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/

Eating carrots may help prevent death from heart disease is a post from: dnawellnessinfo.com

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

TGen-Mayo Clinic study discovers role of DNA methylation in multiple myeloma blood cancer is a post from: dnawellnessinfo.com

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

Cancer treatment found among junk DNA is a post from: dnawellnessinfo.com

Last Updated: Wednesday, May 5, 2010 | 1:11 PM ET

Canadian researchers have unraveled a genetic “code within a code” that helps explain how the instructions for building complex organisms, like humans, can be found in a small number of genes.

University of Toronto scientists Brendan Frey and Benjamin Blencowe said they have found a hidden code in DNA that helps explain how a small number of genes can contain instructions for a larger number of proteins and structures.

When researchers fully sequenced the human genome in 2004, they were surprised at how few genes humans actually have.

“Human DNA has 22,000 genes. That might seem like a lot, but not when you consider that a poplar tree has 45,000,” said Frey, in a statement.

Frey said his team, including Blencowe and Yoseph Barash, found a second level of information that the cells of living organisms use to create a larger set of instructions.

“We discovered a hidden code within DNA that living cells use to turn 20,000 genes into hundreds of thousands of genetic messages, by rearranging their parts,” he said.

Barash and Frey, who is also a professor of computer science and engineering, created a computer program that analyzes DNA to find “code words” in the genome.

The code words together are called the “splicing code,” containing the biological information needed to splice together different parts of the genetic code in different orders to generate a greater number of messages.

“For example, three neurexin genes can generate over 3,000 genetic messages that help control the wiring of the brain,” said Frey.

Neurexin is a protein that glues together the connections between nerve cells in the brain.

Frey said their work is the result of a close collaboration between computer scientists and experimental biologists.

“Understanding a complex biological system is like understanding a complex electronic circuit. Our team ‘reverse-engineered’ the splicing code using large-scale experimental data generated by the group,” he said.

The research was the cover story in this week’s issue of the journal Nature.

DNAWellnessinfo.com Resource: http://www.cbc.ca/technology/story/2010/05/05/tech-dna-splicing-code.html#ixzz0n9Wn5yO0

Canadian scientists crack hidden DNA code is a post from: dnawellnessinfo.com

April 14, 2010, 4:59 PM EDT  BusinessWeek

By Kristen Hallam

April 14 (Bloomberg) — Scientists discovered a way to transfer DNA from one fertilized human egg to another in a pioneering effort to avert the spread of a host of genetic disorders such as learning disabilities and diabetes.

The researchers at Newcastle University in northern England extracted the genetic material contributed by the egg and sperm and implanted it into a donor egg, according to the study published today by the journal Nature. It’s the first time DNA has been transferred between two fertilized human eggs.

The approach discards almost all the defective DNA inherited from the mother that disrupts the tiny energy generators inside cells, and may prevent related disorders such as blindness and liver failure, the researchers said. They are planning further experiments to see whether the technique could help people who carry mutated genes to have healthy babies — an end result that may still be a decade away.

“We have no way of curing these diseases at the moment, but this technique could allow us to prevent the diseases occurring in the first place,” said Doug Turnbull, the lead researcher and a professor at the university’s medical school, in a statement. “It is important that we do all we can to help these families and give them the chance to have healthy children, something most of us take for granted.”

Parents contribute a total of 23,000 genes to a child. In a fertilized egg, this genetic material is housed in two pronuclei, one from the egg and one from the sperm. The egg also contains mitochondria, tiny structures found in every cell that produce the chemical fuel needed for life. Mutations in the mitochondrial DNA, which are passed on from the mother, can disrupt the functioning of these energy generators.

‘Changing the Batteries’

The Newcastle scientists were able to extract both pronuclei and implant the material that makes each child unique into a donor egg with healthy mitochondria. They created 80 fertilized eggs using the technique and grew them in a laboratory for six to eight days. That showed for the first time that eggs produced in this way could reach the stage at which they each had divided into about 100 cells.

“It’s like changing the batteries,” Turnbull said today at a news conference in London. “These are diseases where there is battery failure. Because mitochondria are everywhere, these diseases can affect all parts of the body. None of my patients is exactly the same.”

About 1 out of every 200 children is born each year with mutations in mitochondrial DNA that cause no symptoms or only mild conditions. One in every 6,500 children is born with a more serious mitochondrial disease, ranging from muscular weakness to fatal heart failure. Some disorders lead to death in early infancy.

The research was funded by the Muscular Dystrophy Campaign, the U.K. Medical Research Council and the London-based Wellcome Trust, the world’s second-biggest medical research charity.

–Editors: Phil Serafino, Angela Cullen

To contact the reporter on this story: Kristen Hallam in London at khallam@bloomberg.net

To contact the editor responsible for this story: Phil Serafino at pserafino@bloomberg.net

DNAWellnessinfo.com Resource:  http://www.businessweek.com/news/2010-04-14/dna-swap-between-eggs-may-curb-inherited-disorders-study-finds.html

DNA Swap Between Eggs May Curb Inherited Disorders, Study Finds is a post from: dnawellnessinfo.com

April 11, 2010- physorg.com

Scientists have shown in multiple contexts that DNA damage over our lifetimes is a key mechanism behind the development of cancer and other age-related diseases. Not everyone gets these diseases, because the body has multiple mechanisms for repairing the damage caused to DNA by aging, the environment and other human behaviors – but the mechanisms behind certain kinds of DNA repair have not been well-understood.

In a paper published today in the journal Nature, researchers at the University of North Carolina at Chapel Hill’s Lineberger Comprehensive Cancer Center have shown that a particular protein – called Ku – is particularly adept at healing damaged strands of DNA.

According to Dale Ramsden, PhD, associate professor in the department of biochemistry and biophysics and a member of the curriculum in genetics and molecular biology, Ku is a very exciting protein because it employs a unique mechanism to repair a particularly drastic form of DNA damage.

“Damage to DNA in the form of a broken chromosome, or double strand break, can be very difficult to repair – it is not a clean break and areas along the strand may be damaged at the level of the fundamental building blocks of DNA – called nucleotides,” he notes.

Broken chromosomes can be compared to a break in a strand of yarn made up of several different threads or plies. Unless scissors are used to cut the yarn, the strand frays and may break or be damaged at several different places up and down the length of the yarn. These rough ends get “dirty” – making them harder to repair.

Provided by University of North Carolina

DNAWellnessinfo.com Resource:  http://www.physorg.com/news190207556.html

Key protein aids in DNA repair is a post from: dnawellnessinfo.com

scienceblog.com  4/8/10

A new discovery raises hope that autism may be more easily diagnosed and that its effects may be more reversible than previously thought. In a new study appearing online in The FASEB Journal (http://www.fasebj.org), scientists have identified a way to detect the disorder using blood and have discovered that drugs which affect the methylation state (“DNA tagging”) of genes could reverse autism’s effects. This type of drug is already being used in some cancer treatments.

“As the mother of a now 22-year-old son with an autism spectrum disorder, I hope that our studies as well as those of others, will lead to therapies that are designed to address specific deficiencies that are caused by autism, thus improving the lives of affected individuals,” said Valerie W. Hu, Ph.D., one of the researchers involved in the work from the Department of Biochemistry and Molecular Biology at The George Washington University Medical Center in Washington, D.C. “Since autism is very diverse in the array of symptoms present in any given individual, it is first necessary to be able to identify specific deficits in each individual in order to design and then prescribe the best treatment. As an example of this personalized approach to medicine, we identified RORA as one of the genes that was altered specifically in the sub group of autistic individuals who exhibited severe language deficits.”

To make their discovery, Hu and colleagues identified chemical changes in DNA taken from cells of identical twins and sibling pairs, in which only one of the twins or siblings was diagnosed with autism. The researchers then compared genes that showed changes in DNA tagging (methylation) with a list of genes that showed different levels of expression from these same individuals. Then the scientists studied the amount of protein product produced by two genes that appear on both lists in autistic and control regions of the cerebellum and frontal cortex of the brain. They found that both proteins, as predicted by the observed increase in DNA tagging, were reduced in the autistic brain. This suggests that blocking the chemical tagging of these genes may reverse symptoms of the disorder and demonstrates the feasibility of using more easily accessible cells from blood (or other non-brain tissues) for diagnostic screening.

“For far too long, autism research has been side-tracked by the cranky notion that it’s caused by the MMR vaccine,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “Studies like this, which define genetic and epigenetic changes in discrete subgroups of the autism spectrum, offer real hope that effective treatments and accurate diagnosis are closer at hand.”

Receive monthly highlights from The FASEB Journal by e-mail. Sign up at http://www.faseb.org/fjupdate.aspx. The FASEB Journal (http://www.fasebj.org) is published by the Federation of the American Societies for Experimental Biology (FASEB). The journal has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century and is the most cited biology journal worldwide according to the Institute for Scientific Information.

FASEB comprises 23 societies with more than 90,000 members, making it the largest coalition of biomedical research associations in the United States. FASEB enhances the ability of scientists and engineers to improve — through their research — the health, well-being and productivity of all people. FASEB’s mission is to advance health and welfare by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

Details: AnhThu Nguyen, Tibor A. Rauch, Gerd P. Pfeifer, and Valerie W. Hu. Global methylation profiling of lymphoblastoid cell lines reveals epigenetic contributions to autism spectrum disorders and a novel autism candidate gene, RORA, whose protein product is reduced in autistic brain. FASEB J. doi:10.1096/fj.10-154484 ; http://www.fasebj.org/cgi/content/abstract/fj.10-154484v1

DNAWellnessinfo.com Resource:  http://www.scienceblog.com/cms/new-study-autism-reveals-dna-tag-methylation-amenable-treatment.html

New study of autism reveals a ‘DNA tag’ (methylation) amenable to treatment is a post from: dnawellnessinfo.com

By a GenomeWeb staff reporter – 4/6/10

NEW YORK (GenomeWeb News) – Chronix Biomedical today announced that a study published in the current online edition of the Journal of Molecular Diagnostics supports the use of the firm’s technology in monitoring the clinical status of chronic disease.

The San Jose, Calif.-based firm said that the study is the first to show that its approach, which identifies disease-specific genetic fingerprints based on circulating DNA released into the bloodstream by damaged and dying cells, can be used for such monitoring purposes.

In the study, researchers used Chronix’s techniques to identify genomic fingerprints in the bloodstream of 28 multiple sclerosis patients known to have relapsing or stable disease. They compared these patients with 50 healthy volunteers.

According to Chronix, the researchers were able to distinguish the MS patients from the healthy volunteers. They also were able to use the circulating DNA fingerprints to differentiate periods of active disease attacks from the stable periods of disease remission characterizing relapsing-remitting MS, which affects about 85 percent of MS patients, the firm said.

“These positive data further validate the premise underlying the Chronix approach, showing that the many genetic anomalies associated with active and stable relapsing-remitting MS can be detected by analyzing DNA fragments circulating in the blood serum,” Mario Clerici, chair of immunology in the Department of Biomedical Sciences and Technologies at the University of Milano in Italy, and a co-author of the study, said in a statement. “The prognostic value achieved in this study supports the ability of this new approach to help manage relapsing-remitting multiple sclerosis, potentially offering clinicians a new tool to easily assess which MS treatment options are most effective for their patients, as well as providing critical information that will facilitate development of the next generation of MS therapeutics.”

The firm noted that Clerici is a member of the Chronix Medical Advisory Board and has an equity position in the company.

Chronix also is conducting studies on its approach for cancer diagnostics. The firm said that it intends to offer its serum DNA-based assays in a CLIA laboratory setting.

DNAWellnessinfo.com Resource:  http://www.genomeweb.com/dxpgx/chronix-study-supports-use-circulating-dna-monitoring-disease-status

Chronix Study Supports Use of Circulating DNA in Monitoring Disease Status is a post from: dnawellnessinfo.com

Article by Nicholas Wade – New York Times
Published: March 10, 2010

Two research teams have independently decoded the entire genome of patients to find the exact genetic cause of their diseases. The approach may offer a new start in the so far disappointing effort to identify the genetic roots of major killers like heart disease, diabetes and Alzheimer’s.

In the decade since the first full genetic code of a human was sequenced for some $500 million, less than a dozen genomes had been decoded, all of healthy people.

Geneticists said the new research showed it was now possible to sequence the entire genome of a patient at reasonable cost and with sufficient accuracy to be of practical use to medical researchers. One subject’s genome cost just $50,000 to decode.

“We are finally about to turn the corner, and I suspect that in the next few years human genetics will finally begin to systematically deliver clinically meaningful findings,” said David B. Goldstein, a Duke University geneticist who has criticized the current approach to identifying genetic causes of common diseases.

Besides identifying disease genes, one team, in Seattle, was able to make the first direct estimate of the number of mutations, or changes in DNA, that are passed on from parent to child. They calculate that of the three billion units in the human genome, 60 per generation are changed by random mutation — considerably less than previously thought.

The three diseases analyzed in the two reports, published online Wednesday, are caused by single, rare mutations in a gene.

In one case, Richard A. Gibbs of the Baylor College of Medicine sequenced the whole genome of his colleague Dr. James R. Lupski, a prominent medical geneticist who has a nerve disease, Charcot-Marie-Tooth neuropathy.

In the second, Leroy Hood and David J. Galas of the Institute for Systems Biology in Seattle have decoded the genomes of two children with two rare genetic diseases, and their parents.

More common diseases, like cancer, are thought to be caused by mutations in several genes, and finding the causes was the principal goal of the $3 billion human genome project. To that end, medical geneticists have invested heavily over the last eight years in an alluring shortcut.

But the shortcut was based on a premise that is turning out to be incorrect. Scientists thought the mutations that caused common diseases would themselves be common. So they first identified the common mutations in the human population in a $100 million project called the HapMap. Then they compared patients’ genomes with those of healthy genomes. The comparisons relied on ingenious devices called SNP chips, which scan just a tiny portion of the genome. (SNP, pronounced “snip,” stands for single nucleotide polymorphism.) These projects, called genome-wide association studies, each cost around $10 million or more.

The results of this costly international exercise have been disappointing. About 2,000 sites on the human genome have been statistically linked with various diseases, but in many cases the sites are not inside working genes, suggesting there may be some conceptual flaw in the statistics. And in most diseases the culprit DNA was linked to only a small portion of all the cases of the disease. It seemed that natural selection has weeded out any disease-causing mutation before it becomes common.

The finding implies that common diseases, surprisingly, are caused by rare, not common, mutations. In the last few months, researchers have begun to conclude that a new approach is needed, one based on decoding the entire genome of patients.

The new reports, though involving only single-gene diseases, suggest that the whole-genome approach can be developed into a way of exploring the roots of the common multigene diseases.

“We need a way of assessing rare variants better than the genomewide association studies can do, and whole-genome sequencing is the only way to do that,” Dr. Lupski said.

With 10 genomes of healthy humans sequenced, Dr. Gibbs, a specialist in DNA sequencing, decided it was time to decode the genome of someone with a genetic disease and asked his colleague Dr. Lupski to volunteer.

Mutations in any of 39 genes can cause Charcot-Marie-Tooth, a disease that impairs nerves to the hands and feet and causes muscle weakness.

Fifty thousand dollars later, Dr. Lupski turned out to have mutations in an obscure gene called SH3TC2. The copy of the gene he inherited from his father is mutated in one place, and the copy from his mother in a second.

Both his parents had one good copy of the gene in addition to the mutated one. A single good copy can generate enough, or nearly enough, of the gene’s product for the nerves to work properly. Dr. Lupski’s mother was free of the disease and his father had only mild symptoms.

In the genetic lottery that is human procreation, two of their eight children inherited good copies of SH3TC2 from each parent; two inherited the mother’s mutation but the father’s good copy and are free of the disease; and four siblings including Dr. Lupski inherited mutated copies from both parents. These four all have Charcot-Marie-Tooth disease. The results are reported in The New England Journal of Medicine.

In Seattle, Dr. Hood and Dr. Galas have also applied whole-genome sequencing to disease. They analyzed the genome of a family of four, in which the two children each have two single-gene diseases, called Miller syndrome and ciliary dyskinesia. With four related genomes available, the researchers could identify the causative genes. They also improved the accuracy of the sequencing because DNA changes that did not obey Mendel’s rules of inheritance could be classed as errors in the decoding process.

The Seattle team believes whole-genome sequencing can be applied to the study of the common multigene diseases and plans to sequence more than 100 genomes next year, starting with multigenerational families.

The family whose genomes they report in Science were sequenced by a company with a new DNA sequencing method, Complete Genomics of Mountain View, Calif., at a cost of $25,000 each. Clifford Reid, the chief executive, said that the company was scaling up to sequence 500 genomes a month and that for large projects the price per genome would soon drop below $10,000. “We are on our way to the $5,000 genome,” he said.

Dr. Reid said the HapMap and genomewide association studies were not a mistake but “the best we could do at the time.” But they have not yet revolutionized medicine, “which we are on the verge of doing,” he said.

Dr. Goldstein, of Duke University, said the whole-genome sequencing approach that was now possible should allow rapid progress. “I think we are finally headed where we have long wanted to go,” he said.

DNAWellnessinfo.com Resource:  http://www.nytimes.com/2010/03/11/health/research/11gene.html

Disease Cause Is Pinpointed With Genome is a post from: dnawellnessinfo.com

Naveen Kumar, TNN, Mar 6, 2010, 10.23pm IST

VARANASI: Now, the study of DNA repairing gene using single nucleotide polymorphism (SNP) marker would provide vital cue for cancer prevention, especially neck and head that comprises of as many as seven different types of cancer in the facial region. In addition, the study would also enable early prediction of much feared breast cancer in women.

While a team of scientists is studying the genomics in cancer, especially the squamous cell carcinoma in neck, head and breast region under the Hap Map project, the case studies in the last five years have revealed interesting contribution of DNA repairing genes including P53 associated genes, where SNP can be used as a marker for prompt diagnostic purpose.

Senior scientist Central Drug Research Institute Lucknow Dr SK Rath told TOI on Saturday, “The studies have shown that P53 associated genes play a vital role in DNA repair and act as tumour suppressor. It changes the DNA repair scene and plays pivotal role in protection against mutagenic and cytotoxic effects of DNA damage that also prevents cancer.” Similarly, SNP could also provide vital cue for DNA repairing in BRAC 1 and 2 genes that are believed to cause breast cancer in women, he added.

It is to be mentioned here that Dr Rath is a key member of the team that studied genotype of cancerous and non-cancerous cells under the project in the Xth five-year plan. Now, the team is researching on SNP of different people including smokers and non-smokers, drinkers and non-drinkers, where the cause of cancer

could not be ascertained.

Saying that million of SNPs exist in human genome that occur in gene within the regulatory region, Dr Rath emphasised that the method detects the most common type of variation in the genome, as it cater to small alteration, providing better scope for prediction. The SNP markers are preferred for population genomic disease association and are good indicators of squamous cell carcinoma in neck and head region that includes cancers of oral cavity, pharynx, nasopharynx, oropharynx, hypopharynx and tongue, he added.

Stressing that cancers of neck and head region are growing at alarming rate in states like UP, he said the case studies in Lucknow revealed that out of 100 cancer patients, the number of patients with cancer in the neck and head region increased from 30 to 49 (150 per cent increase) in the last five years. Worldwide, it is the fifth most common type of cancer affecting over one million population annually, he concluded.

DNAWellnessinfo.com Resource:  http://timesofindia.indiatimes.com/city/varanasi/-Vital-cues-for-cancer-prevention-through-DNA-repairing-gene/articleshow/5648729.cms

Vital cues for cancer prevention through DNA repairing gene is a post from: dnawellnessinfo.com