Clarkson University Researchers Developing Personalized Medicine
Clarkson University researchers have developed a new way to personalize medicine, according to a report by the Royal Society of Chemistry. The enzymatic logi...

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Season1 (episode1)OneWill MotivationshowRecovering spinal cord injury
show about OneWill recovery process motivation.

By: Willie Hutchinson

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IMG 0421
Lunges to help with gait training.

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Spinal Cord Injury, "Push Girls," and Female Pleasure - K. Kane
"The Site of Insult: Spinal Cord Injury, "Push Girls" and the Ground Zero of Female Pleasure," Krista Kane, Division of Humanities, University of Louisville ...

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On the Road Again: Driving after Spinal Cord Injury
sci.washington.edu Driving can give someone tremendous independence after SCI. Being in control of your transportation may make life a little easier and help...

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Sarasota, FL (PRWEB) March 12, 2014

Erectile dysfunction (ED) is the most commonly studied disorder when it comes to male sexual dysfunction. It is estimated that 18 million men in the US alone suffer from erectile dysfunction and that it appears to be affecting 1 in 4 males under age 40 according to a study published in The Journal of Sexual Medicine.

While the emphasis of treatments for ED focuses on relieving the symptoms, they only provide a temporary solution rather than a cure or reversing the cause.

The DaSilva Institute is excited to announce the recruitment of males suffering from ED, in an IRB study, which will look at the safety, and efficacy of autologous, adipose derived stem cells (ADSCs) in regenerating the causes of ED.

The evidence shows that ADSCs reverses the pathophysiological changes leading to ED, rather than treating the symptoms of ED. Not only is the data in the literature compelling, but our own, in-house, results on our patients have been phenomenal, states Dr. DaSilva.

The many underlying causes for ED that are being investigated range from those secondary to aging, to injury of the cavernous nerve secondary to injury, surgery and/or radiation of the prostate, to diabetic ED and Peyronies Disease to name a few. According to Dr. DaSilva, the possibilities for ADSCs in reversing ED are limitless.

Currently, there is an expansive and growing body of evidence in the medical literature strongly indicating that ADSCs might be a potential cure for ED, rather than merely symptom relief, which is indicative of the increasing interest in ADSC-regenerative options for sexual medicine over the past decade. The DaSilva Institutes goal is to take this from pre-clinical studies to the clinical world offering it to all males that suffer from intractable ED under an IRB approved protocol.

More information about Dr. DaSilva and the DaSilva Institute Guy DaSilva, MD is currently the medical director of the DaSilva Institute of Anti-Aging, Regenerative & Functional Medicine, located in Sarasota, Florida. Dr. DaSilvas enthusiasm for using autologous stem cells in regenerative medicine comes from his early days as a pathologist in New York City back in 1987 and later as a fellow in hematology in1990 following his residency in internal medicine.

He later brought his expertise in molecular and cellular medicine to the University of Kansas Medical Center where he served as chief of Hematology & Hematopathology. He later became the CEO and medical director of HemePath Institute, a diagnostic leader in diagnosing the most difficult cases of leukemia and lymphomas. Most recently, Dr. DaSilva teamed up with one of the most influential stem cell scientist in the world to bring the highest quality and viability of the harvested stem cells, bar none, to the DaSilva Institute.

Dr. DaSilva is board certified and fellowship trained in Anti-Aging and Regenerative Medicine. For more information about Dr. DaSilva or the DaSilva Institute go to http://www.dasilvainstitute.com.

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Boca Raton, Florida (PRWEB) March 12, 2014

The Miami Stem Cell Treatment Center, PC, located in Miami, Ft. Lauderdale, and Boca Raton, Florida, offers a free public seminar on the use of stem cells for various degenerative and inflammatory conditions. They will be provided by Dr. Thomas A. Gionis, Surgeon-in-Chief, and, Dr. Nia Smyrniotis, Medical Director. The next upcoming seminar will be held on March 16th at the Comfort Suites Weston, 2201 N. Commerce Parkway, Weston, Florida 33326, at 2pm.

Regenerative Medicine: Our Procedure The Miami Stem Cell Treatment Center uses Autologous Adult Adipose Stem Cells to provide care for patients suffering from chronic conditions that may benefit from adult stem cell-based regenerative medicine.

The Miami Stem Cell Treatment Center follows the regenerative medicine procedures developed by the California Stem Cell Treatment Centers (CSCTC) and Cell Surgical Network (CSN) which involves the initial screening, examination and evaluation of every potential candidate for stem cell investigational therapy by one of our physicians. Once a patient is deemed to be an appropriate candidate, the procedure itself is performed by our Surgeon-in-Chief, who is assisted by a team of experienced surgical team members and surgical technicians. The entire process from start to finish takes less than two hours. It is relatively painless, and recovery time is minimal.

In recent times, the bone marrow has been a source for stem cells. Taking bone marrow, however, is a painful procedure. Fat, however, contains many times more stem cells than bone marrow and is much easier and safer to harvest.

For many disease types such as cardiac pathology, adipose derived cells appear to be showing superiority to bone marrow derived cells. This may be related to the well documented fact that chronic disease causes bone marrow suppression. Fat derived cells are a natural choice for our investigational work considering their easy and rapid availability in extremely high numbers.

With our current technology, we can harvest your own fat cells, digest the fat cells and separate out the stem cells. The most significant advantage of using your fat as a source for the stem cells, is that the procedure can be done in the office in only a few hours, as the stem cells can be ready for injection after only 60 minutes of processing with our state of the art equipment. Your stem cells do NOT need to be sent out for processing and there is no need for you to travel outside of the U.S. to have them injected.

Indeed, adipose tissue is an abundant source of mesenchymal stem cells, which have shown promise in the field of regenerative medicine. Furthermore, these cells can be readily harvested in large numbers with low donor-site morbidity. During the past decade, numerous studies have provided pre-clinical data on the safety and efficacy of adipose-derived stem cells, supporting the use of these cells in clinical applications. Various clinical trials have shown the regenerative capability of adipose-derived stem cells in numerous fields of medicine. In addition, a great deal of knowledge concerning the harvesting, characterization, and culture of adipose-derived stem cells has been reported.

Our current areas of study include: Heart Failure, Emphysema, COPD, Asthma, Parkinsons Disease, Stroke, Multiple Sclerosis, and orthopedic joint injections. . The investigational protocols utilized by the Miami Stem Cell Treatment Center have been reviewed and approved by an IRB (Institutional Review Board) which is registered with the U.S. Department of Research Protections; and the study is registered with http://www.Clinicaltrials.gov, a service of the U.S. National Institutes of Health (NIH). For more information contact: Miami(at)MiamiStemCellsUSA(dot)com or visit our website: http://www.MiamiStemCellsUSA.com.

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Newswise COLUMBUS, Ohio -- Imagine a world where malfunctioning organs are replaced by new ones made from your own tissues, where infected wounds are cured with a signal from your smartphone, where doctors find the perfect medicine for whatever ails you simply by studying your stem cells.

Its a world thats inching closer to reality because of the work of some of the nations top scientists, many of whom will gather March 13-15 at The Ohio State University for the 7th Annual Translational to Clinical (T2C) Regenerative Medicine Conference to discuss their recent successes and challenges in coaxing the body to heal itself in extraordinary ways.

Regenerative medicine will change the way you and I experience sickness, health and healthcare, said Chandan Sen, director of the Center for Regenerative Medicine and Cell Based Therapies at Ohio States Wexner Medical Center. Because the field is so new, we as researchers are also changing the way we work to be synergistic not competitive, so patients are able to access the benefits more quickly.

And the benefits are desperately needed, says keynote speaker Dr. Anthony Atala, director of the Wake Forest Institute for Regenerative Medicine at Wake Forest Baptist Medical Center.

From chronic diseases such as kidney failure that costs billions of dollars each year to the medical needs of our aging population and the significant injuries sustained by military troops in Afghanistan, developing new treatment paradigms is essential, said Atala, who was selected to lead the $75 million Armed Forces Institute of Regenerative Medicine (AFIRM), a consortium of 30 academic and industry partners in applying regenerative medicine techniques to battlefield injuries.

In theory, every tissue in the body has the ability to regenerate and heal itself. Its good to come to this meeting and exchange ideas that will enable us to harness that remarkable ability.

Other speakers include Elaine Fuchs, Howard Hughes Medical Institute investigator and Rebecca C. Lancefield Professor at Rockefeller University in New York, who has advanced multiple areas of stem cell research through her work in skin cells and genetics; and Dr. Michael Longaker, director of the Hagey Laboratory for Stem Cell Biology for Pediatric Regenerative Medicine at Stanford University. Longaker is considered one of the nations experts in using a combination of stem cell- and bioengineering-based technologies for craniofacial reconstruction.

Several Ohio State College of Medicine and Wexner Medical Center clinician-scientists are also sharing research updates during pre-conference lectures and the meeting:

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The parents of a 2-year-old Pasadena girl who was diagnosed with an aggressive form of leukemia were this week renewing calls for help in their search for a bone marrow donor after stem cells donated from the girls father failed to help.

Sofia Flores, shown in a family photo, needs a bone marrow donor.

Sofia Flores story first came to light in October 2013 when her parents asked for help in finding a bone marrow donor for their daughter.

Sofia needed a marrow transplant to combat acute myeloid leukemia, according to A3M, a Los Angeles nonprofit that is helping Sofias parents seek a match for the little girl.

However, after an extensive search, no match was found.

On Jan. 23, her father donated his stem cells to her, which was the only alternative available at the time, according to Erica Westfall, Sofias mother.

But the treatment was not successful and Sofias cancer relapsed.

Sofias last chance for survival would be a transplant from an unrelated donor in the next two months, according to her mother.

Weve been searching for a bone marrow match even harder because this is her last chance, her father Ignacio Flores said in a video released to news media on Monday.

Sofia has not found a donor through the Be the Match registry, in part because her mixed-race ethnicity makes it difficult to find a compatible donor, according to A3M. Sofia is half white and half Mexican.

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Debbie Nelson swabs her cheek to register for a bone marrow match as Granger Medical Clinic hosts a bone marrow donor registry drive in West Valley City, Tuesday, March 11, 2014.

Ravell Call, Deseret News

WEST VALLEY CITY Heroes sometimes come from unlikely places.

Ethan VanLeuven's hero came in the form of his 21-month-old brother Blake.

Ethan, 4, has been a cancer patient for most of his life. His initial diagnosis of acute lymphoblastic leukemia came in September of 2011. The cancer that was in remission returned in June. His family soon found out that he would need a bone marrow transplant to survive.

In January, Ethan received that transplant from his brother. Siblings have a 25 percent chance of generating a successful bone marrow match.

On Tuesday, Granger Medical Clinic, Be the Match and the American Childhood Cancer Organization held a bone marrow donor drive to help gather potential donors for those who do not find a donor match within their family. The sample collection process is quick, free and may be a lifesaver.

"Really, it's their chance to be a hero. It's their chance to save someone's life," said Jennifer VanLeuven, the boys' mother.

About 20,000 people in the United States needed a bone marrow or umbilical cord transplant in 2011, according to the U.S. Department of Health and Human Services. Of these, only seven out of 10 patients find a match within their families.

To gather the sample, volunteers at the Granger clinic used cotton swabs to collect samples of cheek cells from potential donors. The samples were sent on for testing and the potential donors' name put on an international registry.

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;

A photo of a stem cell testing kit.

TORONTO A 36-year-old leukemia patient is searching for a bone marrow donor for the third time, after his first two donors backed out for medical or unknown reasons.

Chris Taylor was diagnosed with leukemia in 2012. He originally went to Mount Sinai hospital with chest pains and spent several days in the ICU though doctors couldnt figure out what was wrong with him, he said.

But several weeks later, Princess Margaret Hospital found his cancer at the chromosomal level. HE immediately started chemotherapy and it went into remission.

It came back after ten months, he said. I was starting to feel better and the side effects were starting to wear off and then the cancer came back.

They found a match around Christmas of 2013, he said. They started preliminary testing and even got a proposed date but two days before, the donor pulled out.

Unfortunately that donor was medically unfit to donate, Taylor said.

So they went back to searching. They found another donor.

We began again the process of getting ready to go in for the transplant, he said. Unfortunately for unknown reasons that donor had to opt-out of the procedure.

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Man hoping for third stem cell match after first 2 donors back out

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11-Mar-2014

Contact: Karen Richardson krchrdsn@wakehealth.edu 336-716-4453 Wake Forest Baptist Medical Center

WINSTON-SALEM, N.C. March 11, 2014 Discovering where a common virus hides in the body has been a long-term quest for scientists. Up to 80 percent of adults harbor the human cytomegalovirus (HCMV), which can cause severe illness and death in people with weakened immune systems.

Now, researchers at Wake Forest Baptist Medical Center's Institute for Regenerative Medicine report that stem cells that encircle blood vessels can be a hiding place, suggesting a potential treatment target.

In the American Journal of Transplantation (online ahead of print), senior scientist Graca Almeida-Porada, M.D., Ph.D., professor of regenerative medicine at Wake Forest Baptist, and colleagues report that perivascular stem cells, which are found in bone marrow and surround blood vessels in the body's organs, are a reservoir of HCMV.

The virus, which is part of the herpes family, is unnoticed in healthy people. Half to 80 percent of all adults in the U.S. are infected with HCMV, according to the Centers for Disease Control and Prevention. In people with weakened immune systems, including those with HIV, undergoing chemotherapy, or who are organ or bone marrow transplant recipients, the virus can become re-activated.

Once re-activated, HCMV can cause a host of problems from pneumonia to inflammation of the liver and brain that are associated with organ rejection and death.

"There are anti-viral medications designed to prevent HCMV from re-activating, but HVMC infection remains one of the major complications after both organ and bone marrow transplants," said Almeida-Porada. "The question scientists have been asking for years is, 'Where does the virus hide when it is latent?' Maybe if we knew, we could target it."

Scientists have previously shown that one hiding place is hematopoietic stem cells, which give rise to blood cells. "There has been research on and off looking for the other hiding places," said Almeida-Porada. "Identifying the cells that can harbor the virus and are responsible for its re-activation could potentially lead to development of novel targeted therapies."

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Richard France has been visiting Pine Island for 18 years. Each winter he escapes the Ohio winters for the sunny warmth of Pine Island for about six months a year.

"In 2008 I was diagnosed when I was 68 years old with acute leukemia," France said. "I underwent treatments for a fair amount of time, 4 or 5 months - chemotherapy. We usually come down in January but that year we were here for March and April."

He continued, "After that I was in remission for three years but then in 2011 we were here in Florida and I got a call from my doctor. He said the cancer had returned and that I needed to get back to Ohio. They recommended that I have a bone marrow transplant and I got on the transplant list. I think it was under a year when I got word that they had a donor. By then they had decided against a bone marrow transplant and were looking for a stem cell donor. It was the day before Thanksgiving that I went into the hospital and I stayed until almost Christmas. On Nov. 30, I got Laurie Burnworth's stem cells."

Laurie Burnworth stem cell donor and Richard France recipient.

PHOTO PROVIDED

A stem cell (blood or marrow) transplant is the infusion, or injection, of healthy stem cells into your body to replace damaged or diseased stem cells. A stem cell transplant may be necessary if your bone marrow stops working and doesn't produce enough healthy stem cells. A stem cell transplant also may be performed if high-dose chemotherapy or radiation therapy is given in the treatment of blood disorders such as leukemia, lymphoma or multiple myeloma.

"I've been donating blood for years," Burnworth said. "I think I may have signed up for this at one of those times I signed up for blood but I really don't remember. It seems one thing led to another and I believe we were matched up in 2008 and they called me. But that's when Richard went into remission and they held off. Then in 2011 they contacted me again and said 'You are the perfect match for this gentleman and if you're still interested we're going to do this.' After extensive testing we went ahead.

"I think a lot of people don't sign up because they think they take the material from the bone," Burnworth continued. "But in my case you just go to the blood bank, which for me was in Rockford, Ill., and sit in a chair and then you just get hooked up like you're donating blood the difference being though is you're hooked up with both arms. One arm collects the blood where it is sent to a centrifuge that separates the platelets and then the blood is returned through the other arm to your body.

"It's really not a bad process," Burnworth said. "It takes a little time but this is the result. For the first year you can correspond with each other anonymously. Then after a year you sign forms releasing the information. It was Christmas 2012 that I got my phone call from Richard. And, of course, I didn't recognize the phone number so I didn't answer but he left a message and I immediately called back. That's when it really hit me and I cried because Richard and his family got to celebrate Christmas. Then this year they got to celebrate their 50th wedding anniversary and I cried again."

"We meant to get together last year but didn't," France said. "My wife urged that we get together this year and here we are. It's been two years since I got my transplant and I've got another three to go before I'm considered cured. I'm getting pretty much everything back and I feel wonderful and I'm so thankful for Laurie. I wish more people would look into donating organs in general."

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Auckland scientists have discovered new cells with stem cell properties in human skin, opening the door to a range of new treatments for skin diseases and unhealed wounds.

Auckland scientists have discovered new cells with stem cell properties in human skin, opening the door to a range of new treatments for skin diseases and unhealed wounds.

The scientists, Professor Rod Dunbar, Dr Vaughan Feisst, Dr Anna Brooks and Jenni Chen, are members of the Maurice Wilkins Centre for Molecular Biodiscovery, and the research was carried out in the School of Biological Sciences at the University of Auckland.

They identified mesenchymal progenitor cells (MPCs) in the dermis, the middle layer of skin, and discovered that these could turn themselves into fat cells. This signals that they can probably become other types of cells that repair and regenerate tissue, like similar stem cells found in fat and bone marrow.

"Nobody has identified these cells before, so this opens the door to advances in both skin healing and skin diseases," says Professor Dunbar. "Every time you find new cells with stem cell-like properties, you know youre onto something that could have major implications."

"Its a really exciting discovery," he adds. "We try to avoid getting too carried away about our results because were constitutionally cautious - but this discovery is a pretty fundamental finding."

The team hopes that its research, which started in 2011, could eventually lead to treatments for conditions that severely thicken the skin such as keloid scarring, in which tough, irregularly-shaped scars grow and spread. The team also suspects loss of these MPC cells may prevent proper healing, when, for example, radiation treatment for cancer has damaged the skin.

The tissue used in the research came from men and women who had undergone procedures such as liposuction, abdominoplasty or breast reduction with Auckland surgeons Ms Michelle Locke, Mr Jonathan Wheeler and Mr Julian Lofts. All patients consented to their tissue being used for the study.

The research involved sorting many millions of cells - "like sorting mixed-up flocks of sheep into their different breeds", says Professor Dunbar - with a laser-based technology called flow cytometry.

The research is published this week as the cover article in the March 2014 edition of the international journal Stem Cells and Development.

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Newswise SAN DIEGO Elaine Fuchs, Ph.D., will receive the 2014 Pezcoller Foundation-American Association for Cancer Research (AACR) International Award for Cancer Research at the AACR Annual Meeting 2014, to be held in San Diego, Calif., April 5-9, in recognition of her seminal work contributing to the understanding of mammalian skin, skin stem cells, and skin-related diseases, particularly cancers, genetic diseases, and proinflammatory disorders.

Fuchs is the Rebecca C. Lancefield professor and head of the Laboratory of Mammalian Cell Biology and Development at The Rockefeller University in New York, N.Y., and an investigator of the Howard Hughes Medical Institute. She will give her lecture, Stem Cells in Silence, Action, and Cancer, Sunday, April 6, 4:30 p.m. PT, in Halls F-G in the San Diego Convention Center.

Dr. Fuchs is an exceptional scientist, and we are delighted to recognize her pioneering research on the biology of skin stem cells and how they go awry in human diseases of the skin, including cancer, said Margaret Foti, Ph.D., M.D. (hon.), chief executive officer of the AACR. Her seminal studies have had a profound impact not only on the field of cancer research, but also on the research disciplines of genetics and dermatology.

Fuchs is highly regarded for her studies using reverse genetics to understand the biological basis of normal and abnormal skin development and function. Among her important research discoveries was the clarification of the molecular mechanisms underlying the ability of skin stem cells to produce the epidermis and its appendages, including hair follicles and sweat and oil glands. She has also defined how the normal biology of skin stem cells can be deregulated in skin cancers and other hyperproliferative disorders of the skin.

I'm honored, delighted, and humbled to receive this award from the AACR, said Fuchs. My students, postdocs, and staff, present and past, are the ones who truly merit recognition. My group has long had an interest in skin stem cells, how they make and repair tissues, and how this goes awry in cancers. As a basic scientist who studies the fundamental mechanisms underlying stem cell biology and cancer, it is particular pleasing to be recognized not only by basic cancer biologists, but also by physician scientists and clinicians. It is the diversity and breadth of the AACR that make this Society and this honor so special.

The Pezcoller Foundation-AACR International Award, now in its 17th year, recognizes an individual scientist of international renown who has made a major scientific discovery in basic or translational cancer research.

As recipient of this award, Fuchs will also present the Ninth Annual Stanley J. Korsmeyer Lecture at the Venetian Institute for Molecular Medicine in Padua, Italy, prior to the Pezcoller Foundations official award ceremony in Trento, Italy, May 2014.

Fuchs was named one of the inaugural Fellows of the AACR Academy last year. She has received many additional honors throughout her career, including the AACR-Women in Cancer Research Charlotte Friend Memorial Lectureship, the National Medal of Science, the Albany Prize in Medicine, the Kligman-Frost Leadership Award from the Society of Investigative Dermatology, LOreal-Unesco Award, the March of Dimes Prize, and the Pasarow Award for Cancer Research. She is an elected member of the National Academy of Sciences, the Institute of Medicine, the American Philosophical Society, the American Academy of Arts and Sciences, and the European National Academy of Sciences (EMBO).

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PUBLIC RELEASE DATE:

11-Mar-2014

Contact: Lauren Riley lauren.riley@aacr.org 215-446-7155 American Association for Cancer Research

SAN DIEGO Elaine Fuchs, Ph.D., will receive the 2014 Pezcoller Foundation-American Association for Cancer Research (AACR) International Award for Cancer Research at the AACR Annual Meeting 2014, to be held in San Diego, Calif., April 5-9, in recognition of her seminal work contributing to the understanding of mammalian skin, skin stem cells, and skin-related diseases, particularly cancers, genetic diseases, and proinflammatory disorders.

Fuchs is the Rebecca C. Lancefield professor and head of the Laboratory of Mammalian Cell Biology and Development at The Rockefeller University in New York, N.Y., and an investigator of the Howard Hughes Medical Institute. She will give her lecture, "Stem Cells in Silence, Action, and Cancer," Sunday, April 6, 4:30 p.m. PT, in Halls F-G in the San Diego Convention Center.

"Dr. Fuchs is an exceptional scientist, and we are delighted to recognize her pioneering research on the biology of skin stem cells and how they go awry in human diseases of the skin, including cancer," said Margaret Foti, Ph.D., M.D. (hon.), chief executive officer of the AACR. "Her seminal studies have had a profound impact not only on the field of cancer research, but also on the research disciplines of genetics and dermatology."

Fuchs is highly regarded for her studies using reverse genetics to understand the biological basis of normal and abnormal skin development and function. Among her important research discoveries was the clarification of the molecular mechanisms underlying the ability of skin stem cells to produce the epidermis and its appendages, including hair follicles and sweat and oil glands. She has also defined how the normal biology of skin stem cells can be deregulated in skin cancers and other hyperproliferative disorders of the skin.

"I'm honored, delighted, and humbled to receive this award from the AACR," said Fuchs. "My students, postdocs, and staff, present and past, are the ones who truly merit recognition. My group has long had an interest in skin stem cells, how they make and repair tissues, and how this goes awry in cancers. As a basic scientist who studies the fundamental mechanisms underlying stem cell biology and cancer, it is particular pleasing to be recognized not only by basic cancer biologists, but also by physician scientists and clinicians. It is the diversity and breadth of the AACR that make this Society and this honor so special."

The Pezcoller Foundation-AACR International Award, now in its 17th year, recognizes an individual scientist of international renown who has made a major scientific discovery in basic or translational cancer research.

As recipient of this award, Fuchs will also present the Ninth Annual Stanley J. Korsmeyer Lecture at the Venetian Institute for Molecular Medicine in Padua, Italy, prior to the Pezcoller Foundation's official award ceremony in Trento, Italy, May 2014.

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PUBLIC RELEASE DATE:

12-Mar-2014

Contact: Camille Gamboa camille.gamboa@sagepub.com 805-410-7441 SAGE Publications

Los Angeles, CA (March 12, 2014) Researchers have found that sutures embedded with stem cells led to quicker and stronger healing of Achilles tendon tears than traditional sutures, according to a new study published in the March 2014 issue of Foot & Ankle International (published by SAGE).

Achilles tendon injuries are common for professional, collegiate and recreational athletes. These injuries are often treated surgically to reattach or repair the tendon if it has been torn. Patients have to keep their legs immobilized for a while after surgery before beginning their rehabilitation. Athletes may return to their activities sooner, but risk rerupturing the tendon if it has not healed completely.

Drs. Lew Schon, Samuel Adams, and Elizabeth Allen and Researchers Margaret Thorpe, Brent Parks, and Gary Aghazarian from MedStar Union Memorial Hospital in Baltimore, Maryland, conducted the study. They compared traditional surgery, surgery with stem cells injected in the injury area, and surgery with special sutures embedded with stem cells in rats. The results showed that the group receiving the stem cell sutures healed better.

"The exciting news from this early work is that the stem cells stayed in the tendon, promoting healing right away, during a time when patients are not able to begin aggressive rehabilitation. When people can't fully use their leg, the risk is that atrophy sets in and adhesions can develop which can impact how strong and functional the muscle and tendon are after it is reattached," said Dr. Schon. "Not only did the stem cells encourage better healing at the cellular level, the tendon strength itself was also stronger four weeks following surgery than in the other groups in our study," he added.

###

For further information on how to take care of your feet and ankles, or to find a local orthopaedic foot and ankle surgeon, visit the American Orthopaedic Foot & Ankle Society patient website at http://www.footcaremd.org.

"Stem Cell-Bearing Suture Improves Achilles Tendon Healing in a Rat Model" by Samuel B. Adams, Jr, MD; Margaret A. Thorpe, BS; Brent G. Parks, MSc; Gary Aghazarian, BS; Elizabeth Allen, MD; and Lew C. Schon, MD in the March 2014 Foot & Ankle International.

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Mark Mercola, a scientist who studies heart disease at Sanford-Burnham Medical Research Institute.

A team including Sanford-Burnham Medical Research scientists has identified a form of RNA that plays a key role in inducing heart failure.

Called miR-25, the molecule is a short fragment of RNA, called microRNA. In a model of heart failure in mice, increasing the level of miR-25 reduced the efficiency of heart muscle contraction. Inhibiting miR-25 halted heart failure that had already been established.

The study was published Wednesday in the journal Nature. (If link is not live, check later). Scientists from the Icahn School of Medicine at Mount Sinai and UC San Diego collaborated with Sanford-Burnham scientists in the study.

The microRNA molecule blocks activity of a gene called SERCA2a, which regulates the flow of calcium ions into cardiac tissue. The gene has been identified in another study as a target for gene therapy in heart failure.

In this study, led by Sanford-Burnham heart disease researcher Mark Mercola, the gene activity was boosted by using antisense technology to inactivate miR-25. Antisense RNA molecules form a complementary sequence to the specific RNA molecule, called the "sense" molecule, they inactivate. The antisense molecules bind to the targeted RNA molecules, which prevents them from serving as a template for protein production.

The culprit molecule was identified with a functional screening system developed at Sanford-Burnham Mercola said in a Sanford-Burnham press release. Mercola is a professor in the Development, Aging, and Regeneration Program at Sanford-Burnham and a professor of bioengineering at UC San Diego Jacobs School of Engineering.

"Before the availability of high-throughput functional screening, our chance of teasing apart complex biological processes involved in disease progression like heart failure was like finding a needle in a haystack," Mercola said in the press release. "The results of this study validate our approach to identifying microRNAs as potential therapeutic targets with significant clinical value."

The screen searched through all human microRNAs to find those linked to heart failure. Colleagues at the Cardiovascular Research Center at Icahn School of Medicine at Mount Sinai found that injecting the antisense complement to miR-25 stopped heart-failure progression in mice, improved cardiac function and survival.

Heart failure is a progressive loss of the heart's ability to pump blood. It can be caused by heart attacks, high blood pressure, diabetes and other conditions. As heart failure worsens, patients become increasingly restricted in their physical activities. The disease affects nearly six million Americans.

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CHICAGO These days, its faster and cheaper than ever to decipher a persons entire DNA. But a small study suggests that looking for disease risks that way may not be ready for the masses.

For one thing, the research found that gene variants most likely linked with significant disease were the least likely to be accurately identified.

And analyzing the mass of data from the DNA scan is a daunting task, researchers said.

Some experts think more targeted gene-mapping is a better approach. But while whole genome sequencing is mostly done for research, it has far-reaching potential for diagnosing and treating genetic diseases, even in people with no known risks. The new results show its promise and its challenges.

Stanford University researchers performed whole genome sequencing in 12 healthy people. Most of the millions of genetic variants they found were of uncertain significance, although one woman was found to have a high genetic risk for cancer.

DNA is recovered by a simple blood test and deciphered by machines. The difficulty lies in interpreting the findings and figuring out which variants are important and which ones can be ignored. That takes days of sophisticated follow-up lab tests and interpretation to reveal potentially meaningful genetic information, the researchers said.

Dr. Euan Ashley, a senior co-author and Stanford associate professor of medicine and genetics, likened the technology to an unruly teenager who has grown up very fast. Theres huge potential.

This paper is like parental tough love we have to be really honest about where we are in order to bring it up to clinical standards, he said.

For the test, they used two commercially available instruments to sequence the DNA the second one to validate the initial findings. But less than one-third of variants in inherited disease genes were confirmed.

Several specialists including medical geneticists, genetic counselors and a pathologist examined the findings and recommended follow-up tests. Medical intervention was considered appropriate for one participant, a woman with no family history of breast or ovarian cancer found to have a genetic variant strongly linked with those diseases. That finding led to surgery to remove her ovaries and increased breast cancer screening.

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Gene mapping study shows promise, challenges - The ...

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Researchers may have been focusing on the wrong gene

Obesity may be related to the gene IRX3, which is highly expressed in an area of the brain that regulates feeding behavior. Credit: Tony Alter/Flickr

Scientists studying what they thought was a fat gene seem to have been looking in the wrong place, according to research published today inNature. It suggests instead that the real culprit is another gene that the suspected obesity gene interacts with.

In 2007, several genome studies identified mutations in a gene called FTOthat were strongly associated with an increased risk of obesity and type 2 diabetes in humans. Subsequent studies in mice showed a link between the gene and body mass. So researchers, including Marcelo Nbrega, a geneticist at the University of Chicago, thought that they had found a promising candidate for a gene that helped cause obesity.

The mutations were located in non-coding portions ofFTOinvolved in regulating gene expression. But when Nbrega looked closer, he found that something was amiss. These regulatory regions contained some elements that are specific for the lungs, one of the few tissues in which FTOis not expressed. This made us pause, he says. Why are there regulatory elements that presumably regulateFTOin the tissue where it isnt expressed?

This was not the first red flag. Previous attempts to find a link between the presence of the obesity-associated mutations and the expression levels ofFTOhad been a miserable failure, he says. When Nbrega presented his new results at meetings, he adds that many people came to him to say I just knew there was something wrong here.

So Nbregas team cast the net wider, looking for genes in the broader neighborhood ofFTO whose expression matched that of the mutations, and foundIRX3, a gene about half a million base pairs away.IRX3encodes a transcription factor a type of protein involved in regulating the expression of other genes and is highly expressed in the brain, consistent with a role in regulating energy metabolism and eating behavior.

When they examined the looping three-dimensional structure of the chromosome on which both genes sit in mice, zebrafish and human cells, they found that the obesity-associated regions in FTOwere physically in contact with the promoter (the initial gene sequence which acts as an on/off switch) ofIRX3.So the switches that turn onIRX3are actually located far away fromIRX3itself, inside another gene.We think of the genome as a linear thing, but its really a complex 3D structure that coils back onto itself, he says.

Distant genes IRX3also appeared to be strongly linked with obesity. People with one of the obesity-associated mutations showed higher expression ofIRX3,but notFTO, in brain tissue samples, the team found. Nbrega and his colleagues also found that mice lacking the gene weighed 2530% less than mice with a functionalIRX3gene; did not gain weight on a high-fat diet; were resistant to metabolic disorders such as diabetes and had more of the energy-burning cells known as brown fat. The same results were seen in mice in which the expression ofIRX3was blocked in the hypothalamus, a brain region known to regulate feeding behavior and energy balance.

Ins Barroso, a geneticist at the Wellcome Trust Sanger Institute in Hinxton, UK, says that the work answers some of the questions around the biology of the link found in the genome-wide association studies (GWAS). Thats always the tricky thing; a GWAS gives you an association, but its just a marker on the genome, it doesnt actually say anything about which gene its affecting, she says. This strongly suggests that mediation of body mass is going to be throughIRX3rather thanFTO.

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New Contender for 'Fat Gene' Found

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The gene known to be associated with breast cancer susceptibility, BRCA 1, plays a critical role in the normal metabolic function of skeletal muscle, according to a new study led by University of Maryland School of Public Health researchers. Dr. Espen Spangenburg, associate professor of kinesiology, and his laboratory team are the first to identify that the BRCA1 protein is expressed in the skeletal muscle of both mice and humans, and that it plays a key role in fat storage, insulin response and mitochondrial function in skeletal muscle cells. The research is published in the Journal of Lipid Research.

"Our findings suggest that certain mutations in the BRCA1 gene may put people at increased risk for metabolic diseases like obesity and type 2 diabetes," said Dr. Spangenburg. "Without BRCA1, muscle cells store excess fat and start to look diabetic. We believe that the significance of the BRCA1 gene goes well beyond breast cancer risk."

Dr. Spangenburg and colleagues, including researchers from the University of Maryland School of Medicine, Brigham Young University, Karolinska Institutet in Sweden, and East Carolina University, found that the BRCA1 protein exists in both mouse and in human skeletal muscle. This is the first evidence since the discovery of BRCA1 in 1994 that the gene is expressed in human muscle cells.

They further established that the protein produced by the BRCA 1 gene binds with a protein known to play an important role in the metabolism of fat in muscle cells known as Acetyl-CoA carboxylase or ACC. After a period of exercise, the BRCA 1 protein binds to ACC, which helps "turns it off." This deactivation of ACC encourages the utilization of fatty acids by the muscle.

Once they established that the two proteins complex together, they sought to answer if BRCA1 plays a critical role in regulating muscle metabolic function. To do so, they "knocked out" the gene so that it was no longer being expressed in the muscle cells cultured from healthy, active and lean female subjects. This was done using shRNA technology specific for BRCA1 in human myotubes (skeletal muscle fiber cells).

The result was that the muscle cells started to look diseased. The removal of BRCA1 from the cells, which simulated what could happen in the cells of a person with a BRCA1 mutation, resulted in increased lipid storage, decreased insulin signaling, reduced mitochondrial function and increased oxidative stress. These are all key risk factors for the development of metabolic diseases, such as obesity, type 2 diabetes and cardiovascular disease.

"Our findings make it clear that BRCA1 plays a protective role against the development of metabolic disease," Dr. Spangenburg explains. "This gene needs to be there, and should be considered a target to consider in the treatment of type 2 diabetes and/or obesity."

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The above story is based on materials provided by University of Maryland. Note: Materials may be edited for content and length.

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Breast cancer gene could play critical role in obesity, diabetes

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Microarray analysis -- a complex technology commonly used in many applications such as discovering genes, disease diagnosis, drug development and toxicological research -- has just become easier and more user-friendly. A new advanced software program called Eureka-DMA provides a cost-free, graphical interface that allows bioinformaticians and bench-biologists alike to initiate analyses, and to investigate the data produced by microarrays. The program was developed by Ph.D. student Sagi Abelson of the Rappaport Faculty of Medicine at the Technion-Israel Institute of Technology in Haifa, Israel.

DNA microarray analysis, a high-speed method by which the expression of thousands of genes can be analyzed simultaneously, was invented in the late 1980s and developed in the 1990s. Genetic researchers used a glass slide with tiny dots of copies of DNA to test match genes they were trying to identify. Because the array of dots was so small, it was called a "microarray." There is a strong correlation between the field of molecular biology and medical research, and microarray technology is used routinely in the area of cancer research and other epidemiology studies. Many research groups apply it to detect genetic variations between biological samples and information about aberrant gene expression levels can be used in what is called "personalized medicine." This includes customized approaches to medical care, including finding new drugs for gene targets where diseases have genetic causes and potential cures are based on an individual's aberrant gene's signal.

An article written by Abelson published in the current issue of BMC Bioinformatics (2014,15:53) describes the new software tool and provides examples of its uses.

"Eureka-DMA combines simplicity of operation and ease of data management with the rapid execution of multiple task analyses," says Abelson. "This ability can help researchers who have less experience in bioinformatics to transform the high throughput data they generate into meaningful and understandable information."

Eureka-DMA has a distinct advantage over other software programs that only work "behind the scenes" and provide only a final output. It provides users with an understanding of how their actions influence the outcome throughout all the data elucidation steps, keeping them connected to the data, and enabling them to reach optimal conclusions.

"It is very gratifying to see the insightful initiative of Sagi Abelson, a leading 'out-of-the-box' thoughtful Technion doctorate student whom I have had the privilege of supervising," said Prof. Karl Skorecki, the Director of the Rappaport Family Institute for Research in the Medical Sciences at the Technion Faculty of Medicine and Director of Medical and Research Development at the Rambam Health Care Campus. "Over and above his outstanding PhD thesis research project on cancer stem cells, Sagi has developed -- on his own -- a user-friendly computer-based graphical interface for health and biological research studies. Eureka-DMA enables users to easily interpret massive DNA expression data outputs, empowering researchers (and in the future, clinicians) to generate new testable hypotheses with great intuitive ease, and to examine complex genetic expression signatures of genes that provide information relevant to health and disease conditions. This was enabled by combining outstanding insight and expertise in biological and computer sciences, demonstrating the unique multidisciplinary strengths and intellectual freedom that fosters creative innovation at the Technion."

According to Abelson, Eureka-DMA was programmed in MATLAB, a high-level language and interactive environment for numerical computation, visualization, and programming. Advanced users of MATLAB can analyze data, develop algorithms, and create models and applications to explore multiple hypotheses and reach solutions faster than with spreadsheets or traditional software. Eureka-DMA uses many of MATLAB's toolbox features to provide ways to search for enriched pathways and genetic terms and then combines them with other relevant features.

Raw data input is through Windows Excel or text files. This, says Abelson, spares the user from dealing with multiple and less common microarray files received by different manufacturers. Results can then be exported into a 'txt' file format,' or Windows Excel, making Eureka-DMA a unified and flexible platform for microarray data analysis, interpretation and visualization. It can also be used as a fast validation tool for results obtained by different methods.

Eureka-DMA loads and exports genetic data, "normalizes" raw data, filters non-relevant data, and enables pathway enrichment analysis for mapping genes on cellular pathways. The user can browse through the enriched pathways and create an illustration of the pathway with the differentially expressed genes highlighted.

After identifying the differentially expressed genes, biological meaning is ascribed via the software so that the identification of significant co-clustered genes with similar properties -- cellular components, a biological process, or a molecular function -- can be achieved.

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11-Mar-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5271 The JAMA Network Journals

In an exploratory study involving 12 adults, the use of whole-genome sequencing (WGS) was associated with incomplete coverage of inherited-disease genes, low reproducibility of detection of genetic variation with the highest potential clinical effects, and uncertainty about clinically reportable findings, although in certain cases WGS will identify genetic variants warranting early medical intervention, according to a study in the March 12 issue of JAMA.

As technical barriers to human DNA sequencing decrease and costs approach $1,000, whole-genome sequencing (WGS) is increasingly being used in clinical medicine. Sequencing can successfully aid clinical diagnosis and reveal the genetic basis of rare familial diseases. Regardless of context, even in apparently healthy individuals, WGS is expected to uncover genetic findings of potential clinical importance. However, comprehensive clinical interpretation and reporting of clinically significant findings are seldom performed, according to background information in the article. The technical sensitivity and reproducibility of clinical genetic findings using sequencing and the clinical opportunities and costs associated with discovery and reporting of these and other clinical findings remain undefined.

Frederick E. Dewey, M.D., of the Stanford Center for Inherited Cardiovascular Disease, Stanford, Calif., and colleagues recruited 12 volunteer adult participants who underwent WGS between November 2011 and March 2012. A multidisciplinary team reviewed all potentially reportable genetic findings. Five physicians proposed initial clinical follow-up based on the genetic findings.

The researchers found that the use of WGS was associated with incomplete coverage of inherited-disease genes (important parts of the genome for diseases that run in families are not as easy to read as other regions); there was low reproducibility of detection of genetic variation with the highest potential clinical effects (disagreement around the types of variation particularly important for disease); and there was uncertainty about clinically reportable WGS findings (experts disagree on which findings are most meaningful). Two to 6 personal disease-risk findings were discovered in each participant. Physician review of sequencing findings prompted consideration of a median (midpoint) of 1 to 3 initial diagnostic tests and referrals per participant.

The authors write that their clinical experience with this technology illustrates several challenges to clinical adoption of WGS, including that although analytical validity of WGS is improving, technical challenges to sensitive and accurate assessment of individual genetic variation remain. In addition, the human resource needs for full clinical interpretation of WGS data remains considerable, and much uncertainty remains in classification of potentially disease-causing genetic variants.

"These issues should be considered when determining the role of WGS in clinical medicine."

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Examining potential of clinical applications of whole-genome sequencing

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Newswise (PHILADELPHIA) Researchers at the Scheie Eye Institute, the department of Ophthalmology of the University of Pennsylvania have been awarded a five-year, $11.2 million grant from the National Institutes of Health (NIH) to study the genetic risk factors that make African Americans disproportionately more likely to develop primary open-angle glaucoma (POAG). POAG appears almost ten years earlier and progresses more rapidly in African Americans than among Caucasian individuals, making it the leading cause of irreversible blindness in this population. Approximately two million Americans suffer from this form of glaucoma.

The goal of our study is to identify the genetic and other risk factors that underlie POAG in order to understand this increased burden of disease in African Americans, says Joan OBrien, MD, chair of the department of Ophthalmology in Penns Perelman School of Medicine, director of the Scheie Eye Institute, and primary investigator on the study.

POAG is a group of diseases that cause progressive and irreversible retinal ganglion cell damage, optic nerve degeneration, and corresponding visual field loss. Once a sufficient number of nerve cells are damaged, blind spots begin to form in the patients peripheral field of vision. Even when medical and surgical management are employed, retinal ganglion cell loss can be progressive and irreversible.

We aim to understand more about the disease, its causes, and what makes African Americans more prone to developing POAG at a younger age and experiencing its most severe form, says OBrien. Surprisingly, researchers today still have a poor understanding of what causes POAG, which hinders early identification and focused treatment of the disease.

We know that there is a genetic component to the disease, as family history has a strong influence, says OBrien. The risk of developing POAG increases tenfold when a parent or sibling has the disease, with even larger increases when an identical twin is affected. By dissecting the disease into subtypes (called endophenotyping) and understanding the different genetic underpinnings of the disease, we can begin to develop better, more targeted treatment options.

OBrien will work with Scheie glaucoma specialists, Eydie Miller-Ellis, MD; Prithvi Sankar, MD; and Meredith Regina, MD, PhD, to conduct a comprehensive genetic analysis of POAG in African Americans. Their genome-wide analysis will help identify the biological pathways and networks underlying the disease in 12,766 patients: 4,400 with POAG and 8,365 controls. Additional data will be provided by the Kaiser Permanente Research Program, which received ARRA Stimulus funding to analyze 100,000 genomes, with analysis performed in collaboration with Stanford University. To date, 2,500 Philadelphia-based patients and controls have been enrolled in the study.

Our hypothesis is that genetic variants influence the risk of POAG and the traits related to that risk, such as intraocular pressure and corneal and retinal nerve fiber layer thickness. In addition, we believe that demographic and ocular risk factors, and medical co-morbidities also contribute to the increased risk of POAG in African Americans, says OBrien.

Once these genomes are analyzed in this understudied and over-affected population, the data can be used to create a risk model of POAG in African-Americans, and inexpensively re-analyzed to elucidate the genetics of other diseases that disproportionately affect this population. # # #

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11-Mar-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center

STANFORD, Calif. Whole-genome sequencing has been touted as a game-changer in personalized medicine. Clinicians can identify increases in disease risk for specific patients, as well as their responsiveness to certain drugs, by determining the sequence of the billions of building blocks, called nucleotides, that make up their DNA.

Now, researchers at the Stanford University School of Medicine have discovered that although life-changing discoveries can be made, significant challenges must be overcome before whole-genome sequencing can be routinely clinically useful. In particular, they found that individual risk determination would benefit from a degree of improved sequencing accuracy in disease-associated genes. Furthermore, up to 100 hours of manual assessment by professional genetic counselors or informatics specialists is required for detailed genome analysis.

Although the technique was once prohibitively expensive, plummeting costs have been widely expected to rapidly usher whole-genome sequencing into the arena of mainstream health care. However, the researchers' findings indicate that clinical advances from whole-genome sequencing are, at least in the near future, likely to be significantly more expensive and labor-intensive than some patients and clinicians may have been led to believe.

"We need to be very honest about what we can and cannot do at this point in time," said Euan Ashley, MD, associate professor of medicine and of genetics, one of three senior authors of the paper. "It's clear that if we sequence enough cases, we can change someone's life. But with this opportunity comes the responsibility to do this right. Our hope is that the identification of specific hurdles will allow researchers in this field to focus their efforts on overcoming them to make this technique clinically useful."

The paper will be published March 12 in the Journal of the American Medical Association. Michael Snyder, PhD, professor and chair of genetics, and Thomas Quertermous, MD, professor of medicine, also share senior authorship of the paper. Postdoctoral scholar and cardiology fellow Frederick Dewey, MD, genetic counselor Megan Grove, CGC, and postdoctoral scholar Cuiping Pan, PhD, share lead authorship of the paper.

The researchers analyzed the whole genomes of 12 healthy people and took note of the degree of sequencing accuracy necessary to make clinical decisions in individuals, the time it took to manually analyze each person's results and the projected costs of recommended follow-up medical tests.

"This has been an important project for the Stanford team for a number of reasons, not the least of which is that it represents the initial genetics effort to make use of the Stanford GenePool Biobank," said Quertermous, the William G. Irwin Professor in Cardiovascular Medicine. GenePool was recently launched to promote genomic research in a clinical setting and to improve patient care; the 12 people in the study were the first participants in the effort.

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Whole-genome sequencing for clinical use faces many challenges, Stanford study finds

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