Archive for October, 2013

Gene therapy: Sean Ainsworth at TEDxKalamazoo
In the spirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience. At a TED...

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Gene therapy: Sean Ainsworth at TEDxKalamazoo - Video

Muscular Dystrophy #9: How Can We Pay For Gene Therapy of MD?
Jeff Chamberlain, PhD and Bruce Ransom, MD, PhD of The University of Washington drill down on the realities of what it would cost to take the AAV gene therap...

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Muscular Dystrophy #9: How Can We Pay For Gene Therapy of MD? - Video

Johns Hopkins Medicine Media Relations and Public Affairs

JOHNS HOPKINS MEDICINE NEWS TIPS FROM THE 2013 ANNUAL CLINICAL CONFERENCE OF THE AMERICAN COLLEGE OF SURGEONS, OCT. 6-10, WASHINGTON, D.C.

GENE AND STEM CELL THERAPY COMBINATION COULD AID WOUND HEALING

--Findings in elderly mice offer insight into helping elderly people recover from burns

Newswise Johns Hopkins researchers, working with elderly mice, have determined that combining gene therapy with an extra boost of the same stem cells the body already uses to repair itself leads to faster healing of burns and greater blood flow to the site of the wound.

Their findings offer insight into why older people with burns fail to heal as well as younger patients, and how to potentially harness the power of the bodys own bone marrow stem cells to reverse this age-related discrepancy.

As we get older, it is harder for our wounds to heal, says John W. Harmon, M.D., a professor of surgery at the Johns Hopkins University School of Medicine, who will present his findings to the American College of Surgeons Surgical Biology Club on Sunday at 9 a.m. Our research suggests there may be a way to remedy that.

To heal burns or other wounds, stem cells from the bone marrow rush into action, homing to the wound where they can become blood vessels, skin and other reparative tissue. The migration and homing of the stem cells is organized by a protein called Hypoxia-Inducible Factor-1 (HIF-1). In older people, Harmon says, fewer of these stem cells are released from the bone marrow and there is a deficiency of HIF-1. The protein was first discovered about 15 years ago at Johns Hopkins by Gregg L. Semenza, M.D., Ph.D., one of Harmons collaborators.

Harmon and his colleagues first attempted to boost the healing process in mice with burn wounds by increasing levels of HIF-1 using gene therapy, a process that included injecting the rodents with a better working copy of the gene that codes for the protein. That had worked to improve healing of wounds in diabetic animals, but the burn wound is particularly difficult to heal, and that approach was insufficient. So they supplemented the gene therapy by removing bone marrow from a young mouse and growing out the needed stem cells in the lab. When they had enough, they injected those supercharged cells back into the mice.

After 17 days, there were significantly more mice with completely healed burns in the group treated with the combination therapy than in the other groups, Harmon says. The animals that got the combination therapy also showed better blood flow and more blood vessels supplying the wounds.

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Gene and Stem Cell Therapy Combination Could Aid Wound Healing

Public release date: 9-Oct-2013 [ | E-mail | Share ]

Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego

A research team, headed by Theodore Friedmann, MD, professor of pediatrics at the University of California, San Diego School of Medicine, says a gene mutation that causes a rare but devastating neurological disorder known as Lesch-Nyhan syndrome appears to offer clues to the developmental and neuronal defects found in other, diverse neurological disorders like Alzheimer's, Parkinson's and Huntington's diseases.

The findings, published in the October 9, 2013 issue of the journal PLOS ONE, provide the first experimental picture of how gene expression errors impair the ability of stem cells to produce normal neurons, resulting instead in neurological disease. More broadly, they indicate that at least some distinctly different neurodevelopmental and neurodegenerative disorders share basic, causative defects.

The scientists say that understanding defects in Lesch-Nyhan could help identify errant processes in other, more common neurological disorders, perhaps pointing the way to new kinds of therapies.

Lesch-Nyhan syndrome is caused by defects in the HPRT1 gene (short for hypoxanthine guanine phosphoribosyltransferace, the enzyme it encodes), a gene that is well-known for its essential "housekeeping duties," among them helping generate purine nucleotides the building blocks of DNA and RNA.

Mutations in the gene result in deficiencies in the HPRT enzyme, leading to defective expression of the neurotransmitter dopamine and subsequent abnormal neuron function. HPRT mutation is known to be the specific cause of Lesch-Nyhan, an inherited neurodevelopmental disorder characterized by uncontrollable repetitive body movements, cognitive defects and compulsive self-mutilating behaviors. The disorder was first described in 1964 by medical student Michael Lesch and his mentor, William Nyhan, MD, professor emeritus at UC San Diego School of Medicine.

Using mouse embryonic stem cells modified to be HPRT-deficient, Friedmann and colleagues discovered that the cells do not develop normally. Instead, they differentiate from full-fledged neurons into cells that resemble and partially function as neurons, but also perform functions more typical of glial cells, a kind of supporting cell in the central nervous system. In addition, they noted that HPRT deficiency causes abnormal regulation of many cellular functions controlling important operational and reproduction mechanisms, DNA replication and repair and many metabolic processes.

"We believe that the neural aberrations of HPRT deficiency are the consequence of these combined, multi-system metabolic errors," said Friedmann. "And since some of these aberrations are also found in other neurological disorders, we think they almost certainly play some role in causing the neurological abnormalities in diseases like Alzheimer's, Parkinson's, Huntington's and possibly others. That makes them potential therapeutic targets for conditions that currently have limited or no treatments, let alone cures."

The task now is to further parse and better understand the many pathways that cause abnormal brain and brain cell development, and how those pathways are also disturbed in other neurological disorders. Those defects will probably not affect HPRT directly, said Friedmann, but rather will correspond to some of the same metabolic and genetic errors that occur as a result of HPRT deficiency. Once those pathways are identified, they may become good targets for more effective forms of therapy.

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Single gene mutation linked to diverse neurological disorders

Washington, Oct. 9 (ANI): A new research has found that sunscreen when applied properly can prevent three types of skin cancer and protect the superhero gene p53, which works to repair sun-damaged skin.

According to researchers, sunscreen provides 100 per cent protection against all three forms of skin cancer: BCC (basal cell carcinoma); SCC (squamous cell carcinoma); and malignant melanoma.

Lead researcher Dr Elke Hacker, from QUT's AusSun Research Lab, said sunscreen also shielded the important p53 gene, a gene that works to prevent cancer.

She said that as soon as our skin becomes sun damaged, the p53 gene goes to work repairing that damage and thereby preventing skin cancer occurring, but over time if skin gets burnt regularly the p53 gene mutates and can no longer do the job it was intended for - it no longer repairs sun damaged skin and without this protection skin cancers are far more likely to occur.

The study looked at the impact of sunlight on human skin, both with and without sunscreen, and found no evidence of UV-induced skin damage when proper application of sunscreen (SPF30+) had been applied to exposed area.

The study has been published in the Pigment Cell and Melanoma Research journal. (ANI)

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Sunscreen protects sun-damaged skin repairing 'superhero' gene

Gene Munster, Senior Research Analyst at Piper Jaffray, reports that teens are overwhelmingly buying Apple products. What does that mean for Apple in the long-run?

Kids these days are said to show no brand allegiance. But when it comes to the Apple, teens are fiercely loyal fans, according to new research by one noted analyst. As the new iPad is set for its debut on October 22, is Apple a long-term generational play?

Gene Munster, Senior Research Analyst at Piper Jaffray, is one of the best-known Apple analysts. He and his team recently conducted a survey of 8,643 teenagers about what kind of mobile phone and tablet devices they use. The winner was Apple by wide margin.

(Read: Julian Robertson sells Apple because Steve Jobs was 'mean')

Teen ownership of iPhones has gone from 40% in the fall of 2012 to 55% today. That number is expected to grow as 65% of teens expect their next phone to be an iPhone.

When it comes to teen ownership of table devices, Apple trounces its competition. While 44% of teens don't own tablets, the ones that do emphatically choose the iPad; 68% own an iPad (60% have the full-sized version while 8% have the iPad mini). Of those that plan on buying a tablet in the next six month, 64% say they want an Apple product.

(Read: Forget the iPhone 5S, let's talk about the iPhone 6)

Now Apple is expected to release its latest iPad, a thinner version of its previous full-sized models with an A7X processor, its newest. It may even include a fingerprint scanner like the ones found in the latest iPhones, according to Current Editorials.

What does this all mean for Apple's stock? We talk numbers with Gene Munster on his research and the expected new iPad.

To see what Gene Munster has to say on Apple's future, watch the video above.

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This is good for Apple’s long-term growth: Munster

Public release date: 9-Oct-2013 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, October 9, 2013A national survey has found that uterine fibroids have a disproportionate impact on African American women, causing more severe symptoms, interfering with their daily life, and causing them to miss work. These new findings are reported in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Women's Health website at http://www.liebertpub.com/jwh.

African American women have a 3-fold higher incidence of uterine fibroids and tend to have them at an earlier age. In "The Burden of Uterine Fibroids for African American Women: Results of a National Survey," authors Elizabeth Stewart, MD, Wanda Nicholson, MD, MPH, MBA, Linda Bradley, MD, and Bijan Borah, PhD, Mayo Clinic and Mayo Medical School, Rochester, MN, University of North Carolina School of Medicine, Chapel Hill, and Cleveland Clinic, OH, describe the symptoms, concerns, and quality of life issues African American women are more likely to face than are other women with uterine fibroids.

Early intervention to reduce the high risk of hysterectomy and preserve the fertility of this disproportionately affected group of women should be considered, proposes Gloria Richard-Davis, MD, University of Arkansas Medical Sciences, Little Rock, AR, in the accompanying Editorial, "Uterine Fibroid: The Burden Borne by African American Women."

"Uterine fibroids are a major source of morbidity for reproductive-aged women, and this is especially true for African American women," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA, and President of the Academy of Women's Health.

###

About the Journal

Journal of Women's Health, published monthly, is a core multidisciplinary journal dedicated to the diseases and conditions that hold greater risk for or are more prevalent among women, as well as diseases that present differently in women. The Journal covers the latest advances and clinical applications of new diagnostic procedures and therapeutic protocols for the prevention and management of women's healthcare issues. Complete tables of content and a sample issue may be viewed on the Journal of Women's Health website at http://www.liebertpub.com/jwh. Journal of Women's Health is the Official Journal of the Academy of Women's Health and the Society for Women's Health Research.

About the Academy

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New study shows uterine fibroids have greater impact in African-American women

Will Martin, with his mother, Lori. Will was 2 when Lori learned he was born with Leigh's Syndrome, a progressive genetic condition. So far it's given him low muscle tone and some difficulty with speech.

Mark Sauer of the Columbia University Medical Center, a member of one of two teams of U.S. scientists pursuing the research, calls the effort to prevent infants from getting devastating genetic diseases "noble." Sauer says the groups are hoping "to cure disease and to help women deliver healthy, normal children."

But the research also raises a variety of concerns, including worries it could open the door to creating "designer babies." The Food and Drug Administration has scheduled an Oct. 22 hearing to consider the issues.

Specifically, the research would create an egg with healthy mitochondrial DNA (mtDNA). Unlike the DNA that most people are familiar with the 23 pairs of human chromosomes that program most of our body processes mtDNA is the bit of genetic material inside mitochondria, living structures inside a cell that provide its energy.

Scientists estimate that 1 in every 200 women carries defects in her mtDNA. Between 1 in 2,000 and 1 in 4,000 babies may be born each year with syndromes caused by these genetic glitches; the syndromes range from mild to severe. In many cases, there is no treatment, and the affected child dies early in life.

Lori Martin, 33, of Houston, found out her son, Will, was born with the mitochondrial disease known as Leigh's syndrome, when he was about 2 years old.

"The experience of being told that your son is basically going to die and you don't know when or how, but it's obviously life-changing, and it completely wrecks your world," Martin says.

Martin and her husband are trying to help Will live as long and as happy a life as they can. And they want more kids. But her doctor advised against it.

"Since I am a carrier, I've been told it's recommended I do not have any more biological children using my eggs," Martin says. "It's a really devastating blow to be told not to have more children."

The proposed research might help Martin and women like her.

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Proposed Treatment To Fix Genetic Diseases Raises Ethics Issues

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Somewhere between the ideas of resurrecting extinct species and engaging in genetic engineering of existing ones lies space for a conversation about a third potential approach to fending off conservation disaster.

"Facilitated adaptation" is the name given this concept, and the suggestion to talk about it comes in part from Brett Dickson, assistant research professor at Northern Arizona University.

As coauthor of a comment piece in Nature, Dickson helps bring the topic to the forefront of scientific discussion. As a researcher, his dual affiliation and multiple pursuits illustrate the complexity of proactively facing the potential loss of 40 percent of species by 2050.

At NAU, Dickson directs the Lab of Landscape Ecology and Conservation Biology in the Landscape Conservation Initiative. But he is also president and chief scientist of Conservation Science Partners, a nonprofit organization that brings together experts in various disciplines to address conservation issues such as habitat fragmentation, landscape connectivity and the spread and distribution of infectious diseases across animal populations.

Considering the looming loss of species, Dickson said it is surprising that facilitated adaptationessentially, taking a genetically proactive approach to improve the prospects of a particular animal populationhas not gotten much attention.

"My colleagues and I thought this would be a compelling idea ready for debate, although it's not necessarily ready to be put immediately into widespread practice," Dickson said.

Rather than taking the "very challenging" step of physically moving animal populations threatened by climate change, which has been tried with mixed success, facilitated adaptation entails "moving adaptive alleles from one population to another," Dickson said. Alleles determine traits (such as a thick coat of hair versus thin in mammals). So traits that bolster a well-adapted population of a particular species could be transferred to a population under stress.

From a technical standpoint, Dickson said, the science is already being demonstrated with genetically modified organisms in the plant world. Although facilitated adaptation does not go as far as genetic engineering, the Nature coauthors agree that even such a mitigated step would be drastic, with profound ethical implications.

"If we feel strongly as a society this is something we should explore, then perhaps piloting a program would be warranted," Dickson said, with a caveat: "Facilitated adaptation should not be considered a substitute for preventing the loss of habitats or the species that depend on them."

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Impending species loss opens 'compelling' genetic discussion

Oct. 9, 2013 Using mice, lab-grown cells and clues from a related disorder, Johns Hopkins researchers have greatly increased understanding of the causes of systemic sclerosis, showing that a critical culprit is a defect in the way certain cells communicate with their structural scaffolding. They say the new insights point the way toward potentially developing drugs for the disease, which affects approximately 100,000 people in the United States.

"Until now we've had little insight and no effective treatment strategies for systemic sclerosis, and many patients die within a year of diagnosis," says Hal Dietz, M.D., the Victor A. McKusick Professor of Genetics and Medicine in the Johns Hopkins' Institute of Genetic Medicine, director of the Smilow Center for Marfan Syndrome Research at Johns Hopkins and Howard Hughes Medical Institute investigator. "Our group created mouse models that allowed us to learn about the sequence of events that leads to the disease's symptoms, and we hope drugs can be developed that target one or more of these events." The Dietz team's results are described in the Oct. 10 issue of Nature.

Patients with systemic sclerosis, also known as systemic scleroderma, experience a sudden hardening, or fibrosis, of the skin. For some patients, this hardening occurs only in limited areas, but for others, it quickly spreads across the body and to organs such as the heart, intestines and kidneys. It is this fibrosis of the internal organs that is often fatal.

Systemic sclerosis rarely runs in families, Dietz says, making the gene for the disease, if it exists, very difficult to find. Without a known genetic mutation, researchers had not been able to create a genetically altered mouse with which to study the condition. But Dietz's group was struck by the similarities between systemic sclerosis and a less severe, much rarer condition called stiff skin syndrome (SSS), which does run in families, and they suspected that learning more about SSS would also shed light on systemic sclerosis.

In a previous experiment , they pinpointed the genetic mutation responsible for SSS in a gene for a protein called fibrillin-1, which plays a role in other connective tissue disorders. In certain types of tissues, including skin, fibrillin-1 helps make up the scaffolding for cells. The specific changes in fibrillin-1 seen in SSS patients were predicted to impair the ability of cells to make contact with fibrillin-1 through bridging molecules called integrins.

In the current study, M.D./Ph.D. student Elizabeth Gerber created a line of mice with a genetic variant similar to that found in SSS patients. To test the group's hypothesis, Gerber also created a line of mice with a variant the team knew would prevent fibrillin-1 from interacting with integrin. As the team expected, both groups of mice developed patches of stiff skin, along with elevated levels of proteins and cells involved in the immune response -- much like humans with SSS or systemic sclerosis. "It seemed we were right that the SSS mutation causes the condition by blocking fibrillin's interaction with integrin," Dietz says. "Something else we found was that both types of mice had high levels of integrin in their skin, which made us think their cells were trying to compensate for the lack of fibrillin-integrin interaction by making more and more integrin."

This still left open the question of what was ultimately causing fibrosis, however: Was it the integrin levels or the immune response? Dietz's group delved deeper into the question by creating mice that had both the SSS mutation and artificially low levels of integrin, and found that the mice never developed fibrosis or an abnormal immune response. "They looked normal," Dietz says.

The team next tried waiting until mice with the SSS mutation had developed fibrosis, then treating them with a compound known to block a key molecule with known connections to both fibrosis and the immune response. This reversed the mice's skin fibrosis and immunologic abnormalities. The team also tested the compounds on lab-grown human skin cells with systemic sclerosis, with the same results. This raises the possibility that systemic sclerosis patients could eventually be treated with similar compounds in humans, Dietz says. A number of the compounds that proved effective in SSS mice and systemic sclerosis cells are currently being explored by drug companies for the treatment of other conditions, prominently including cancer.

The results raised another big question for the team: Which of the several types of skin cells were responsible for the runaway immune response and fibrosis? They traced the activity to so-called plasmacytoid dendritic cells, or pDCs, a cell type known to either tamp down or ramp up immune response, depending on the circumstances.

"Dietz's work gives scleroderma patients hope that we have gained fundamental insights into the process of fibrosis in scleroderma. In particular, I am confident that within a relatively short time, novel therapies can be tested in patients, and I am optimistic that such treatments will have a profound effect," says Luke Evnin, Ph.D., chairman of the board of directors of the Scleroderma Research Foundation and a scleroderma patient.

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Likely causes and treatment strategies for systemic scleroderma identified

MONTREAL, Oct. 9, 2013 /PRNewswire/ - Hundreds of researchers from North America, Europe, Australia and Asia have joined together in a consortium to identify the genetic basis of the five most common forms of cancer - breast, prostate, lung, ovarian and colorectal. The group, called the OncoArray Consortium, developed a new customized genotyping tool - the OncoArray - manufactured by the U.S. genomics firm Illumina, Inc.

"The U.S. National Cancer Institute (NCI)-funded Genetic Associations and Mechanisms of Oncology (GAME-ON) initiative has been instrumental in bringing together multiple consortia and provides primary funding for the OncoArray Consortium. It allowed us to design a custom array that incorporates some 530,000 markers, which is planned for genotyping on over 425,000 samples from patients with one of the five types of cancer and control subjects from around the world. The sheer size of the sample is unprecedented for a study on the genetic factors involved in cancer. The OncoArray Consortium's work will provide insight into the inherited genetic basis of cancer and help scientists understand the underlying biology of cancer," explained Professor Christopher Amos, Head of Dartmouth's Center for Genomic Medicine, in the US, and the leader of the Lung Cancer consortium.

This project is a direct extension of the work that has been achieved in recent years through the Collaborative Oncological Gene-Environment Study (COGS). "The OncoArray will allow us to enhance our current understanding of the genetic factors associated with the risk of multiple cancers," explained Cancer Research UK funded Professor Douglas Easton of University of Cambridge (United Kingdom). "We are proud to be involved in this international initiative, which will significantly accelerate the pace of discovery and lead to a greater understanding of a disease that affects one in three people," he continued.

About 200 studies are involved in this project and nearly 50 countries participate in the consortium.

Breast cancer samples will represent more than one-third of the samples under analysis. "This is the largest number of samples ever used for research into the genetic basis of breast cancer risk," noted Universit Laval Professor Jacques Simard, who works at the Genomics Centre of the CHU de Qubec Research Centre, and chair holder of the Canada Research Chair in Oncogenetics. Qubec is at the forefront of this study, since the results will be used for a Qubec-based project aiming to improve the early detection of breast cancer, an initiative funded by Gnome Qubec, Genome Canada, the CIHR and the Qubec Breast Cancer Foundation. "The work of Professor Jacques Simard will broaden our current understanding of this terrible disease, leading to better risk stratification tools that will increase our ability to deliver better-targeted screening services to those women at higher risk," said Marc LePage, President and CEO of Gnome Qubec.

Leading efforts in prostate cancer are Brian Henderson and Ros Eeles. "The OncoArray will provide fresh clues to the origin of these cancers and will hasten novel approaches to prevention and treatment," Dr. Henderson said. "Every year 220,000 men in the US are diagnosed with prostate cancer, and there are 30,000 deaths. This indicates many people are being treated who don't need it. We hope this product will help us focus on the men who have the highest risk to the more fatal forms of this disease."

"This new research consortium will give us a fantastic opportunity to look at huge numbers of gene variants in prostate cancer patients across the world, helping expand our knowledge of the genetic basis of this disease," said Ros Eeles, Professor of Oncogenetics at The Institute of Cancer Research, London, which along with the University of Cambridge.

Leading efforts in colorectal cancer is Kenneth T. Norris Jr. Chair in Cancer Prevention, Keck Medicine of USC, and Stephen Gruber, director, USC Norris Comprehensive Cancer Center, Keck Medicine of USC. Leading efforts in breast cancer on behalf of the US NCI are David J. Hunter, Dean for Academic Affairs, Harvard School of Public Health; for ovarian cancer the US NCI leader is Tom Sellers, Director of the Moffit Cancer Center in Florida. In addition, the Consortium of Investigators of Modifiers of BRCA1/2, led by Georgia Chenevix-Trench, will genotype the OncoArray on about 30,000 women and men who carry mutations in the BRCA1 or BRCA2 genes.

The project is funded through major grants from the U.S. National Cancer Institute to the GAME-ON initiative and the Division of Cancer Epidemiology and Genetics; Genome Canada/Gnome Qubec/CIHR/Qubec Breast Cancer Foundation through the Personalized Risk Stratification for Prevention and Early Detection of Breast Cancer; Cancer Research UK (Cambridge University and The Institute of Cancer Research); Movember and Prostate Cancer UK (The Institute of Cancer Research) and EU's FP7 grant program (COGS), together with many other partners.

Link:
New Discoveries for Cancer Risk: Researchers Worldwide Take Part in one of History's Largest Scientific Consortium

This micrograph shows a single mitochondrion (yellow), one of many little energy factories inside a cell.

The federal government is considering whether to allow scientists to take a controversial step: make changes in some of the genetic material in a woman's egg that would be passed down through generations.

Mark Sauer of the Columbia University Medical Center, a member of one of two teams of U.S. scientists pursuing the research, calls the effort to prevent infants from getting devastating genetic diseases "noble." Sauer says the groups are hoping "to cure disease and to help women deliver healthy, normal children."

But the research also raises a variety of concerns, including worries it could open the door to creating "designer babies." The Food and Drug Administration has scheduled an Oct. 22 hearing to consider the issues.

Specifically, the research would create an egg with healthy mitochondrial DNA (mtDNA). Unlike the DNA that most people are familiar with the 23 pairs of human chromosomes that program most of our body processes mtDNA is the bit of genetic material inside mitochondria, living structures inside a cell that provide its energy.

Scientists estimate that 1 in every 200 women carries defects in her mtDNA. Between 1 in 2,000 and 1 in 4,000 babies may be born each year with syndromes caused by these genetic glitches; the syndromes range from mild to severe. In many cases, there is no treatment, and the affected child dies early in life.

Lori Martin, 33, of Houston, found out her son, Will, was born with a genetic malady known as Leigh's syndrome, when he was about 2 years old. The progressive illness was linked to genetic problems in his mitochondria.

Will Martin, with his mother, Lori. Will was 2 when Lori learned he was born with Leigh's syndrome, a progressive genetic condition. So far it's given him low muscle tone and some difficulty with speech.

Will Martin, with his mother, Lori. Will was 2 when Lori learned he was born with Leigh's syndrome, a progressive genetic condition. So far it's given him low muscle tone and some difficulty with speech.

"The experience of being told that your son is basically going to die and you don't know when or how, but it's obviously life-changing, and it completely wrecks your world," Martin says.

Original post:
Proposed Treatment To Fix Genetic Diseases Raising Ethics Issues

This micrograph shows a single mitochondrion (yellow), one of many little energy factories inside a cell.

The federal government is considering whether to allow scientists to take a controversial step: make changes in some of the genetic material in a woman's egg that would be passed down through generations.

Mark Sauer of the Columbia University Medical Center, a member of one of two teams of U.S. scientists pursuing the research, calls the effort to prevent infants from getting devastating genetic diseases "noble." Sauer says the groups are hoping "to cure disease and to help women deliver healthy, normal children."

But the research also raises a variety of concerns, including worries it could open the door to creating "designer babies." The Food and Drug Administration has scheduled an Oct. 22 hearing to consider the issues.

Specifically, the research would create an egg with healthy mitochondrial DNA (mtDNA). Unlike the DNA that most people are familiar with the 23 pairs of human chromosomes that program most of our body processes mtDNA is the bit of genetic material inside mitochondria, living structures inside a cell that provide its energy.

Scientists estimate that 1 in every 200 women carries defects in her mtDNA. Between 1 in 2,000 and 1 in 4,000 babies may be born each year with syndromes caused by these genetic glitches; the syndromes range from mild to severe. In many cases, there is no treatment, and the affected child dies early in life.

Lori Martin, 33, of Houston, found out her son, Will, was born with a genetic malady known as Leigh's syndrome, when he was about 2 years old. The progressive illness was linked to genetic problems in his mitochondria.

Will Martin, with his mother, Lori. Will was 2 when Lori learned he was born with Leigh's syndrome, a progressive genetic condition. So far it's given him low muscle tone and some difficulty with speech.

Will Martin, with his mother, Lori. Will was 2 when Lori learned he was born with Leigh's syndrome, a progressive genetic condition. So far it's given him low muscle tone and some difficulty with speech.

"The experience of being told that your son is basically going to die and you don't know when or how, but it's obviously life-changing, and it completely wrecks your world," Martin says.

Read more:
Proposed Treatment To Fix Genetic Diseases Raises Ethical Issues

PHILADELPHIA D. Gary Gilliland, MD, PhD, has been named the inaugural Vice Dean and Vice President for Precision Medicine, a newly created role to position Penn Medicine as the nations top leader in the delivery of individualized medicine.

Dr. Gilliland, a cancer genetics expert and pioneer in the development of targeted therapies, will synthesize Penn Medicines research and clinical care initiatives across all disciplines to create a national model for the delivery of precise, personalized medicine to patients with diseases of all kinds. He will work with the institutions top leaders in cancer, heart and vascular medicine, neurosciences, genetics, pathology, and many other specialties.

We are proud to be among the first institutions in the country to create a position to oversee the tremendous opportunities and challenges that face us as our physicians and scientists work to hone the promise of the burgeoning and exciting field of precision medicine, says J. Larry Jameson, MD, PhD, Executive Vice President of the University of Pennsylvania for the Health System and Dean of the Perelman School of Medicine. Dr. Gillilands experience as a leader in both academic medicine and the pharmaceutical industry will help Penn Medicine forge a roadmap for the most effective and efficient ways to conduct research and deliver care in this new field.

The establishment of the new role builds on such existing Penn Medicine efforts as the Institute for Translational Medicine and Therapeutics and the newly launched Center for Personalized Diagnostics.

Penn Medicine already has a strong base in this new field, and Dr. Gillilands background and accomplishments will provide experienced leadership to take us to the next level of excellence, says Ralph W. Muller, Chief Executive Officer of the University of Pennsylvania Health System. No matter what its called precision medicine, personalized medicine, or individualized medicine this extremely promising approach will better equip physicians to match the most effective treatment to each patients specific disease.

Gilliland joins Penn Medicine from Merck, where he was recruited in 2009 as Senior Vice President of Merck Research Laboratories and Oncology Franchise Head, following a long career at Harvard Medical School. At Merck, he was responsible for end-to-end research and development of its Global Oncology Programs. He oversaw first-in-human studies, proof-of-concept trials, and Phase II/III registration trials, and managed all preclinical and clinical oncology licensing activities.

Prior to joining Merck, Gilliland was a member of the faculty at Harvard Medical School for nearly 20 years, where he served as Professor of Medicine and a Professor of Stem Cell and Regenerative Biology. He was also an Investigator of the Howard Hughes Medical Institute, Director of the Leukemia Program at the Dana-Farber/Harvard Cancer Center, and Director of the Cancer Stem Cell Program of the Harvard Stem Cell Institute.He saw patients at numerous top Boston hospitals, serving as an attending physician in the Bone Marrow Transplant Service of Childrens Hospital; attending physician in medical oncology at Dana-Farber Cancer Institute; and senior attending physician at Brigham and Womens Hospital.

As an investigator studying hematologic malignancies, Gilliland made seminal discoveries that have contributed to the understanding of the genetic basis of leukemias and other cancers that affect the blood and bone marrow. He has worked to help apply these findings into the development of new investigational cancer treatments, including molecularly targeted therapies, and has advanced this research into all phases of clinical development.

His work has earned him numerous honors, including the William Dameshek Prize from the American Society of Hematology, the Emil J. Freireich Award from the MD Anderson Cancer Center, and the Stanley J. Korsmeyer Award from the American Society for Clinical Investigation. He is an elected member of the America Society for Clinical Investigation and the American Association of Physicians.

He received his Ph.D. in Microbiology from the University of California, Los Angeles, and his M.D. from the University of California, San Francisco. He completed his internship and residency, including serving as Chief Medical Resident, at Brigham and Women's Hospital, Harvard Medical School. He completed his Hematology and Medical Oncology training at the Brigham and Womens Hospital and the Dana-Farber Cancer Institute, respectively.

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Penn Medicine Names First Leader of Precision Medicine to Speed Delivery of Tailored Treatments to Patients

SALT LAKE CITY, Oct. 9, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced it will present data showing the high prevalence and overlap between hereditary colon cancer and hereditary breast and ovarian cancer in patients previously diagnosed with endometrial and ovarian cancer. Myriad is presenting this data and another hereditary cancer study at the 2013 National Society of Genetic Counselors annual meeting in Anaheim, California.

"Myriad is committed to advancing the scientific understanding of hereditary cancers and developing innovative diagnostic tests to benefit a broad range of cancer patients," said Richard J. Wenstrup, chief medical officer of Myriad. "Our data show there is both a high prevalence and overlap of hereditary cancer syndromes in patients with endometrial and ovarian cancers, which supports the use of myRisk Hereditary Cancer testing to accurately diagnose patients and select appropriate medical management."

Key data being presented at the NSGC annual meeting include:

Prevalence of Lynch Syndrome and HBOC among Patients with Primary Endometrial and Primary Ovarian Cancers [Raymond et al., Oct. 11, 2013 2:45 -- 3:00 p.m.]

This study assessed the prevalence of hereditary colon cancer and hereditary breast and ovarian cancer in patients with both primary endometrial and ovarian cancer. Under current National Comprehensive Cancer Network guidelines these patients would meet the medical criteria for both hereditary breast and ovarian cancer testing and hereditary colon cancer testing. Results showed that among 1,529 patients evaluated, 11.2 percent had a deleterious mutation with 73.3 percent of the mutations in hereditary colon cancer genes and 26.7 percent in hereditary breast cancer genes. Although the prevalence of hereditary colon cancer was higher than hereditary breast cancer in patients with endometrial and ovarian cancers, these patients showed a strong family history overlap between the two syndromes. The findings suggest these patients would be appropriate candidates for testing with a hereditary cancer panel to prevent a missed diagnosis of hereditary cancer.

Prevalence of Lynch Syndrome Mutations in Patients with Colorectal and Endometrial Cancer Based on Decade of Diagnosis [Mendonca et al., Oct. 11, 2013 12:45 -- 1:45 p.m.]

This study evaluated the prevalence of deleterious mutations in patients with colorectal and endometrial cancer based on a decade of diagnosis. Data was obtained from 20,000 patients with colorectal cancer and/or endometrial cancer. The deleterious mutation rate was analysed based on the age of diagnoses. Colorectal cancer patients diagnosed in their 40s had an 11.5 percent mutation rate and patients diagnosed in their 50s saw a 10.9 percent mutation rate, while patients in their 60s experienced a still very high 8.3 percent mutation rate. Although hereditary colon cancer is associated with onset at an earlier age, these data show the importance of genetic testing for deleterious mutations in all patients, regardless of their age at diagnosis.

Additionally, Myriad scientists will participate in the following highlighted symposia:

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests is based on an understanding of the role genes play in human disease and was developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website at: http://www.myriad.com and our social media channels: Twitter and Facebook.

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Myriad Genetics Study Highlights Importance of myRisk(TM) Hereditary Cancer Testing

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IBM is going through gene therapy, and by that we don't mean an expensive course of Freudian analysis for its Blue Gene/Q supercomputer, but rather a wholesale change in how the company approaches cloud computing.

The bout of "gene therapy" is due to IBM's buy of bare-metal cloud specialist SoftLayer in June, Mac Devine, CTO of IBM's cloud services division, told El Reg.

The acquisition is leading to major changes in how the company approaches the cloud sector: Big Blue is splicing its existing tech into SoftLayer and vice versa, and the resulting gear was announced on Tuesday.

These changes should let IBM "alter the DNA" of the way in which it approaches cloud technology, Devine said.

To that end, IBM is starting to move cloud products over to infrastructure hosted on SoftLayer. The first such move is IBM's "Social Learning Platform", which is a cloud-based technology platform for sharing videos and other information between institutions such as hospitals.

"When you move from a different type of software development approach to a cloud-first approach you have to be willing to get things out quickly," Devine said. "One of the things that was attractive about SoftLayer [was] when they go to deploy a new service if they couldn't 100 per cent automate the configuration and operations... they wouldn't deploy."

This is a very different approach to the technologies IBM had put in place with much of its prior SmartCloud portfolio, Devine admitted. "Softlayer is the center of gravity of all of our cloud strategy," Devine said. "We believe that we need to adapt the processes and ways we did traditional business."

IBM is also planning to upgrade SoftLayer, he said, by tearing off the provisioning and infrastructure components of SmartCloud and injecting them into SoftLayer's systems.

It has already done part of this by combining SoftLayer and SmartCloud technologies in another bid for a strategically important $600m IBM cloud contract with the CIA, which Big Blue is battling Amazon for. (A judge ruled on Monday that Amazon's spook cloud may still go ahead, but IBM is appealing that decision.)

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IBM checks itself into therapy after touting Frankencloud to the CIA

Public release date: 9-Oct-2013 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, October 9, 2013Cancer immunotherapy can successfully use the body's own immune system to kill tumor cells. But some current approaches to stimulate an antitumor immune response are short-lived, with limited clinical effectiveness. A new gene transfer strategy that introduces modified, immune-stimulating human stem cells is both feasible and effective for achieving persistent immunotherapy to treat leukemias and lymophomas, according to a study published in Human Gene Therapy, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Human Gene Therapy website.

Satiro Nakamura De Oliveira and coauthors from the David Geffen School of Medicine, University of California, Los Angeles and University of Texas MD Anderson Cancer Center, Houston, describe the gene transfer method they developed to deliver chimeric antigen receptors, or CARS, that direct the immune system to target tumor cells derived from B-lymphocytes.

In the article "Modification of Hematopoietic Stem/Progenitor Cells with CD19-specific Chimeric Antigen Receptors as a Novel Approach for Cancer Immunotherapy" the authors show that by packaging the CARS in human hematopoietic stem cells, the immunotherapeutic receptors will be produced in the bloodstream for a long period of time. This persistent expression should improve their effectiveness in the treatment of blood cancers such as leukemia and lymphoma.

"This study represents an interesting new direction for an approach that has generated substantial interest," says Dr. Wilson, Director of the Gene Therapy Program, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia.

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About the Journal

Human Gene Therapy, the official journal of the European Society of Gene and Cell Therapy, British Society for Gene and Cell Therapy, French Society of Cell and Gene Therapy, German Society of Gene Therapy, and five other gene therapy societies, is an authoritative peer-reviewed journal published monthly in print and online. Human Gene Therapy presents reports on the transfer and expression of genes in mammals, including humans. Related topics include improvements in vector development, delivery systems, and animal models, particularly in the areas of cancer, heart disease, viral disease, genetic disease, and neurological disease, as well as ethical, legal, and regulatory issues related to the gene transfer in humans. Its sister journal, Human Gene Therapy Methods, published bimonthly, focuses on the application of gene therapy to product testing and development, and Human Gene Therapy Clinical Development, new in 2013, publishes data relevant to the regulatory review and commercial development of cell and gene therapy products. Complete tables of content for all three publications and a free sample issue may be viewed on the Human Gene Therapy website.

About the Publisher

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Novel gene therapy enables persistent anti-tumor immune response

Employment after Spinal Cord Injury: How Do You Get There?
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Cell Therapy - Hormonal Treatment
For More Information Visit: http://www.progenacell.com/

By: Charles Studios

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Cell Therapy - Hormonal Treatment - Video

Cell Therapy - Introduction
For More Information Visit: http://www.progenacell.com/

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Cell Therapy - Introduction - Video

SAN DIEGO--(BUSINESS WIRE)--

OncoSec Medical Inc. (ONCS), a company developing its advanced-stage ImmunoPulse DNA-based immunotherapy and NeoPulse therapy to treat solid tumors, has announced positive preliminary animal data demonstrating the benefits of combining the companys ImmunoPulse with anti-CTLA4 and anti-PD1 antibodies.

Dr. Richard Heller, professor at Old Dominion University, summarized the initial results of this study at the Cancer Vaccines and Gene Therapy Meeting in Philadelphia, Pennsylvania. The study was conducted using a single tumor model where a total of forty mice (eight treatment groups) were treated with either ImmunoPulse alone, or in combination with anti-CTLA4, anti-PD1 or both at varying concentrations. Safety and anti-tumor activity were assessed. Results indicate that all treatment groups showed 100% regression of treated lesions in all mice, and that no mice died as a result of toxicity from treatment. The results from this initial study demonstrate that ImmunoPulse in combination with anti-CTLA4 or anti-PD1 is safe, effective and does not have any contraindicated outcomes. Based on these positive results the company intends to continue testing combination approaches in more aggressive melanoma models that will support further evaluation of this approach in humans.

Results are encouraging and indicate that using gene electrotransfer to deliver plasmid IL-12 into tumors can be an effective and safe delivery tool. Additional studies are being conducted to demonstrate that the combination may lead to immune responses against distant untreated lesions in mice. We will investigate the anti-tumor response and plan to present these findings in the near future, commented Dr. Heller.

In addition, Dr. Adil Daud, principal investigator and co-director of melanoma research at the University of California San Francisco School of Medicine, reviewed previously presented data from OncoSecs Phase II melanoma program. In his presentation titled Gene Electrotransfer in Solid Tumors, Dr. Daud discussed that continual analysis of the data so far confirms signals demonstrated in the positive interim immune response data presented earlier in the year.

About the Sponsored Research Agreement with Old Dominion University for Combination Study in Melanoma

In June of 2013, OncoSec signed a Sponsored Research Agreement (SRA) withOld Dominion University(ODU) and the Frank Reidy Research Center for Bioelectrics. Under the agreement, OncoSec and the University agreed to collaborate on nonclinical research focused on developing new technology related to electroporation and delivery of different agents into solid tumors by electroporation. The first research experiment under the SRA was to evaluate the effects of ImmunoPulse in combination with Anti-CTLA4, Anti-PD1 and Anti-PDL-1 in a melanoma mouse model.

About OncoSec Medical Inc.

OncoSec Medical Inc. isa biopharmaceutical companydeveloping its advanced-stage ImmunoPulse DNA-based immunotherapy and NeoPulse therapy to treat solid tumors.ImmunoPulse and NeoPulse therapiesaddress an unmet medical needandrepresenta potential solution for less invasive and less expensive therapies that are able to minimize detrimental effects resulting from currently available cancer treatments such as surgery, systemic chemotherapy or immunotherapy and other treatment alternatives. OncoSec Medical's core technology is based upon its proprietaryuse of anelectroporation platform to enhancethedelivery and uptake of a locally delivered DNA-based immunocytokine (ImmunoPulse) or chemotherapeutic agent(NeoPulse). Treatment ofvarious solid cancersusing these targetedanti-cancer agentshas demonstratedselective destruction of cancerous cellswhile potentially sparing healthy normal tissues during early and late stage clinical trials. OncoSec's clinical programs include three Phase II clinical trials for ImmunoPulse targeting lethal skin cancers. More information is available athttp://www.oncosec.com/.

This press release contains forward-looking statements within the meaning of the U.S. Private Securities Litigation Reform Act of 1995. Any statements in this release that are not historical facts may be considered such "forward-looking statements." Forward-looking statements are based on management's current preliminary expectations and are subject to risks and uncertainties which may cause our results to differ materially and adversely from the statements contained herein. Some of the potential risks and uncertainties that could cause actual results to differ from those predicted include our ability to raise additional funding, our ability to acquire, develop or commercialize new products, uncertainties inherent in pre-clinical studies and clinical trials, unexpected new data, safety and technical issues, competition and market conditions. These and additional risks and uncertainties are more fully described in OncoSec Medical's filings with the Securities and Exchange Commission. Undue reliance should not be placed on forward-looking statements which speak only as of the date they are made. OncoSec Medical disclaims any obligation to update any forward-looking statements to reflect new information, events or circumstances after the date they are made, or to reflect the occurrence of unanticipated events.

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OncoSec Medical Announces Positive Preliminary Safety Data in Combination Study

October 8, 2013

Lee Rannals for redOrbit.com Your Universe Online

Sunscreen not only helps prevent three types of skin cancer, it also shields a superhero gene that repairs sun-damaged skin.

Scientists performing the worlds first human study to assess the impact of sunscreen at the molecular level have confirmed that the skin protector provides 100 percent protection against all three-forms of skin cancer, including basal cell carcinoma, squamous cell carcinoma, and malignant melanoma.

Researchers writing in the journal Pigment Cell & Melanoma Research looked at the impact of sunlight on human skin, both with and without sunscreen. They found no evidence of UV-induced skin damage when of sunscreen had been properly applied to an exposed area.

The team determined that not only does sunscreen provide 100 percent protection against the skin cancers, but it also shielded the p53 gene, which works to prevent cancer.

As soon as our skin becomes sun damaged, the p53 gene goes to work repairing that damage and thereby preventing skin cancer occurring, Lead researcher Dr. Elke Hacker, from Queensland University of Technologys AusSun Research Lab, said in a press release. But over time if skin is burnt regularly the p53 gene mutates and can no longer do the job it was intended for it no longer repairs sun damaged skin and without this protection skin cancers are far more likely to occur.

The study involved 57 people undergoing a series of skin biopsies to determine molecular changes to the skin before and after UV exposure and with and without sunscreen. First, the team took small skin biopsies of peoples unexposed skin. After this, they exposed two skin sites to a mild burning dose of UV light. One site was covered with sunscreen, while the other was not.

After 24 hours, we took another set of biopsies and compared the skin samples, Hacker said. What we found was that, after 24 hours, where the sunscreen had been applied there were no DNA changes to the skin and no impact on the p53 gene.

She said that this study looked beyond the redness of skin to determine whether sunscreen helps prevent molecular changes that have been linked to skin cancers.

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Sunscreen Helps Protect 'Superhero' Gene, Prevents Skin Cancer

Oct. 8, 2013 ext time your kids complain about putting on sunscreen, tell them this: Sunscreen shields a superhero gene that protects them from getting cancer.

It is widely accepted that sunscreen stops you from getting burnt but to date there has been academic debate about the effectiveness of sunscreen in preventing skin cancers.

Now QUT has undertaken a world-first human study to assess the impact of sunscreen at the molecular level.

Researchers found sunscreen provides 100 per cent protection against all three forms of skin cancer: BCC (basal cell carcinoma); SCC (squamous cell carcinoma); and malignant melanoma.

Lead researcher Dr Elke Hacker, from QUT's AusSun Research Lab, said sunscreen not only provided 100 per cent protection against the damage that can lead to skin cancer but it shielded the important p53 gene, a gene that works to prevent cancer.

"As soon as our skin becomes sun damaged, the p53 gene goes to work repairing that damage and thereby preventing skin cancer occurring.

"But over time if skin is burnt regularly the p53 gene mutates and can no longer do the job it was intended for -- it no longer repairs sun damaged skin and without this protection skin cancers are far more likely to occur."

The study, published in the Pigment Cell & Melanoma Research journal, looked at the impact of sunlight on human skin, both with and without sunscreen, and found no evidence of UV-induced skin damage when proper application of sunscreen (SPF30+) had been applied to exposed area.

"Melanoma is the most lethal form of skin cancer with research showing damage of melanocytes -- the pigment-producing cells of the skin -- after sun exposure plays a role in the development of skin cancer," Dr Hacker said.

Dr Hacker said the study, funded by Cancer Council Queensland, involved 57 people undergoing a series of skin biopsies to determine molecular changes to the skin before and after UV exposure and with and without sunscreen.

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Sunscreen saves superhero gene

Newswise LOS ANGELES (Oct. 8, 2013) Julie Miller is a key part of an extensive effort at Cedars-Sinai to increase awareness of and support for womens cancer research. She not only has registered to participate in clinical research, but shes also lacing up her running shoes.

Miller, who lives in Westwood, Calif., is a participant in both Research for Her and the Run for Her 5K Run and Friendship Walk.

Millers journey started more than four years ago when she made an appointment with Ora Karp Gordon, MD, director of the Cedars-Sinai GenRISK Adult Genetics Program, to learn if she may be a carrier of the BRCA gene, a genetic mutation that greatly increased her risk of developing breast and ovarian cancers. With a long lineage of family members diagnosed with these cancers, the odds were stacked against her, and Miller soon learned that she too was a carrier.

With this knowledge, Miller made a proactive decision to dramatically lessen her chances of developing cancer by undergoing prophylactic surgeries to remove her breasts, ovaries and fallopian tubes. Her experience prompted Miller to become an advocate for not only herself, but womens cancer research and awareness.

This commitment also led Miller to participate in the new Research for Her program at the Samuel Oschin Comprehensive Cancer Institute. The program is aimed at increasing womens representation in medical research and intended to help scientists understand how cancers develop and how treatments affect people.

Research for Her is the research arm of a Cedars-Sinai commitment to increasing treatment options and public awareness of womens cancers. Research for Her is supported by Run for Her, the annual 5K run and friendship walk.

In 2005, the inaugural Run for Her event took place in a Cedars-Sinai parking lot with 700 people. Since then, thousands of individuals have joined the cause to help increase ovarian cancer awareness. Miller will be participating in this years event Sunday, Nov. 10, 2013.

Run for Her began when Kelli Sargent created a marketing and operations plan for an ovarian cancer 5k run/walk for her master's degree thesis. She later partnered with the Cedars-Sinai Womens Cancer Program at the Samuel Oschin Comprehensive Cancer Institute to create the event. Sargents passion for the event stemmed from her mothers eight-year battle with ovarian cancer, a battle she lost in 2008.

Run for Her supports more than vital funds for ovarian cancer research and awareness, Sargent said. It provides an outlet for people to share their experiences, cry and laugh. Its a day to remember the loved ones we lost to this disease and continue fighting for those whose battle continues.

Both research-driven programs are providing women an empowering opportunity to change the landscape of womens cancer.

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Ovarian Cancer Research and Awareness Remain a Focus at Cedars-Sinai