people were diagnosed with bowel cancer in Northern Ireland last year; 400 of these died from the disease. Ten per cent of bowel cancer cases are hereditary and by taking aspirin regularly the number of those dying from the hereditary form of the disease could be halved.

Professor Patrick Morrison from Queen's University in Belfast, who led the Northern Ireland part of the study, said: "The results of this study, which has been ongoing for over a decade, proves that the regular intake of aspirin over a prolonged period halves the risk of developing hereditary cancers. The effects of aspirin in the first five years of the study were not clear but in those who took aspirin for between five and ten years the results were very clear."

"This is a huge breakthrough in terms of cancer prevention. For those who have a history of hereditary cancers in their family, like bowel and womb cancers, this will be welcome news. Not only does it show we can reduce cancer rates and ultimately deaths, it opens up other avenues for further cancer prevention research. We aim now to go forward with another trial to assess the most effective dosage of aspirin for hereditary cancer prevention and to look at the use of aspirin in the general population as a way of reducing the risk of bowel cancer.

"For anyone considering taking aspirin I would recommend discussing this with your GP first as aspirin is known to bring with it a risk of stomach complaints, including ulcers."

The research was published online Oct. 28 in The Lancet.

Recommend this story on Facebook, Twitter,
and Google +1:

Other bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Queen's University Belfast.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Sir John Burn, Anne-Marie Gerdes, Finlay Macrae, Jukka-Pekka Mecklin, Gabriela Moeslein, Sylviane Olschwang, Diane Eccles, Gareth Evans, Eamonn R. Maher, Lucio Bertario, Marie-Luise Bisgaard, Malcolm G. Dunlop, Judy W.C. Ho, Shirley V. Hodgson, Annika Lindblom, Jan Lubinski, Patrick J. Morrison, Victoria Murday, Raj Ramesar, Lucy Side, Rodney J. Scott, Huw J.W. Thomas, Hans F. Vasen, Gail Barker, Gillian Crawford, Faye Elliott, Mohammad Movahedi, Kirsi Pylvanainen, Juul T. Wijnen, Riccardo Fodde, Henry T. Lynch, John C. Mathers, D. Timothy Bishop, on behalf of the CAPP2 Investigators. Long-term effect of aspirin on cancer risk in carriers of hereditary colorectal cancer: an analysis from the CAPP2 randomised controlled trial. The Lancet, Pubished online Oct. 28, 2011; DOI: 10.1016/S0140-6736(11)61049-0

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Read More