Vital cues for cancer prevention through DNA repairing gene

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

A First: Diagnosis By DNA

Matthew Herper, 02.25.10, 11:20 AM EST
Forbes Magazine dated March 15, 2010

Last year a five-month-old boy in Turkey stopped gaining weight and became dehydrated despite getting plenty of liquids. Specialists in Istanbul suspected Bartter’s syndrome, a potentially fatal kidney disorder that afflicts one in 100,000 babies, causing dangerously low levels of potassium and salt.

To confirm their hunch they sent a blood sample to Yale Medical School geneticist Richard Lifton. They asked him to determine whether the baby had the gene defect implicated in Bartter’s. But Lifton thought that Bartter’s might not be the culprit. So he did something that would have been prohibitively expensive a few years ago. He deciphered the DNA letters for all the baby’s genes. The gene scan revealed that the baby’s problem was not Bartter’s but something else called congenital chloride diarrhea, which also lowers salt levels. The result means that the baby, now doing better on a special diet, could be treated with drugs if his condition gets worse.

The case, published in the Proceedings of the National Academies of the Sciences in October, may be the first in which the results of DNA sequencing have altered treatment of a patient. Does this herald the beginning of a new kind of medicine in which patients with unexplained symptoms get their DNA sequenced? Yes, says Lifton: “This will be a court of last resort to try and identify causes of disease.”

Gene researchers have talked for years about how sequencing will transform medicine. Now that sequencing is cheap this transformation is under way. The cost of deciphering all 6 billion letters in the human genome has dropped from $1 million in 2007 to less than $20,000 today. Lifton used a two-step method to extract and sequence only the 1% of those letters that contain known genes, lowering the price to $2,500. New DNA sequencers just introduced by Illumina ( ILMN – news – people ) (whose model Lifton used) and Life Technologies ( LIFE – news – people ) could lower the cost of sequencing a whole genome to below $3,000 by year-end.

DNA sequencers haven’t been approved for use in medical testing, and insurers don’t pay for sequencing. But peering into DNA is becoming an option for wealthy patients with rare and scary diseases. Knome, a privately held company in Cambridge, Mass., started out in 2008 charging $350,000 to arrange sequencing and interpret the data for wealthy patrons as a vanity project. Now it offers the scans for as little as $25,000. Chief Executive Jorge Conde says several patients hoping to improve their care are among his customers.

The $600 million annual market for DNA sequencers is still all about research, with Illumina holding a 60% market share. But numerous companies are already jockeying for position in anticipation of a big future medical-test market.

Cancer patients may be among the first to benefit from DNA sequencing technology. In one early example of how this may work, Marco Marra, a researcher at the Michael Smith Genome Sciences Centre in Vancouver, last year sequenced the genes from a tumor that had spread from an 80-year-old patient’s tongue to his lungs. There is no standard therapy for this type of tumor. But the gene scan found the tumor was making large amounts of a growth-promoting protein called RET. When the patient’s medicine was switched to Pfizer ( PFE – news – people )’s Sutent, a drug that blocks this protein, the tumor shrank, according to a report in Nature.

A looming question is how the Food & Drug Administration will regulate sequencing technology. It could treat DNA sequencing like genetic tests and require separate approvals for each use. Some equipment makers hope for a faster path in which doctors practicing a new medical specialty emerge to evaluate and interpret gene scans, as radiologists do with X-rays. Clifford Reid, chief executive of Complete Genomics, which has finished 50 genomes, is skeptical that it will be that easy. “The FDA has been very quiet up until now,” he says. “We all have to expect the FDA to be intimately involved with these new tests.”

DNAWellnessinfo.com Resource:  http://www.forbes.com/forbes/2010/0315/health-illumina-genome-cancer-diagnosis-by-dna.html

From Uncharted Region of Human Genome, Clues Emerge About Origins of Coronary Artery Disease

ScienceDaily (Feb. 22, 2010) — Scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory have learned how an interval of DNA in an unexplored region of the human genome increases the risk for coronary artery disease, the leading cause of death worldwide.

Their research paints a fuller picture of a genetic risk for the disease that was discovered only three years ago and which lurks in one out of two people.

It also reinforces the tantalizing possibility that many more disease risks — and potential therapies — are hidden in the vast and uncharted part of the genome that doesn’t contain instructions for making proteins.

The research is reported in the February 21 advance online publication of the journal Nature.

The team focused on an interval of DNA in chromosome 9p21. People who carry variations of this interval have an increased chance of developing coronary artery disease, which is an accumulation of plaque in coronary arteries that restricts blood flow to the heart and causes heart attacks.

Determining how this DNA contributes to the disease is difficult because it’s in the poorly understood part of the genome that doesn’t code for proteins, the workhorses of cellular function.

In groundbreaking research, the Berkeley Lab scientists found that the DNA interval regulates a pair of genes that inhibit cell division, and that bad copies of the interval reduce the genes’ expression. Although more work is needed to understand how this mechanism contributes to coronary artery disease, the researchers speculate that the hobbled genes allow vascular cells to proliferate unchecked and narrow coronary arteries.

“We show that this non-coding interval affects the expression of two cell cycle inhibitor genes located almost 100,000 base pairs away. We believe that something goes awry in variants of this interval, causing vascular cells to divide and multiply more quickly than usual,” says Len Pennacchio, a geneticist with Berkeley Lab’s Genomics Division who conducted the research with Axel Visel and several other scientists from Berkeley Lab, as well as Jonathan Cohen of the University of Texas Southwestern Medical Center.

The link between an interval of DNA in chromosome 9p21 and a risk for coronary artery disease was established in several recent studies, one of which was published in the journal Science in 2007. In that study, led by Cohen and co-authored by several scientists including Pennacchio, the researchers scoured the human genome for differences in people who have coronary artery disease versus people who don’t.

This genome-wide association analysis alighted on a stretch of DNA in chromosome 9p21 that spans 58,000 base pairs of DNA. The study found that people with bad copies of this interval have a moderately higher risk of developing coronary artery disease. In addition, 50 percent of people have one bad copy and 25 percent have two bad copies.

“The risk of coronary artery disease isn’t very high in any give person with bad copies. But they are so common that population-wide the effect is significant,” says Pennacchio.

Remarkably, the study also found that the DNA interval isn’t associated with known risks for coronary artery disease such as diabetes, high blood pressure, and high cholesterol level. An unknown mechanism was at work.

“We landed on this risk interval and immediately said ‘wow!’ why doesn’t it link to problems that we know cause coronary artery disease?” says Pennacchio. “So the big question became: what is this DNA doing?”

Adding to the mystery, the DNA interval is among the 98 percent of our genome that doesn’t code for proteins. Most efforts to determine the function of the genome have focused on the two percent of our DNA that overlaps protein-coding genes. Scientists are just now beginning to explore the non-coding region, once referred to as “junk DNA.”

As part of this effort, the Berkeley Lab scientists set out to determine the function of the DNA interval in chromosome 9p21 that’s linked to coronary artery disease. They removed an analogous section of DNA from mice, then tracked what happened.

The expression level of two genes located far away, Cdkn2a and Cdkn2b, plummeted by about 90 percent in the “knock-out” mice compared to normal mice. These genes are important in controlling cell cycles and have been linked to cancer when mutated, but they had never been linked to coronary artery disease.

The scientists also studied heart tissue of the “knock-out” mice and found that the smooth muscle cells from their aortas had increased proliferation, a hallmark of coronary artery disease.

“Our research shows that the DNA interval plays a pivotal role in regulating the expression of two genes that control cell cycles. It also suggests that variants of the interval spur the progression of coronary artery disease by altering the dynamics of vascular cells,” says Pennacchio.

With this mechanism identified, scientists can develop therapies that fight coronary artery disease by targeting the two genes and jumpstarting them into action, says Pennacchio. He also believes that the genetic roots of many other diseases will be unearthed as scientists learn how to decipher the function of non-coding DNA.

“Non-coding DNA is a huge area of the genome, waiting to be explored, which could have huge dividends for understanding and treating disease,” says Pennacchio.

The research was funded by the National Institutes of Health.

Other Berkeley Lab scientists involved in the research include Yiwen Zhu, Dalit May, Veena Afzal, Elaine Gong, Cattia Attanasio, Matthew Blow, and Eddy Rubin.

DNAWellnessinfo.com Resource:  http://www.sciencedaily.com/releases/2010/02/100222094801.htm

Blood Tests May Reveal Tumor Size

Feb. 22, 2010 – cbsnews.com

(CBS) This article was written by Discover’sAndrew Moseman.

Doctors who are torn over how aggressively to treat a cancer patient, not knowing whether a tumor has fully regressed or is coming back, might someday be able to find out just by testing the patient’s blood. In a study forthcoming his week in Science Translational Medicine, John Hopkins researchers say they have tested a way to spot the “fingerprint” of cancer-the changes to the

Jeffery Schloss of the National Human Genome Research Institute, who wasn’t involved in the study, likened the approach to drawing a map. Sequencing the letters of the genetic code would be akin to plotting every house in a large neighborhood. The Hopkins team was looking only for neighborhoods-in particular, neighborhoods out of place compared with where they would be in normal tissue. The researchers in the study looked at tissue from people with breast or bowel cancer, and found multiple DNA rearrangements in each of the samples of cancerous tissue.

In each patient, the genetic changes in the cancerous cells amount to a unique marker of the patient’s tumor, the researchers say. Using blood samples from two of the colorectal cancer patients, they found the test was sensitive enough to detect this marker or “fingerprint” DNA that had been shed by tumors into the bloodstream.

The study’s approach could be invaluable for tracking the progress of a tumor. When a cancer is operated on or treated with radio – or chemotherapy, the levels of the fingerprint should fall, and vanish altogether if the tumor has been eradicated. Indeed, in one of their patients, the study authors saw the cancer biomarker drop after surgery but then rise again, suggesting to them that the cancer wasn’t fully eradicated.

Because the technique requires sequencing a person’s whole genome, it’s not coming to a hospital near you in the immediate future, says study author Bert Vogelstein: “This is really personalized medicine. This is not something off the shelf…. This is something that has to be designed for each individual patient”. But with the cost of genome sequencing rapidly coming down in price, this kind of approach might not be too far away, and doctors could use it to catch a recurring cancer before it’s large enough to be visible to other methods, like CT scans.


By Andrew Moseman
Reprinted with permission from Discover

DNAWellnessinfo.com Resource: http://www.cbsnews.com/stories/2010/02/22/tech/main6232081.shtml

Secrets of attraction may lie in immune system DNA

BY Rosemary Black
DAILY NEWS STAFF WRITER

Wednesday, February 17th 2010, 5:04 PM

Here’s some new information about the science of attraction: Your body odor may provide your mate with subconscious clues about the strength of your immune system.

Researchers from the University of Western Australia, reporting in the journal “Animal Behavior,” say that whether or not the object of your desire finds you irresistible may depend on how sweet your sweat smells, according to a report in the Daily Mail. A woman’s sweat holds genetic information that signals to a potential hubby whether their offspring would possess the best chance of fighting off illness.

The more varied a woman’s histocompatibility, or MHC, genes are, the more attractive she appears to the opposite sex.

The researchers studied the DNA of nearly 150 college students, who filled out questionnaires about their love lives. They looked at the students’ DNA to find variation in genes that are known to have an influence on the immune system, and found that the more diverse these genes were, the more disease-resistant a person was.

The researchers then matched the results of the genetic tests with the survey answers and learned that the women with the most varied histocompatibility (MHC) genes also had the greatest number of sexual partners.

Previous research has shown that the more different a person’s perspiration is to yours, the more pleasant you’re likely to find him or her. It’s theorized that this phenomenon came about so people wouldn’t accidentally marry their relatives or anyone else who’s genetically similar.

Another theory is that women with varied MHC genes could be more outgoing.

“It is possible that MHC-diverse women have more sexual partners because they actively seek more partners, rather than because males prefer diverse partners,” wrote the researchers.

Relationship expert Laurent Mackler says parents may affect how successful a woman is at finding a boyfriend – but not necessarily because of genetics.

“We are invariably attracted to people based on how familiar that person is to us from childhood,” says Mackler, author of “SoleMate: Master the Art of Aloneness & Transform Your Life.”

“As human beings, we are always seeking homeostasis, or balance, and looking for the parts of us that got lost as we grew up and had to adapt to the family system. So we’re attracted unconsciously to the people who embody these traits. We are looking for our other half and may not always find him.”

DNAWellnessinfo.com Resource:  http://www.nydailynews.com/lifestyle/health/2010/02/17/2010-02-17_secrets_of_attraction_may_lie_in_immune_system_dna_thats_sensed_through_sweat_sc.html

Scientists develop universal DNA reader to advance faster, cheaper sequencing efforts

2/11/10 – physorg.com

Led by ASU Regents’ Professor Stuart Lindsay, director of the Biodesign Institute’s Center for Single Molecule Biophysics, the ASU team is one of a handful that has received stimulus funds for a National Human Genome Research Initiative, part of the National Institutes of Health, to make DNA genome sequencing as widespread as a routine medical checkup.

The broad goal of this “$1000 genome” initiative is to develop a next-generation DNA sequencing technology to usher in the age of personalized medicine, where knowledge of an individual’s complete, 3 billion-long code of DNA information, or genome, will allow for a more tailored approach to disease diagnosis and treatment. With current technologies taking almost a year to complete at a cost of several hundreds of thousands of dollars, less than 20 individuals on the planet have had their whole genomes sequenced to date.

To make their research dream a reality, Lindsay’s team has envisioned building a tiny, nanoscale DNA reader that could work like a supermarket checkout scanner, distinguishing between the four chemical letters of the DNA genetic code, abbreviated by A, G, C, and T, as they rapidly pass by the reader.

To do so, they needed to develop the nanotechnology equivalent of threading the eye of a needle. In this case, the DNA would be the thread that could be recognized as it moved past the reader ‘eye.’ During the past few years, Lindsay’s team has made steady progress, and first demonstrated the ability to read individual DNA sequences in 2008—but this approach was limited because they had to use four separate readers to recognize each of the DNA bases. More recently, they demonstrated the ability to thread DNA sequences through the narrow hole of a fundamental building block of nanotechnology, the carbon nanotube.

Lindsay’s team relies on the eyes of nanotechnology, scanning tunneling- (STM) and atomic force- (ATM) microscopes, to make their measurements. The microscopes have a delicate electrode tip that is held very close to the DNA sample.

In their latest innovation, Lindsay’s team made two electrodes, one on the end of microscope probe, and another on the surface, that had their tiny ends chemically modified to attract and catch the DNA between a gap like a pair of chemical tweezers. The gap between these functionalized electrodes had to be adjusted to find the chemical bonding sweet spot, so that when a single chemical base of DNA passed through a tiny, 2.5 nanometer gap between two gold electrodes, it momentarily sticks to the electrodes and a small increase in the current is detected. Any smaller, and the molecules would be able to bind in many configurations, confusing the readout, any bigger and smaller bases would not be detected.

“What we did was to narrow the number of types of bound configurations to just one per DNA base,” said Lindsay. “The beauty of the approach is that all the four bases just fit the 2.5 nanometer gap, so it is one size fits all, but only just so!”

At this scale, which is just a few atomic diameters wide, quantum phenomena are at play where the electrons can actually leak from one electrode to the other, tunneling through the DNA bases in the process.

Each of the chemical bases of the DNA genetic code, abbreviated A, C, T or G, gives a unique electrical signature as they pass between the gap in the electrodes. By trial and error, and a bit of serendipity, they discovered that just a single chemical modification to both electrodes could distinguish between all 4 DNA bases.

“We’ve now made a generic DNA sequence reader and are the first group to report the detection of all 4 DNA bases in one tunnel gap,” said Lindsay. “Also, the control experiments show that there is a certain (poor) level of discrimination with even bare electrodes (the control experiments) and this is in itself, a first too.”

“We were quite surprised about binding to bare electrodes because, like many physicists, we had always assumed that the bases would just tumble through. But actually, any surface chemist will tell you that the bases have weak chemical interactions with metal surfaces.”

Next, Lindsay’s group is hard at work trying to adapt the reader to work in water-based solutions, a critically practical step for DNA sequencing applications. Also, the team would like to combine the reader capabilities with the carbon nanotube technology to work on reading short stretches of DNA.

More information: The Nano Letters research article can be accessed online at URL: http://pubs.acs.org/doi/pdfplus/10.1021/nl1001185

Provided by Arizona State University (news : web)

DNAWellnessinfo.com Resource:  http://www.physorg.com/news185129971.html

A new theory of how low doses of antibioitics create antibiotic resistance

Feb 11, 2010 – usatoday.com

E.coli bacteria is seen under a microscope.

CAPTION

By Centers for Disease Control

Exposure to low levels of antibiotics increases mutations in E. coli and Staphylococcus bacteria hundreds of time more than normal, making the creation of drug-resistance strains more likely, says a paper in today’s edition of the journal Molecular Cell.

This finding adds to concerns about antibiotic resistance brought on by poor prescriptions practices among doctors, patients who don’t take all their medicine and even low doses of antibiotics given to help animals grow faster.

The researchers found that while low levels of antibiotics may not be enough to kill off the bacteria, they still stress them. That stress causes them to produce free radicals, says James Collins, a biomedical engineer at Boston University and one of the paper’s authors.

Those free radicals are produced by oxidation, a process that’s known to damage cells. In the case of bacteria, the free radicals damage the bacteria’s DNA, causing some of the affected bugs to mutate.

Two and a half years ago Collins’ group began looking at how bacteria respond to antibiotics. It was then that they discovered that antibiotics can stimulate the pathways that create free radicals in bacteria.

A year ago they started considering what other implications their discovery might have.

“We wondered whether sub-lethal levels still produce free radicals. We know the cells wouldn’t die, but we know that free radicals can damage DNA, and that increases mutenigenesis,” he says.

And that’s exactly what they found. Basically, if the antibiotic dose isn’t high enough to kill every bacteria in sight, “you could be creating a zoo with a wide range of mutations,” he says.

The  finding is important “within the context of our understanding — or lack of understanding — of how bacteria become resistant to antibiotics,” says Deborah Hung, a molecular biologist at Massachusetts General Hospital, who wrote an accompanying Perspective piece on the article.

The  truth is that no one really knows exactly how bacteria become resistant to antibiotics, says Hung. So knowing that low levels of antibiotics might potentially increase the random chance that bacteria might mutate into resistant forms could have important implications for medicine.

By Elizabeth Weise

DNAWellnessinfo.com Resource:  http://content.usatoday.com/communities/sciencefair/post/2010/02/a-new-theory-of-how-low-doses-of-antibioitics-create-antibiotic-resistance/1

Tiny DNA circles advance stem cell therapy prospects

Thursday Feb 11 2010 Stanford News

By Krista Conger

The promise of stem cells sometimes seems no more than a distant glow on the horizon, particularly for patients afflicted with devastating conditions that could potentially benefit from stem-cell-based treatments.

One hurdle has been the difficulty of creating stem cells that match a patient’s genetic background–a must to avoid immune rejection or to study a person’s unique disease fingerprint. The most commonly used protocols to create so-called induced pluripotent stem cells (or iPS cells) have relied on viruses or bacterially based DNA circles called plasmids to introduce the genes necessary to transform a cell from an adult tissue like skin. Unfortunately, these methods work by either popping the genes willy nilly into a cell’s genome without regard to what they might muck up in the process, or they introduce foreign DNA that compromises the ability of the cell to express the necessary genes.

Now Stanford researchers Joseph Wu, MD, PhD; Michael Longaker, MD; and Mark Kay, MD, PhD, have devised a way to use tiny DNA minicircles–about one half the size of regular plasmids–to reprogram stem cells found in human fat. Their research was recently published in Nature Methods (subscription required). You can read our release about the work here.

DNAWellnessinfo.com Resource: http://scopeblog.stanford.edu/archives/2010/02/the-promise-of.html

Colorado company using DNA to predict athletic performance

Posted: 5:19 PM Feb 8, 2010
Reporter: KKTV

Colorado company is testing young athletes’ DNA to find out if they have what it takes to compete at an elite level.

Atlas Sports Genetics uses a cotton swab to take a saliva sample to be sent and analyzed by an Australian lab. The test screens for variants of the gene ACTN3, which is associated with a muscle protein that is commonly found in high levels in elite athletes, such as Olympians. Atlas says the results can help guide young athletes to play in particular sports that are better suited to their physical make-up.

Atlas president Kevin Reiley says if they can direct a young athlete to such a sport at an early age and it can help them get ready to make a run at a college scholarship by the end of their high school career.

“Now the expectation is, when you recruit an athlete at a collegiate level, you want the recruit to be an impact player right away,” says Reiley. “That puts emphasis on high school and junior high to get them up to the point where they can be an impact player right away.”‘

Dr. Matthew Taylor, the Director of Adult Clinical Genetics at the University of Colorado School of Medicine says Atlas can indeed test for the presence of the gene ACTN3 and the associated proteins, but he feels it’s way to early to say the results can predict better performance in certain sports.

“At the moment, you’re welcome to use the test. You might find it interesting,” admits Dr. Taylor. “But anybody who thinks you should use the test to guide or dictate your own athletic work or what your kids do is probably not getting the message. I think it’s too premature.”

Atlas admits there is still plenty of research to be done with such testing, but it feels like the results, combined with a proper training regimen is the best way to identify athletic talent at the present time.

The test costs $169.00 and can be purchased on Atlas’s website at www.atlasgene.com

DNAWellnessinfo.com Resource:  http://www.kktv.com/sports/headlines/83841927.html

Stem Cell Research Makes Another Advance

February 8, 2010 – health Day

MONDAY, Feb. 8 (HealthDay News) — Scientists say they’ve developed a new and easier way to create what’s known as pluripotent stem cells

— cells that can develop into one of many cell types for use in regenerative medicine.

Unlike many other methods, this new technique doesn’t use viruses to introduce genes into cells or permanently alter a cell’s genome. Instead, tiny circles of DNA are used to transform stem cells taken from human fat into induced pluripotent stem cells, which are the starting point for research into many human diseases.

This is the first time that adult (non-embryonic) stem cells have been reprogrammed this way and it could be an important advance toward the use of such cells in humans, according to the Stanford University School of Medicine researchers.

“This technique is not only safer, it’s relatively simple,” study co-author Dr. Michael Longaker, a professor of surgery and deputy director of Stanford’s Institute for Stem Cell Biology and Regenerative Medicine, said in a Stanford news release. “It will be a relatively straightforward process for labs around the world to begin using this technique. We are moving toward clinically applicable regenerative medicine.”

The researchers plan to create pluripotent stem cells to learn more about, and perhaps some day treat, human heart disease.

“Imagine doing a fat or skin biopsy from a member of a family with heart problems, reprogramming the cells to pluripotency and then making cardiac cells to study in a laboratory dish. This would be much easier and less invasive than taking cell samples from a patient’s heart,” study senior author Dr. Joseph Wu, an assistant professor of cardiology and radiology and a member of Stanford’s Cardiovascular Institute, said in the news release.

The study was published online Feb. 7 in the journal Nature Methods.

More information

The U.S. National Institutes of Health has more about stem cells.

DNAWellnessinfo.com Resource:  http://www.usnews.com/health/managing-your-healthcare/womens-health/articles/2010/02/08/stem-cell-research-makes-another-advance.html