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Posted on August 12th, 2011
DNAWellness
By Pete Spotts, Staff writer / August 12, 2011 /csmonitor.com
If you’re out watching the Perseid meteor shower tonight, you’ll be witnessing a process that scientists have increasingly come to regard as the vehicle for delivering basic building blocks of organic life to Earth.
A team of scientists led by NASA‘s Michael Callahan appears to have added some critical components to the list of space-borne building blocks raining onto Earth’s surface: a class of chemicals called nucleobases. Nucleobases combine to carry the genetic information found in DNA molecules, the molecules that orchestrate an organism’s form and functions.
In results reported this week in the Proceedings of the National Academy of Sciences, the team analyzed the chemical makeup of a dozen carbon-rich meteorites plucked from different locations in Antarctica and Australia.
They not only found nucleobases widely found in organisms on Earth, compounds such as adenine and guanine, two of the four bases found in DNA. They also found related compounds, which the team dubbed “nucleobase analogues,” that aren’t found on Earth and in effect are new to science.
Over the years, scientists have found amino acids, which are needed to form proteins, with unambiguous space-based origins. And meteorites have carried the chemicals necessary to make cell walls.
Even nucleobases have been detected in meteorites before, notes Dr. Callahan. But scientists have had a hard time convincing themselves and others that the nucleobases came from space. They could represent contamination a space rock picked up after it landed.
“We do see biological nucleobases in ice and soil samples” collected from the places where the meteorites were found, he says. “That’s only natural.”
But, he adds, the mix and distribution of the nucleobases typically found in ice and soil are far different that those found in the meteorites the team analyzed.
And those new-to-science compounds are definitely not earth contamination. “We don’t see any nucleobase analogues whatsoever” in the ice and soil, he says.
Many biologically important molecules form from water, hydrogen cyanide, and ammonia – all substances that are abundant in the clouds of dust and gas that collapse to form stars and planets.
As an additional test, the team conducted simple experiments in the lab in which they mixed ammonia, hydrogen cyanide, and water and ended up with the same variety of nucleobases and nucleobase analogues they found in meteorites.
They concluded that some of the key components of DNA may have been delivered to Earth ready-made by chemical reactions that took place on asteroids or comets as the solar system evolved.
And if it can happen in our solar system, Callahan suggests, under the right conditions these building blocks can find their way to hospitable planets elsewhere.
DNAWellnessinfo.com Resource: http://www.csmonitor.com/Science/2011/0812/Are-we-all-extraterrestrials-Scientists-discover-traces-of-DNA-in-space.
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Posted on August 9th, 2011
DNAWellness
Lauren Brown| Aug. 9, 2011, 7:28 PM
New research shows that half of human intelligence can be attributed to genes. A forthcoming issue of
Molecular Psychiatry also showed that a multitude of genes, rather than a single gene, contributes to people’s thinking skills, according to
HealthDay.For the last century, the
majority of studies on the heritability of I.Q. have concluded that genes account for more like 75 percent of intelligence.
Authors of the study analyzed over 3,500 unrelated adults by scanning data on the portion of their DNA that accounts for the greatest genetic variability. Knowledge and problem-solving skills were tested and researchers found that 40 to 50 percent in the variation came from genetic differences.
This calls into question how influential education and environmental factors are in shaping the rest of human intelligence.
The 50 percent figure, however, is “likely to be an underestimate because we could only detect variation that is correlated with common DNA markers,” researcher Peter Visscher told HealthDay.
DNAWellnessinfo.com Resource: http://www.businessinsider.com/genes-peter-visscher-human-intelligence-2011-8#ixzz1V1qLFWvs
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Posted on August 9th, 2011
DNAWellness
Testing for fetal DNA in a pregnant woman’s blood can accurately predict the child’s sex, researchers have found.
In a review of previous research, such tests were able to accurately pin down sex at least 95 percent of the time, Stephanie Devaney of the National Institutes of Health in Bethesda, Md. and colleagues reported in the August 10 issue of the Journal of the American Medical Association.
Non-invasive DNA testing may provide an alternative to more invasive tests, such as chorionic villus sampling and amniocentesis — which can carry a slight risk of pregnancy loss — for determining the gender of a fetus and related heritable disorders, the researchers wrote.
Read this story on www.medpagetoday.com.
Those disorders include ambiguous genitalia, X-linked conditions, and single-gene disorders such as congenital adrenal hyperplasia.
The presence of cell-free circulating Y-chromosome DNA sequences in the blood of pregnant women was first described in 1997, and has been widely studied since then, albeit in studies that have been limited methodologically.
In some countries — the Netherlands, U.K., France, and Spain — cell-free fetal DNA testing has already become a part of routine clinical care despite the lack of large performance studies.
Gender can typically be accurately assessed via sonogram at 13 weeks, but diagnosis with ultrasound isn’t always possible, the researchers explained, and earlier diagnosis is often favorable.
In order to look at overall performance of the blood tests, the researchers conducted a review and meta-analysis of 57 studies conducted between Jan. 1, 1997 and April 17, 2011, totaling 80 data sets on 3,524 male-bearing and 3,017 female-bearing pregnancies.
Generally, they found high sensitivity and specificity for Y-chromosome detection in maternal blood (95 percent and 99 percent, respectively).
They also found that performance was best when performed at 20 weeks’ gestation or later.
Tests done using urine samples and those run prior to seven weeks’ gestation were unreliable, the researchers said.
Devaney and colleagues noted that a disadvantage of fetal DNA blood testing is the need to validate female sex, because the test looks for male, or Y-chromosome, DNA. Also, the test is not currently available at the doctor’s office, has not yet been approved by the Clinical Laboratory Improvement Amendments (CLIA), and is not currently reimbursed by insurers.
They also noted that many of the included studies were small, so it would be “beneficial to help validate test performance under highly controlled testing conditions.”
This could also help test manufacturers to “ensure that their claims are accurate,” as some companies that directly market the tests to consumers say their products have an accuracy of 95 percent to 99 percent as early as five to seven weeks’ gestation.
DNAWellnessinfo.com Resource: http://abcnews.go.com/Health/ParentingResourceCenter/fetal-dna-test-moms-blood-predicts-babys-sex/story?id=14266954
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Posted on July 19th, 2011
DNAWellness
If the same is true for human sperm, men could pass genetic defects caused by passive smoking to their children
Alok Jha, science correspondent, guardian.co.uk, Monday 18 July 2011 19.59 BST
Passive smoking may cause mutations in the DNA of sperm, according to a study in mice. The finding suggests that men exposed to second-hand smoke could pass on any resulting genetic abnormalities to their children.
Men who smoke are known to be at higher risk of developing abnormalities in their sperm, including reduced motility and increased DNA damage. “Recently, the International Agency for Research on Cancer concluded that there is enough evidence to link paternal smoking in humans with increased risk of childhood cancer, suggesting that tobacco smoking causes heritable germ cell mutation in humans,” wrote Francesco Marchetti of the Lawrence Berkeley National Laboratory in California, who led the new research, in a paper in the Proceedings of the National Academy of Sciences.
Allan Pacey, a fertility expert at the University of Sheffield, said: “What we don’t know, and what we overlook, is the influence of passive smoking. I guess it’s no surprise that passive smoking causes the same kind of damage, because you’re just inhaling the same stuff, albeit at different levels.”
In Marchetti’s study, 32 mice were exposed to the total amount of smoke generated by between three and 16 cigarettes, for varying times up to 90 minutes per day for two weeks. The different conditions modelled the effects of low and high doses of direct smoking and passive smoking. The scientists then examined the sperm of these mice six weeks later, looking at a region of their DNA that doesn’t code for proteins.
The frequency of mutations in the sperm of control mice – which were not exposed to cigarette smoke – was around 1.3%-1.5%. In those mice simulating direct smoking, the average mutation rate was 4% and 4.7% for low and high doses. For those mice simulating passive smoking, mutation rates were 4.6% and 2.6% for low and high doses respectively.
The researchers wrote that while it wasn’t clear whether the same relationship would apply to regions of the genome that code for proteins, “our data suggest that paternal exposure to second-hand smoke may have reproductive consequences that go beyond the passive smoker.”
Marchetti said that the findings provided “compelling evidence in support of the argument that passive smoking should be regarded as a germ cell mutagen in humans”. Male exposure to second-hand smoke was likely to have harmful consequences for reproduction similar to those from first-hand smoke.
Pacey said that, in human terms, the level of “passive smoking” the mice were exposed to in the study was high. “Most people’s experience of passive smoking is maybe on a Friday night entering and exiting a pub. And it might be the odd whiff when somebody exhales when you’re walking down the street.”
He said that while the long-term consequences for human health were uncertain, the advice for would-be fathers was clear. “If you’re trying to conceive, stopping smoking is good advice and removing yourself from the influences of passive smoking is good advice,” he said. “The advice to any man who wants to be a father is to stop smoking at least three months before he tries.”
DNAWellnessinfo.com Resource: http://www.guardian.co.uk/science/2011/jul/18/passive-smoking-dna-sperm-mice
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Posted on November 23rd, 2010
DNAWellness
Posted on efitnessnow.com on 11/23/10
According to a new study, eating foods like carrots and certain fruits, fights disease and may prolong life.
A team of researchers discovered carotenoids including beta-carotene, alpha-carotene and lycopene created by plants and micro-organisms act as antioxidants and counteract this damage.
The researchers determined, oxygen-related damage to DNA, proteins and fats might play a part in the development of chronic diseases like heart disease and cancer. That damage can be eased by the antioxidant action of carotenoids, such as beta-carotene, alpha-carotene and lycopene. Most people get these nutrients through foods, like fruits and veggies, that are loaded with them.
The research team from the U.S. Centers for Disease Control and Prevention (CDC) discovered that over 14 years of follow-up, many people — regardless of lifestyle habits, demographics or overall health risks — had fewer life-limiting health troubles as their blood concentrations of alpha-carotene rose.
The study found that the risk of death in those who had blood alpha-carotene levels ranging from 2 and 3 micrograms per deciliter (mcg/dL) was 23% lower compared to those who had concentrations between 0 and 1.
The research only looked at a person’s alpha-carotene levels. It did not measure blood levels of other antioxidants, so it is difficult to know if alpha-carotene alone is associated with health benefits or if other constituents were also involved.
DNAWellnessInfo.com Resource: http://www.efitnessnow.com/news/2010/11/23/eating-carrots-may-help-prevent-death-from-heart-disease/
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Posted on November 17th, 2010
DNAWellness
BLUE BELL, Pa.–(BUSINESS WIRE)–Nov 17, 2010 – Inovio Pharmaceuticals, Inc. (NYSE Amex: INO), a leader in the development of therapeutic and preventive vaccines against cancers and infectious diseases, announced today that it has achieved high vaccine-induced response rates and strong magnitude of immune responses in its Phase I clinical study of PENNVAX™-B, a DNA vaccine for the prevention of HIV infection. Similar to recently reported results from a Phase I clinical study of Inovio’s therapeutic DNA vaccine for cervical cancer, the response rates and magnitude of responses achieved in this study are significantly higher than those seen previously with other DNA vaccine trials. Dr. Spyros Kalams, principal investigator for the study and Immunology Director of the Vanderbilt Center for AIDS Research at Vanderbilt University Medical Center, presented the interim immune response and safety data at the Annual HIV Vaccine Trials Network (HVTN) Conference being held November 15-17 in Seattle, WA.
Inovio previously reported data from non-human primates demonstrating up to a 100-fold enhancement in immune responses resulting from the vaccine when delivered via in vivo electroporation compared to syringe injection without electroporation. This study, designated HVTN-080, involved vaccination of 48 healthy, HIV-negative volunteers to assess safety and levels of immune responses generated by Inovio’s PENNVAX-B vaccine delivered with its CELLECTRA® electroporation device. PENNVAX-B is a SynCon™ DNA vaccine that targets HIV gag, pol, and env proteins. This randomized, double-blind, multi-center study is being sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), an agency of the National Institutes of Health, and conducted by the NIAID-funded HVTN, at several clinical sites.
Of the 48 total volunteers, eight subjects received a placebo, 10 subjects received a 1 mg dose of PENNVAX™-B vaccine, and 30 subjects received a 1 mg dose of PENNVAX-B along with IL-12 DNA. The IL-12 for this study (Genevax-IL-12), manufactured under a contract with DAIDS, was provided by Profectus Biosciences. All volunteers received vaccine or placebo administered with electroporation at months 0, 1, and 3. The T-cell immune responses were detected using a validated flow cytometry-based intracellular cytokine staining (ICS) assay at the HVTN core immunology laboratory at the Fred Hutchinson Cancer Research Center (Seattle, WA).
Preliminary data from the trial reported at the meeting included safety data from all trial participants (48) and immunogenicity data from 38 out of 40 samples from vaccine recipients post-second-dose and from 31 out of 40 samples from vaccine recipients post-third-dose. The data indicate that antigen-specific T-cell responses were generated by the vaccine in a majority of subjects. Either CD4+ or CD8+ or both T-cell responses were observed against at least one of the vaccine antigens in 61% (23 out of 38) of evaluated subjects after two vaccinations. After three vaccinations, 84% (26 out of 31) of evaluated subjects had positive T-cell responses.
Notably, after three vaccinations:
- 67% (6 out of 9) of evaluated subjects receiving PENNVAX-B and 91% (20 of 22) of evaluated subjects receiving PENNVAX-B + IL-12 were observed to have generated antigen-specific T-cell responses (either CD4+ or CD8+).
- Antigen-specific CD4+ T-cell responses were generated by the vaccine in 70% of evaluated vaccine recipients (21 out of 30).
- Significantly strong antigen-specific, CD8+ T-cell responses were also generated by the vaccine in 55% of evaluated vaccine recipients (17 out of 31).
- Samples from eight placebo recipients and pre-vaccine samples from vaccine recipients were also tested and were negative for both CD4+ T-cell responses and CD8+ T-cell responses.
- PENNVAX-B delivered using the CELLECTRA® intramuscular electroporation delivery device with or without IL-12 was generally safe and well tolerated. There were no vaccine-related serious adverse events. Reported adverse events and injection site reactions were mild to moderate and required no treatment.
Dr. Kalams stated, “The preliminary immune response data from this novel DNA-based vaccine are indeed very encouraging. We look forward to our continuing work with Inovio to develop the potential of this promising vaccine candidate.”
Dr. J. Joseph Kim, Inovio’s President and CEO, said: “After recently announcing best-in-class immunogenicity data from our clinical trial for our cervical cancer DNA vaccine using the same technology platform, we are pleased to again see very strong T-cell immune responses from this vaccine platform for a different disease, and particularly a disease with unmet needs like HIV. They are amongst the highest immune responses seen in other HIV vaccine trials either with DNA or other vaccine platforms including proteins and viral vectors. However, unlike viral vectors, DNA vaccines do not induce unwanted immune responses against the carrier. Taken together these results further support the prospect that Inovio’s DNA vaccine and delivery platform could play an important role in developing new vaccines and therapies for major diseases like cancer and HIV.”
In addition to the interim ICS results presented at the meeting, the complete immunogenicity data including data from the few remaining unanalyzed samples and additional antibody and T-cell results based on ELISpot assays as well as the end-of-study safety data are expected in 2Q 2011.
DNAWellnessinfo.com Resource: http://www.drugs.com/clinical_trials/inovio-pharmaceuticals-hiv-dna-vaccine-achieves-strong-t-cell-immune-responses-phase-human-trial-10673.html
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Posted on November 2nd, 2010
DNAWellness
But applications for diabetes years away, researchers say.
TUESDAY, Nov. 2 (HealthDay News) — A new genetic analysis has uncovered specific regions in the DNA of certain human pancreatic cells that appear central to the regulation of insulin and other functions of the pancreas.
The new effort — conducted by researchers at the National Human Genome Research Institute (NHGRI) — takes scientists a step closer towards understanding the complex genetic underpinnings of insulin deficiency and the onset of type 2 diabetes, which accounts for most of the 23 million cases of diabetes among Americans and the more than 170 million cases worldwide.
By honing in on clusters of hormone-producing pancreatic cells known as islets, the investigators were able to detect about 18,000 “molecular on-off switches” (or so-called “promoters”) that control gene behavior. Several hundred of these gene-adjacent switches were previously unknown.
In a U.S. National Institutes of Health (NIH) news release, study co-author Michael Stitzel explained that previous gene-mapping work has pointed out some genetic differences between type 2 diabetic and non-diabetic individuals in specific regions of the genome.
“But substantial efforts are required to understand how these differences contribute to disease,” he said. “Defining regulatory elements in human islets is a critical first step to understanding the molecular and biological effects for some of the genetic variants statistically associated with type 2 diabetes.”
Stitzel and colleagues from the NIH Intramural Sequencing Center, Duke University in Durham, N.C., and the University of Michigan in Ann Arbor report their findings in the Nov. 3 issue of Cell Metabolism.
The new work has also enabled the authors to identify another 34,000 regulatory “modules” located slightly farther away (than the 18,000 on-off switches) from the genes they control. They believe that these distinct “regulatory elements” may be critical to proper blood glucose levels.
Upwards of 50 genetic abnormalities believed to have an association with islet-related pancreatic dysfunction were also uncovered.
“These findings represent important strides that were not possible just five years ago, but that are now realized with advances in genome sequencing technologies,” Dr. Eric D. Green, NHGRI director, noted in the NIH news release.
“Very exciting” is how Dr. Stuart Weiss, an endocrinologist at New York University Medical Center and a clinical assistant professor at the NYU School of Medicine in New York City, described the current effort.
“It’s clearly the future of medicine,” he said. “However, the fact of the matter is that all sorts of factors are involved in the development of diabetes, and different people require different treatments. And just when you think that you understand it, another curve comes at you. So it’s very difficult to think that we’re going to find a magic bullet. And I would think that the clinical applications from any of this are probably years and years away.”
More information
For more on genetics and diabetes, visit the American Diabetes Association.
SOURCES: U.S. National Institutes of Health, news release, Nov. 2, 2010; Stuart Weiss, M.D., endocrinologist, clinical assistant professor, NYU School of Medicine, New York City
Copyright © 2010 HealthDay. All rights reserved.
DNAWellnessinfo.com Resource: http://www.doctorslounge.com/index.php/news/hd/15338
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Posted on October 1st, 2010
DNAWellness
Science Centric | 1 October 2010 11:18 GMT
DNA methylation – a modification of DNA linked to gene regulation – is altered with increasing severity in a blood cancer called multiple myeloma, according to a study by Mayo Clinic and the Translational Genomics Research Institute (TGen).
And at specific points of DNA, ‘global hypomethylation,’ in which many genes lose the modification, may be associated with the step-by-step development of myeloma, according to a scientific paper published this month in the journal Cancer Research.
‘This is the first study to show that hypomethylation occurs early in the development of multiple myeloma and increases through disease progression,’ said Dr Bodour Salhia, a TGen cancer researcher and the paper’s lead author.
DNA methylation suppresses the expression of viral genes and other harmful elements incorporated over time into an individual’s genome. In cancer, hypermethylation at certain genomic locations can turn tumour suppressing genes off, while hypomethylation in some instances may lead to the over-expression of oncogenes, or those genes that give rise to cancer, and is linked to chromosomal instability.
However, there is still much to learn about the consequences of altered methylation.
In this study, researchers examined the methylation status of more than 1,500 CpGs. This is shorthand for C-phosphate-G, or cytosine and guanine – two of the four chemicals that comprise DNA – separated by a phosphate group, which links the two nucleosides together.
Researchers used a high-throughput universal bead array technology to examine CpG methylation at different stages of multiple myeloma, evaluating DNA methylation events associated with the progression of tumours.
They performed DNA methylation profiling analysis for more than 800 genes, including tumour suppressors, oncogenes, and genes involved in cancer-related cellular processes. This process contrasts with previous studies that focused on the analysis of a single gene.
They found only a few genes that were hypermethylated, but importantly found many more hypomethylated genes, even in the earliest stages of multiple myeloma.
‘Our data suggest that the overall degree of methylation may have some prognostic value, and further studies are needed to determine the functional and clinical significance of our findings,’ said Dr John Carpten, Director of TGen’s Integrated Cancer Genomics Division and the paper’s senior author.
Dr Salhia, added, ‘This study represents the most comprehensive examination to date of the role of methylation in multiple myeloma, and is expected to lead to an improved understanding of the biological mechanisms involved in the development of this type of cancer.’
The study of DNA methylation falls under epigenetics – an emerging field in cancer research. Unlike the study of genetics, epigenetics refers to the study of gene activity that does not involve hardwiring alterations in the genetic code. These epigenetic events, which lay atop the genome, are an intricate and heritable mechanism of regulating the expression of genes.
‘Understanding the full spectrum of epigenetic modifications will be key to improving the clinical management of the disease, and studies should continue to find new ways of treating multiple myeloma by targeting the multiple myeloma epigenome. This study also emphasises that hypomethylating strategies may not be the next necessary steps in drug development.’ said Rafael Fonseca, M.D., Deputy Director of Mayo Clinic Cancer Centre in Arizona.
Source: TGen
DNAWellnessnessinfo.com Resource: http://www.sciencecentric.com/news/10100122-tgen-mayo-clinic-study-discovers-role-dna-methylation-multiple-myeloma-blood-cancer.html
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Posted on October 1st, 2010
DNAWellness
October 1, 2010 8:51 AM - cbsnews.com
Posted by David W Freeman
CBS) What causes attention-deficit hyperactivity disorder, or ADHD?
A new study points the finger not at bad parenting or too much sugar in the diet but at heredity.
Scientists at Cardiff University in Wales compared the DNA of 366 children with ADHD to that of 1,047 kids without the condition. They found that kids with ADHD were more likely to have small segments of DNA that were duplicates or missing.
“We hope that these findings will help overcome the stigma associated with ADHD,” Professor Anita Thapar, the study’s lead author, said in a written statement. “Too often, people dismiss ADHD as being down to bad parenting or poor diet. As a clinician, it was clear to me that this was unlikely to be the case. Now we can say with confidence that ADHD is a genetic disease and that the brains of children with this condition develop differently to those of other children.”
The study was published online in The Lancet, the English medical journal.
Worldwide, about one in 50 children have ADHD. The condition – which makes kids restless, impulsive, and easily distracted – is incurable but can often be controlled with medication and therapy.
DNAWellnessinfo.com Resource: http://www.cbsnews.com/8301-504763_162-20018239-10391704.html
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Posted on September 27th, 2010
DNAWellness
September 27, 2010
AAP
Australian scientists have found a new and potent way to fight cancer among what was once thought of as junk DNA.
The experimental technique, proven to shrink tumours in mice, involves “microRNA”.
Dr Alex Swarbrick said this new class of genes was until recently considered to be junk DNA, the term used to describe the bulk of information contained in the genome that has no apparent purpose.
But far from being junk, he said one specific type of microRNA (microRNA 380) has been found to play a pivotal role in allowing certain types of cancer to grow.
Dr Swarbrick and his research colleagues also found that blocking the action of this microRNA in mice with neuroblastoma cancers caused their tumours to shrink.
“The revolutionary thing about this finding is that it’s the first time anyone has blocked the growth of a primary tumour by the simple delivery of a microRNA inhibitor…,” Dr Swarbrick, from Sydney’s Garvan Institute of Medical Research, said.
“That, of course, makes this microRNA a potential therapeutic target for all cancers that depend on it.”
The discovery points to a new way to combat cancer that could be as simple as a twice-weekly injection of a microRNA inhibitor.
MicroRNA 380 has its cancer-promoting effect on the body by disabling another gene (P53), which is known as the “guardian of the genome” because of its role in suppressing tumour growth.
Dr Swarbrick said the studies in mice showed how their P53 gene was disabled by “overproducing” microRNA 380.
He said this microRNA served a necessary purpose in embryos when cells needed to divide quickly and it should play no role in a “normal adult’s cells”.
It was not yet known why it could become active and with cancer-causing effects later in life.
“By blocking it, you’re effectively returning cells to normal,” Dr Swarbrick said.
“We still don’t know why it gets switched on again in certain cancers.
“(However) understanding that certain cancers appear to be regulated like this gives us a new avenue to explore in their treatment.”
Dr Swarbrick said the technique could also be applied to treat brain tumours as well as melanoma, which are known to be caused by a disabled P53 gene.
The research was conducted along with Brisbane-based Dr Susan Woods from the Queensland Institute of Medical Research, and a colleague in the US.
The results are reported in the journal Nature Medicine on Monday.
© 2010 AAP
DNAWellnessinfo.com Resource: http://news.smh.com.au/breaking-news-national/cancer-treatment-found-among-junk-dna-20100927-15sv8.html
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