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Research and Markets has announced the addition of the "MediPoint: Predictive Breast Cancer Gene Testing - EU Analysis and Market Forecasts" report to their offering.

MediPoint: Predictive Breast Cancer Gene Testing - EU Analysis and Market Forecasts

Breast cancer is the most common form of cancer in women in both the developed and developing world. The incidence of breast cancer is increasing due to the increased life span and increasing adoption of Western lifestyle risk factors. Predictive breast cancer gene tests can be used to identify women who are at increased risk of developing hereditary breast cancer. The Predictive Breast Cancer Gene Testing market has seen exponential growth in the US, dominated by Myriad Genetics. Gene testing in Europe is mostly carried out by the state funded health sector, but increasingly private companies are offering breast cancer gene tests to physicians. Myriad Genetics' position in the market is dependent on it being the leading provider of the most common breast cancer mutations. By the end of our forecast period, the competitive landscape will experience significant change due to the erosion of Myriad Genetics' position, as a result of the expiry of key patents, and the emergence of alternative molecular technologies.

Scope

- An overview of Breast Cancer, which includes epidemiology, etiology, symptoms, diagnosis, pathology and treatment guidelines.

- Annualized EU Breast Cancer Gene Testing market revenue and future forecasts from 2009 to 2011, forecast for 7 years to 2018.

- Investigation of current and future market competition for Breast Cancer Gene Testing

- Insightful review of the key industry drivers, restraints and challenges as well as predicted impact of key events.

- Competitor assessment including device approval analysis and device sales forecasts.

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Research and Markets: MediPoint: Predictive Breast Cancer Gene Testing - EU Analysis and Market Forecasts

Recommendation and review posted by Bethany Smith

Feds Were Watching Tamerlan Tsarnaev and Mother Long Before the Bombing
About 18 months before the Boston Marathon bombings, the CIA added the mother of the two suspects to a terrorism database after Russian authorities raised co...

By: TheAlexJonesChannel

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Feds Were Watching Tamerlan Tsarnaev and Mother Long Before the Bombing - Video

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Bilderberg Sleuth Jim Tucker Remembered
Alex broadcasts from the road. He pays tribute to Bilderberg sleuth Jim Tucker, who passed away last week at the age of 78. He also covers the latest attack ...

By: TheAlexJonesChannel

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Bilderberg Sleuth Jim Tucker Remembered - Video

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Dear EarthTalk: What is the Monsanto Protection Act and why are environmentalists so upset about it?

Rita Redstone

Milwaukee, Wisc.

The so-called Monsanto Protection Act is actually a provision (officially known as Section 735) within a recently passed Congressional spending bill, H.R. 933, which exempts biotech companies from litigation regarding the making, selling and distribution of genetically engineered seeds and plants.

President Barack Obama signed the bill and its controversial rider into law in March, much to the dismay of environmentalists. It means that Monsanto and other companies that supply the majority of the nation's crop seeds can continue to produce genetically engineered products regardless of any potential court orders stating otherwise. Opponents of genetically engineered foods believe that giving such companies a free reign over the production of such potentially dangerous organisms regardless of judicial challenge is a bad idea -- especially given how little we still know about the biological and ecological implications of widespread use of genetically engineered crops.

Today, more than 90 percent of the corn, soybeans, cotton, sugar beets and canola planted in the U.S. is derived from seeds genetically engineered by Monsanto and other companies to resist pests and thus increase yields. Aviva Shen of the ThinkProgress blog reports that, instead of reducing farmers' use of toxic pesticides and herbicides, genetically engineered seeds are having the opposite effect in what has become a race to keep faster and faster developing "superweeds" and "superbugs" at bay. With Congress and the White House refusing to regulate genetically engineered crops, the court system has remained a last line of defense for those fighting the widespread adoption of genetic engineering -- until now, that is, thanks to H.R. 933.

Monsanto isn't the only seed company heavily into genetic engineering, but it is the biggest and most well-known and spends millions of dollars each year on lobbyists to keep it that way. Critics point out that the company has spent decades stacking government agencies with its executives and directors. "Monsanto's board members have worked for the EPA, advised the U.S. Department of Agriculture and served on President Obama's Advisory Committee for Trade Policy and Negotiations," reports the group Food & Water Watch. "The prevalence of Monsanto's directors in these highly influential positions begs a closer look at how they're able to push the pro-genetically engineered agenda within the government and influence public opinion."

"The judicial review process is an essential element of U.S law and serves as a vital check on any Federal Agency decision that may negatively impact human health, the environment or livelihoods," reports Food Democracy Now! "Yet this provision seeks an end-run around such judicial review by preemptively deciding that industry can set its own conditions to continue to sell biotech seeds, even if a court may find them to have been wrongfully approved."

Another concern of safe food advocates now is getting the government to require food makers to list genetically engineered ingredients clearly on product labels so consumers can make informed choices accordingly. "Not only is (genetically engineered) labeling a reasonable and common sense solution to the continued controversy that corporations like Monsanto, DuPont and Dow Chemical have created by subverting our basic democratic rights," adds Food Democracy Now!, "but it is a basic right that citizens in 62 other countries around the world already enjoy, including Europe, Russia, China, India, South Africa and Saudi Arabia."

CONTACTS: ThinkProgress, http://www.thinkprogress.org; Food & Water Watch, http://www.foodandwaterwatch.org; Food Democracy Now!, http://www.fooddemocracynow.org.

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EarthTalk / Efforts to regulate genetic engineering of crops sacked

Recommendation and review posted by Bethany Smith

Researchers studying a genetic mutation, which causes sudden cardiac death, may have discovered a genetic link between German, Danish and Newfoundland families.

Dr. Hendrick Milting, a genetics researcher at the Heart and Diabetes Center North Rhine-Westphalia in Bad Oeynhausen, Germany, has been doing work with a gene mutation for arrhythmogenic right ventricular, or ARVC, a form of heart disease that usually appears in early adulthood and causes sudden cardiac death.

It has affected many members of a German family.

That mutation is the same one that genetic researchers at Memorial University identified in 2008 as affecting 24 Newfoundland families adding up to 1,200 people over several generations.

Not only did Milting discover the Newfoundland research, he also found a similar mutation in a Danish family.

"By chance at the same time, a group in Copenhagen found a similar family in Denmark. We decided to make a genetic fingerprint of these families and we found that all these families are connected," said Milting.

"So they have a common root."

Milting has come to Memorial University to work with genetic researchers Dr. Kathy Hodgkinson, Dr. Terry Lynn Young, and Dr. Sean Connors at the Faculty of Medicine.

He has also planned to meet with history, folklore, geography, and anthropology experts to try to find out more about how the German and Danish families could be linked to the Newfoundland family, which, like many Newfoundland families, was thought to be of English and Irish descent.

"What we have is a piece of DNA that gives us history written in a DNA code," said Hodgkinson.

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Genetic mutation shared by Newfoundland, German, Danish families

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CAMBRIDGE, Mass., April 30, 2013 /PRNewswire/ -- Metamark Genetics, Inc., a leader in the discovery of novel molecular prognostic and diagnostic tests for cancer, today announced that industry veteran Shawn M. Marcell has been named the company's new president and chief executive officer. Mr. Marcell succeeds interim executive Michael Kauffman, M.D., who will remain on Metamark's board of directors.

Metamark lead director Gregory C. Critchfield, M.D., said, "We are excited to welcome Shawn to Metamark as the company prepares to launch its first prognostic test, for prostate cancer. Shawn's broad and deep experience in life sciences, and his success in bringing innovative products to market, make him the ideal leader for Metamark as it grows into to a commercial organization." Dr. Critchfield added, "We also would like to thank Michael Kauffman for his leadership during this important time in the company's evolution."

"Metamark's strategy to develop novel prognostic and diagnostic tests based on advanced quantitative histologic analysis has the potential to transform approaches to cancer and other major diseases," said Mr. Marcell. "I am thrilled to join the company and look forward to working with the entire team as we build a leading commercial stage molecular diagnostics company."

Mr. Marcell has nearly three decades of diverse executive, commercial and operational experience in life science and technology businesses. Most recently, he was the lead executive, serving as general manager of Hologic's (HOLX) wholly owned LIFECODES subsidiary, which was acquired by Immucor. He headed commercial operations at Sequenom (SQNM), which acquired SensiGen, where he served as president and CEO. Mr. Marcell has both CLIA laboratory and product launch experience and has had additional key management roles with Redpoint Bio, Prima Facie, Centocor and Abbott Diagnostics.

Mr. Marcell has been adjunct faculty and lecturer in Entrepreneurial Programs at the Wharton School and has served on numerous for-profit and non-profit boards.

About Metamark

Metamark Genetics is a privately held biotechnology company founded in 2007 to develop new function- based prognostic and diagnostic tests aimed at improving cancer care. The company's proprietary genomic and proteomic discovery platforms have yielded significant discoveries in several disease areas, including prostate, colon and breast cancers. During 2013, Metamark plans to commercialize ProMarkTM its lead prostate cancer prognostic test through its Cambridge, MA CLIA-certified laboratory. For more information, please visit the company's Website at http://www.metamarkgenetics.com.

MetamarkTM and ProMarkTM are trademarks of Metamark Genetics, Inc.

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Metamark Genetics Board of Directors Appoints Shawn M. Marcell President and Chief Executive Officer

Recommendation and review posted by Bethany Smith

Public release date: 30-Apr-2013 [ | E-mail | Share ]

Contact: Phyllis Edelman pedelman@genetics-gsa.org 301-634-7302 Genetics Society of America

Bethesda, MDApril 30, 2013 Listed below are the selected highlights for the May 2013 issue of the Genetics Society of America's journal, GENETICS. The May issue is available online at http://www.genetics.org/content/current. Please credit GENETICS, Vol. 194, MAY 2013, Copyright 2013.

Please feel free to forward to colleagues who may be interested in these articles on a wide array of topics including: developmental and behavioral genetics; genome integrity and transmission; genetics of complex traits; cellular genetics; and population and evolutionary genetics.

ISSUE HIGHLIGHTS

Developmental and Behavioral Genetics An organelle gatekeeper function for Caenorhabditis elegans UNC-16 (JIP3) at the axon initial segment, pp. 143-161 S. L. Edwards, S.-c. Yu, C. M. Hoover, B. C. Phillips, J. E. Richmond, and K. G. Miller Nerve cell bodies have a vastly different organelle composition than axons. This article (see accompanying commentary by Zheng and Nonet, pp. 35-37) provides insight into the basis of this difference. The authors report the discovery of a previously unrecognized organelle gatekeeper function, mediated by UNC-16 (JIP3 in humans), that acts at the axon initial segment to restrict the flow of Golgi and endosomal organelles into the synaptic region of axons.

Genome Integrity and Transmission Novel proteins required for meiotic silencing by unpaired DNA and siRNA generation in Neurospora crassa, pp. 91-100 T. M. Hammond, H. Xiao, E. C. Boone, L. M. Decker, S. A. Lee, T. D. Perdue, P. J. Pukkila, and P. K. Shiu and Identification of small RNAs associated with meiotic silencing by unpaired DNA, pp. 279-284 T. M. Hammond, W. G. Spollen, L. M. Decker, S. M. Blake, G. K. Springer, and P. K. Shiu Genes unpaired during meiosis are silenced in Neurospora by a mechanism known as meiotic silencing by unpaired DNA (MSUD). Two articles in this issue of GENETICS report the identification of novel players in this process, including small RNAs and the first nuclear MSUD protein. This protein is not required for meiosis, providing the first indication that MSUD is not necessarily coupled to sexual development.

Genome Integrity and Transmission Intragenomic conflict between the two major knob repeats of maize, pp. 81-89 L. B. Kanizay, P. S. Albert, J. A. Birchler, and R. K. Dawe Large genomes are often replete with tandem repeats. Why do they exist? Here the authors investigate the distribution of tandem repeats in maize heterochromatic domains called knobs. The data suggest an intragenomic conflict whereby one family of repeats suppresses proliferation of the other. Similar competition may underlie the formation and maintenance of many tandem repeat arrays.

Genome Integrity and Transmission Nonrandom distribution of interhomolog recombination events induced by breakage of a dicentric chromosome in Saccharomyces cerevisiae, pp. 69-80 W. Song, M. Gawel, M. Dominska, P. W. Greenwell, E. Hazkani-Covo, K. Bloom, and T. D. Petes This article presents the first high-resolution mapping of the positions of chromosome breaks that result from the bridge-fusion-breakage cycles of dicentric chromosomes. Sites of recombination between a dicentric chromosome and its normal homolog revealed the locations of breaks in the dicentric chromosome, which were distributed in a quasi-random fashion between the two centromeres.

Genetics of Complex Traits Systems genetics of environmental response in the mature wheat embryo, pp. 265-277 J. D. Munkvold, D. Laudencia-Chingcuanco, and M. E. Sorrells This article illustrates the utility of network approaches for understanding gene expression by environment interaction, even in organisms with highly complex genomes. A unique Weighted Gene Co-Expression Network Analysis approach was used to compare gene expression networks in mature wheat embryos from two distinct growing environments across a segregating population. This approach identified environmentally conserved and unique co-expression modules and their genetic control.

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Genetics Society of America's GENETICS journal highlights for May 2013

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The technique, which has been 20 years in development, could help the 750,000 people in the UK living with heart failure.

The condition results from damage to the heart left over from a heart attack or side-effects of powerful chemotherapy drugs. After the heart is starved of oxygen, cells die and the remaining heart cells become fatigued.

"Once heart failure starts, it progresses into a vicious cycle where the pumping becomes weaker and weaker, as each heart cell simply cannot respond to the increased demand." said Alex Lyon, a cardiologist at the Royal Brompton hospital in London who is leading the trial in the UK.

"Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails," he said.

People with heart failure can find it difficult to walk long distances or climb stairs. The disease is usually progressive, with heart function gradually weakening over time. The only solutions are heart transplant or surgically implanted pumps to maintain blood flow.

The gene therapy adds a repair gene to failing heart cells which produces more of a protein called SERCA2a which regulates the availability of calcium in the heart. Without ample supplies of calcium, heart muscles are unable to contract properly or relax properly between contractions - two key symptoms of heart failure.

Tests on human cells in the laboratory at Imperial College in London and in animals have shown that the SERCA2a gene can be repaired, and reverses some of the symptoms of heart failure.

A US biotech company Celladon has patented a method for inserting the gene into human hearts. They are co-sponsoring the UK element of the trial along with the British Heart Foundation which funded much of the basic research involved.

The technique uses a harmless virus similar related to the common cold. The DNA from the virus is removed and replaced with SERCA2a gene. This virus is then injected into the heart where it infects heart cells. The cells' own machinery then decodes the SERCA2a gene, making more of the calcium regulating protein that is missing in failing hearts.

"When the gene is repaired it produces more of the functional protein and the problem is reversed," said Dr Lyon.

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Gene therapy hope for heart failure patients

Recommendation and review posted by Bethany Smith

The first of 200 patients from around the world will be treated at the Golden Jubilee National Hospital, Clydebank, and the Royal Brompton Hospital, London, in the next three to six weeks.

All suffer from severe chronic heart failure, due to the after-effects of heart attacks and inherited conditions.

Doctors will randomly treat half the patients with a harmless virus carrying a corrective gene. The rest will receive an inactive placebo treatment.

Previous research suggests that a protein produced by the gene can restore function to failing hearts, and reduce the risk of death and the need for heart transplants.

Lead investigator Dr Alexander Lyon, consultant cardiologist at the Royal Brompton, said: "Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails."

The Cupid 2 trial is taking place in conjunction with US biotech company Celladon, which has patented the treatment.

The therapy involves injecting the virus directly into the heart via a catheter. As the virus infects the heart cells, it implants the corrective gene.

This has the effect of increasing levels of a protein called SERCA2a, which plays a key role in a vital signalling mechanism involving calcium.

"When the heart muscle is injured it activates a series of compensatory changes, but over time fatigue sets in which results in the natural version of this gene switching off," said Dr Lyon. "When the gene is repaired it produces more of the functional protein and the problem is reversed."

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Gene hope for heart patients

Recommendation and review posted by Bethany Smith

More than 200 people with heart failure are to receive a pioneering form of gene therapy to try to get their hearts beating properly again. "This is the first ever gene therapy trial to target heart failure," says lead investigator Alexander Lyon of Imperial College London.

Heart failure results after damage to the heart muscle causes it to deteriorate, which in turn progressively weakens cells that govern heartbeat. The result is serious fatigue due to the heart's inability to pump blood efficiently. Each year in the UK alone it affects 120,000 people who have never had the condition before, killing a third of them within 12 months.

Doctors will inject participants with harmless viruses that ferry a gene called SERCA2a into their heart muscle. The gene codes for a protein that recycles calcium within heart muscle cells, vital for driving each heartbeat and priming the next one.

In damaged cells, this recycling is impaired. By loading new copies of the gene the aim is to compensate for this decline. "The gene therapy will reset the calcium control," says Lyon.

A preliminary trial of the same therapy three years ago in 39 people demonstrated that it is safe and delivers benefits. Those who got the highest dose of the virus, for example, spent only a tenth as long in hospital as those given a placebo (Circulation, doi.org/bzvxst). The impending follow-up trial will recruit 200 people split equally between the US and Europe.

In a separate trial of the same therapy, doctors will treat 24 people who already have temporary mechanical implants to aid heartbeat while they await heart transplants.

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Gene therapy to repair failing hearts starts trial

Recommendation and review posted by Bethany Smith

Patients with severe heart failure are to be treated with gene therapy for the first time in Britain.

Earlier clinical trials have suggested the treatment could reverse damaging changes inside cardiac cells that weaken the muscle and reduce the ability of the heart to pump blood.

The condition affects 750,000 people in the UK and is often fatal.

Doctors backed by the British Heart Foundation will give 100 patients an infusion of a harmless virus that has been genetically engineered to carry an extra gene, called SERCA2a.

The virus infects cardiac cells. Once inside, the gene becomes activated and makes a protein crucial to normal beating of the heart.

Dr Alexander Lyon, consultant cardiologist at The Royal Brompton Hospital, is leading the Cupid 2 trial.

He said: "When the heart muscle is injured it activates a series of compensatory changes, but over time fatigue sets in which results in the natural version of this gene switching off.

"When the gene is repaired it produces more of the functional protein and the problem is reversed."

The first patients will be given the treatment in the next three to six weeks at hospitals in London and Glasgow.

They will be tracked and compared to another group of study volunteers who will receive a dummy treatment.

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Heart Failure: First UK Gene Therapy Trial

Recommendation and review posted by Bethany Smith

The first attempt in Britain to treat heart failure patients with gene therapy is to begin within weeks, as part of study aimed at improving the lives of up to a million people in the UK who suffer the debilitating and potentially fatal condition.

Click HERE to view 'how to treat a failing heart' graphic

Two clinical trials are planned for a few dozen British patients who will be deliberately exposed to a virus carrying a synthetic copy of a human gene known to be involved in boosting heartbeat.

The first trial will be carried out at the Royal Brompton Hospital in London and the Golden Jubilee National Hospital in Glasgow. The patients will be part of a group of 200 from around the world who will have the virus injected via a cardiac catheter inserted through a vein in the leg. A second trial at the Harefield and Papworth hospitals will be based entirely within the UK and involve 24 patients with chronic heart failure who are already fitted with an "artificial heart" known as a left ventricular assist device, which helps to pump blood around the body.

The aim in both trials is to inject additional copies of a healthy gene, known to be responsible for a key protein involved in regulating the rhythmic contraction of the heart muscle. It is hoped that the extra genes will remain active within a patient's heart for many months or even years.

Scientists believe the approach could lead to a significant improvement in the efficiency of the diseased heart to pump blood around the body so improving the quality of life of thousands of patients with progressive heart failure who develop serious ailments as well as severe fatigue.

Scientists warned that it will still be several years before the technique can be made widely available. They do not want to raise hopes unduly as many previous gene therapy trials on patients with a range of other illnesses have failed to live up to expectations.

However, the heart researchers said they are optimistic that the gene technique will improve the quality of life in at least some of the patients, who would otherwise suffer deteriorating health and life expectancy a third of patients die within a year of diagnosis.

"Once heart failure starts, it progresses into a vicious cycle where the pumping becomes weaker and weaker, as each heart cell simply cannot respond to the increased demand," said Alexander Lyon, a consultant cardiologist at the Royal Brompton.

"Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails."

Read the original:
Gene therapy to offer up to 1m heart patients new lease of life

Recommendation and review posted by Bethany Smith

The first attempt in Britain to treat heart failure patients with gene therapy is to begin within weeks, as part of study aimed at improving the lives of up to a million people in the UK who suffer the debilitating and potentially fatal condition.

Click HERE to view 'how to treat a failing heart' graphic

Two clinical trials are planned for a few dozen British patients who will be deliberately exposed to a virus carrying a synthetic copy of a human gene known to be involved in boosting heartbeat.

The first trial will be carried out at the Royal Brompton Hospital in London and the Golden Jubilee National Hospital in Glasgow. The patients will be part of a group of 200 from around the world who will have the virus injected via a cardiac catheter inserted through a vein in the leg. A second trial at the Harefield and Papworth hospitals will be based entirely within the UK and involve 24 patients with chronic heart failure who are already fitted with an "artificial heart" known as a left ventricular assist device, which helps to pump blood around the body.

The aim in both trials is to inject additional copies of a healthy gene, known to be responsible for a key protein involved in regulating the rhythmic contraction of the heart muscle. It is hoped that the extra genes will remain active within a patient's heart for many months or even years.

Scientists believe the approach could lead to a significant improvement in the efficiency of the diseased heart to pump blood around the body so improving the quality of life of thousands of patients with progressive heart failure who develop serious ailments as well as severe fatigue.

Scientists warned that it will still be several years before the technique can be made widely available. They do not want to raise hopes unduly as many previous gene therapy trials on patients with a range of other illnesses have failed to live up to expectations.

However, the heart researchers said they are optimistic that the gene technique will improve the quality of life in at least some of the patients, who would otherwise suffer deteriorating health and life expectancy a third of patients die within a year of diagnosis.

"Once heart failure starts, it progresses into a vicious cycle where the pumping becomes weaker and weaker, as each heart cell simply cannot respond to the increased demand," said Alexander Lyon, a consultant cardiologist at the Royal Brompton.

"Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails."

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Gene therapy to offer heart patients new lease of life

Recommendation and review posted by Bethany Smith

Public release date: 28-Apr-2013 [ | E-mail | Share ]

Contact: Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central

Injection of human stem cells into mice with tumors slowed down tumor growth, finds research published in BioMed Central's open access journal Stem Cell Research & Therapy. Human mesenchymal stem cells (MSC), isolated from bone marrow, caused changes in blood vessels supplying the tumor, and it is this modification of blood supply which seems to impact tumor growth.

The use of stem cells in treating cancer has been controversial, with some studies finding that stem cells force tumors to enter programmed cell death. However other studies find that stem cells actually promote tumor growth by inducing infiltration of new blood vessels. In attempting to sort out this puzzle researchers from INSERM groups at Universit Joseph Fourier in collaboration with CHU de Grenoble investigated the impact of MSC on already established subcutaneous or lung metastasis in mice.

For both the subcutaneous and lung tumors, injection of MSC reduced cell division, consequently slowing the rate of tumor growth. Part of the mode of action of stem cells therefore appears to be due to with angiogenesis, but the mechanism behind this is still unclear.

Claire Rome who led this study explained, "We found that MSC altered vasculature inside the tumor - although new blood vessels were generated, overall they were longer and fewer than in untreated tumors. This could be restricting the oxygen and nutrients to the tumor, limiting cell division." She continued, "Our study confirms others which propose that stem cells, in particular MSC, might be one way forwards in treating cancer."

Commenting on this study Celia Gomes, from the University of Coimbra, said, "One of the interesting questions this study raises is when MSC promote tumor growth and when they restrict it. The answer seems to be timing this study looks at already established tumors, while others, which find that MSC increase growth, tend to be investigating new tumors. This is a first step in the path to identifying exactly which patients might benefit from stem cell therapy and who will not."

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Media Contact

Dr Hilary Glover Scientific Press Officer, BioMed Central Tel: +44 (0) 20 3192 2370 Mob: +44 (0) 778 698 1967 Email: hilary.glover@biomedcentral.com

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Clarifying the effect of stem cell therapy on cancer

Recommendation and review posted by simmons

ALLENDALE, N.J., April 29, 2013 (GLOBE NEWSWIRE) -- NeoStem, Inc. (NYSE MKT:NBS) and its subsidiary, Progenitor Cell Therapy LLC ("PCT"), announced today the execution of a Services Agreement with Sentien Biotechnologies, Inc. ("Sentien") under which PCT will provide services to support Sentien's development of its cell therapy product, including technology transfer, staff training, and manufacturing.

Sentien is developing an allogeneic cell therapy product consisting of bone marrow derived mesenchymal stem cells seeded onto a medical device for critical care indications. Sentien has engaged PCT for manufacture of the final formulation of its cell therapy product and intends to transfer and implement Sentien's master cell bank, product working cell bank and product manufacturing processes to PCT. These cell banks will be prepared according to Good Manufacturing Practices ("GMP") guidelines and implemented by PCT to create a cell therapy product for Sentien's Investigational New Drug ("IND") submission to the FDA. Upon obtaining an IND, Sentien intends to have PCT manufacture GMP compliant grade materials to support Sentien's Phase I clinical trial.

"We are excited to enter into this agreement with Sentien, an innovator for acute organ failure," said Robert A. Preti, PhD, President and Chief Scientific Officer of PCT. PCT is an internationally recognized contract development and manufacturing organization with facilities in Allendale, New Jersey and Mountain View, California. The company has expertise in GMP manufacture for cell therapies, including dendritic cells, stem cells and T cells. Notably, PCT provided manufacturing for the pivotal studies for Dendreon's Provenge(R), the first cell therapy approved for cancer treatment.

About NeoStem, Inc.

NeoStem, Inc. ("NeoStem" or the "Company") is a leader in the emerging cellular therapy industry. Our business model includes the development of novel proprietary cell therapy products as well as operating a contract development and manufacturing organization ("CDMO") providing services to others in the regenerative medicine industry. The combination of a therapeutic development business and revenue-generating service provider business provides the Company with capabilities for cost effective in-house product development and immediate revenue and cash flow generation. http://www.neostem.com

Forward-Looking Statements for NeoStem, Inc.

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements reflect management's current expectations, as of the date of this press release, and involve certain risks and uncertainties. Forward-looking statements include statements herein with respect to the successful execution of the Company's business strategy, including with respect to the Company's research and development and clinical evaluation efforts for cellular therapies, including with respect to AMR-001, the future of the regenerative medicine industry and the role of stem cells and cellular therapy in that industry and the Company's ability to successfully grow its contract development and manufacturing business. The Company's actual results could differ materially from those anticipated in these forward- looking statements as a result of various factors. Factors that could cause future results to materially differ from the recent results or those projected in forward-looking statements include the "Risk Factors" described in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 11, 2013 and in the Company's periodic filings with the Securities and Exchange Commission. The Company's further development is highly dependent on future medical and research developments and market acceptance, which is outside its control.

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NeoStem's Subsidiary, Progenitor Cell Therapy, Enters Into a Services Agreement With Sentien Biotechnologies, Inc.

Recommendation and review posted by Bethany Smith

Apr. 29, 2013 University of North Carolina researchers have discovered that disrupting a gene that acts as a regulatory switch to turn on other genes can keep blood vessels from forming and developing properly.

Further study of this gene -- a "transcription factor" called CASZ1 -- may uncover a regulatory network that influences the development of cardiovascular disease. A number of other studies have already shown a genetic link between mutations in CASZ1 and hypertension.

The UNC research, which was carried out in a frog model as well as human cells, will be published April 29, 2013, in the journal Developmental Cell.

"There has been a lot of interest in studying the vasculature because of its role in a wide range of disease states, as well as human development. But there are very few transcription factors that are known to affect the vasculature. To find a new one is quite unique, and then to be able to link it up to a known network of vascular development is surprising and encouraging," said senior study author Frank Conlon, PhD, an associate professor of genetics in the UNC School of Medicine.

During vascular development, specialized cells coalesce into three-dimensional "cords" that then hollow out to provide a path for transporting blood throughout the body. This process involves the complex coordination of molecular entities like growth factors and signaling molecules, defects that have been associated with human illnesses such as cancer, stroke, and atherosclerosis.

Conlon has long been interested in understanding how these various molecular players come together in the cardiovascular system. In 2008, his laboratory showed that a gene called CASZ1 is involved in the development of heart muscle. In this study, he and his colleagues decided to look for its role in the development of blood vessels.

Marta S. Charpentier and Kathleen S. Christine, lead authors of the study and graduate students in Conlon's laboratory, removed CASZ1 from frog embryos and looked to see how its absence affected the development of the vasculature. Without CASZ1, the frogs failed to form branched and functional blood vessels. When they removed the CASZ1 gene from cultured human cells, Charpentier and Christine saw similar defects: the cells did not sprout or branch correctly due to their inability to maintain proper adhesions with the surrounding extracellular matrix.

"If you take out CASZ1, these cultured human cells try to migrate by sending out these filopodia or little feet, but what happens is it is like someone nails down the back end of those growing vessels. They try to move and keep getting thinner and thinner, and like an elastic band it gets to be too much and just snaps back. It appears to cause an adhesion defect that makes the cells too sticky to form normal vessels," said Conlon.

CASZ1 is a transcription factor, a master switch that controls when and where other genes are expressed. Therefore, Charpentier and Christine did a series of experiments to explore CASZ1's influence on a known vascular network, involving other genes called Egfl7 and RhoA. When Charpentier and Christine added the Egfl7 gene to her CASZ1-depleted cells, the defect in blood vessel formation went away, suggesting that the two genes are connected. They then showed that CASZ1 directly acts on the Egfl7 gene, and that this activity in turn activates the RhoA gene, which is known to be required for cellular behaviors associated with adhesion and migration.

Transcription factors themselves are so essential that they are generally considered to be "undruggable," but the researchers say that further studies into how specific transcription factors work and the targets they control could eventually lead to new drug candidates.

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Molecular role of gene linked to blood vessel formation uncovered

Recommendation and review posted by Bethany Smith

Public release date: 29-Apr-2013 [ | E-mail | Share ]

Contact: Megan Fellman fellman@northwestern.edu 847-491-3115 Northwestern University

When a mouse smells a cat, it instinctively avoids the feline or risks becoming dinner. How? A Northwestern University study involving olfactory receptors, which underlie the sense of smell, provides evidence that a single gene is necessary for the behavior.

A research team led by neurobiologist Thomas Bozza has shown that removing one olfactory receptor from mice can have a profound effect on their behavior. The gene, called TAAR4, encodes a receptor that responds to a chemical that is enriched in the urine of carnivores. While normal mice innately avoid the scent marks of predators, mice lacking the TAAR4 receptor do not.

The study, published April 28 in the journal Nature, reveals something new about our sense of smell: individual genes matter.

Unlike our sense of vision, much less is known about how sensory receptors contribute to the perception of smells. Color vision is generated by the cooperative action of three light-sensitive receptors found in sensory neurons in the eye. People with mutations in even one of these receptors experience color blindness.

"It is easy to understand how each of the three color receptors is important and maintained during evolution," said Bozza, an author of the paper, "but the olfactory system is much more complex."

In contrast to the three color receptors, humans have 380 olfactory receptor genes, while mice have more than 1,000. Common smells like the fragrance of coffee and perfumes typically activate many receptors.

"The general consensus in the field is that removing a single olfactory receptor gene would not have a significant effect on odor perception," said Bozza, an assistant professor of neurobiology in the Weinberg College of Arts and Sciences.

Bozza and his colleagues tested this assumption by genetically removing a specific subset of olfactory receptors called trace amine-associated receptors, or TAARs, in mice. Mice have 15 TAARs. One is expressed in the brain and responds to amine neurotransmitters and common drugs of abuse such as amphetamine. The other 14 are found in the nose and have been coopted to detect odors.

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Cat and mouse: A single gene matters

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Public release date: 29-Apr-2013 [ | E-mail | Share ]

Contact: Tom Hughes tahughes@unch.unc.edu 919-966-6047 University of North Carolina Health Care

CHAPEL HILL, N.C. University of North Carolina researchers have discovered that disrupting a gene that acts as a regulatory switch to turn on other genes can keep blood vessels from forming and developing properly.

Further study of this gene a "transcription factor" called CASZ1 may uncover a regulatory network that influences the development of cardiovascular disease. A number of other studies have already shown a genetic link between mutations in CASZ1 and hypertension.

The UNC research, which was carried out in a frog model as well as human cells, will be published April 29, 2013, in the journal Developmental Cell.

"There has been a lot of interest in studying the vasculature because of its role in a wide range of disease states, as well as human development. But there are very few transcription factors that are known to affect the vasculature. To find a new one is quite unique, and then to be able to link it up to a known network of vascular development is surprising and encouraging," said senior study author Frank Conlon, PhD, an associate professor of genetics in the UNC School of Medicine.

During vascular development, specialized cells coalesce into three-dimensional "cords" that then hollow out to provide a path for transporting blood throughout the body. This process involves the complex coordination of molecular entities like growth factors and signaling molecules, defects that have been associated with human illnesses such as cancer, stroke, and atherosclerosis.

Conlon has long been interested in understanding how these various molecular players come together in the cardiovascular system. In 2008, his laboratory showed that a gene called CASZ1 is involved in the development of heart muscle. In this study, he and his colleagues decided to look for its role in the development of blood vessels.

Marta S. Charpentier and Kathleen S. Christine, lead authors of the study and graduate students in Conlon's laboratory, removed CASZ1 from frog embryos and looked to see how its absence affected the development of the vasculature. Without CASZ1, the frogs failed to form branched and functional blood vessels. When they removed the CASZ1 gene from cultured human cells, Charpentier and Christine saw similar defects: the cells did not sprout or branch correctly due to their inability to maintain proper adhesions with the surrounding extracellular matrix.

"If you take out CASZ1, these cultured human cells try to migrate by sending out these filopodia or little feet, but what happens is it is like someone nails down the back end of those growing vessels. They try to move and keep getting thinner and thinner, and like an elastic band it gets to be too much and just snaps back. It appears to cause an adhesion defect that makes the cells too sticky to form normal vessels," said Conlon.

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UNC research uncovers molecular role of gene linked to blood vessel formation

Recommendation and review posted by Bethany Smith

Apr. 29, 2013 When a mouse smells a cat, it instinctively avoids the feline or risks becoming dinner. How? A Northwestern University study involving olfactory receptors, which underlie the sense of smell, provides evidence that a single gene is necessary for the behavior.

A research team led by neurobiologist Thomas Bozza has shown that removing one olfactory receptor from mice can have a profound effect on their behavior. The gene, called TAAR4, encodes a receptor that responds to a chemical that is enriched in the urine of carnivores. While normal mice innately avoid the scent marks of predators, mice lacking the TAAR4 receptor do not.

The study, published April 28 in the journal Nature, reveals something new about our sense of smell: individual genes matter.

Unlike our sense of vision, much less is known about how sensory receptors contribute to the perception of smells. Color vision is generated by the cooperative action of three light-sensitive receptors found in sensory neurons in the eye. People with mutations in even one of these receptors experience color blindness.

"It is easy to understand how each of the three color receptors is important and maintained during evolution," said Bozza, an author of the paper, "but the olfactory system is much more complex."

In contrast to the three color receptors, humans have 380 olfactory receptor genes, while mice have more than 1,000. Common smells like the fragrance of coffee and perfumes typically activate many receptors.

"The general consensus in the field is that removing a single olfactory receptor gene would not have a significant effect on odor perception," said Bozza, an assistant professor of neurobiology in the Weinberg College of Arts and Sciences.

Bozza and his colleagues tested this assumption by genetically removing a specific subset of olfactory receptors called trace amine-associated receptors, or TAARs, in mice. Mice have 15 TAARs. One is expressed in the brain and responds to amine neurotransmitters and common drugs of abuse such as amphetamine. The other 14 are found in the nose and have been coopted to detect odors.

Bozza's group has shown that the TAARs are extremely sensitive to amines -- a class of chemicals that is ubiquitous in biological systems and is enriched in decaying materials and rotting flesh. Mice and humans typically avoid amines since they have a strongly unpleasant, fishy quality.

Bozza's team, including the paper's lead authors, postdoctoral fellow Adam Dewan and graduate student Rodrigo Pacifico, generated mice that lack all 14 olfactory TAAR genes. These mice showed no aversion to amines. In a second experiment, the researchers removed only the TAAR4 gene. TAAR4 responds selectively to phenylethylamine (PEA), an amine that is concentrated in carnivore urine. They found that mice lacking TAAR4 fail to avoid PEA, or the smell of predator cat urine, but still avoid other amines.

Original post:
Cat and mouse: One gene is necessary for mice to avoid predators

Recommendation and review posted by Bethany Smith

Newswise CHAPEL HILL, N.C. University of North Carolina researchers have discovered that disrupting a gene that acts as a regulatory switch to turn on other genes can keep blood vessels from forming and developing properly.

Further study of this gene a transcription factor called CASZ1 may uncover a regulatory network that influences the development of cardiovascular disease. A number of other studies have already shown a genetic link between mutations in CASZ1 and hypertension.

The UNC research, which was carried out in a frog model as well as human cells, will be published April 29, 2013, in the journal Developmental Cell.

There has been a lot of interest in studying the vasculature because of its role in a wide range of disease states, as well as human development. But there are very few transcription factors that are known to affect the vasculature. To find a new one is quite unique, and then to be able to link it up to a known network of vascular development is surprising and encouraging, said senior study author Frank Conlon, PhD, an associate professor of genetics in the UNC School of Medicine.

During vascular development, specialized cells coalesce into three-dimensional cords that then hollow out to provide a path for transporting blood throughout the body. This process involves the complex coordination of molecular entities like growth factors and signaling molecules, defects that have been associated with human illnesses such as cancer, stroke, and atherosclerosis.

Conlon has long been interested in understanding how these various molecular players come together in the cardiovascular system. In 2008, his laboratory showed that a gene called CASZ1 is involved in the development of heart muscle. In this study, he and his colleagues decided to look for its role in the development of blood vessels.

Marta S. Charpentier and Kathleen S. Christine, lead authors of the study and graduate students in Conlons laboratory, removed CASZ1 from frog embryos and looked to see how its absence affected the development of the vasculature. Without CASZ1, the frogs failed to form branched and functional blood vessels. When they removed the CASZ1 gene from cultured human cells, Charpentier and Christine saw similar defects: the cells did not sprout or branch correctly due to their inability to maintain proper adhesions with the surrounding extracellular matrix.

If you take out CASZ1, these cultured human cells try to migrate by sending out these filopodia or little feet, but what happens is it is like someone nails down the back end of those growing vessels. They try to move and keep getting thinner and thinner, and like an elastic band it gets to be too much and just snaps back. It appears to cause an adhesion defect that makes the cells too sticky to form normal vessels, said Conlon.

CASZ1 is a transcription factor, a master switch that controls when and where other genes are expressed. Therefore, Charpentier and Christine did a series of experiments to explore CASZ1s influence on a known vascular network, involving other genes called Egfl7 and RhoA. When Charpentier and Christine added the Egfl7 gene to her CASZ1-depleted cells, the defect in blood vessel formation went away, suggesting that the two genes are connected. They then showed that CASZ1 directly acts on the Egfl7 gene, and that this activity in turn activates the RhoA gene, which is known to be required for cellular behaviors associated with adhesion and migration.

Transcription factors themselves are so essential that they are generally considered to be undruggable, but the researchers say that further studies into how specific transcription factors work and the targets they control could eventually lead to new drug candidates.

Read more from the original source:
Research Uncovers Molecular Role of Gene Linked to Blood Vessel Formation

Recommendation and review posted by Bethany Smith

Thursday, February 22, 2007

By Kenny Goldberg and KPBS Public Broadcasting

All pregnant women in California who get regular prenatal care are offered a genetic screening test. This test indicates whether their baby is at risk of having Down syndrome or other genetic birth defects. What women do with the test results is a matter of personal choice. KPBS health reporter Kenny Goldberg has the story.

Last year, Kim Capello was pregnant with her third child. As part of her routine pre-natal care, she had a blood test that screens for certain genetic disorders.

Capello: And a week later, my midwife called me to say that I had a high risk of having a baby with Down syndrome.

Capello had another screening test. But it was inconclusive. So to find out for sure, she had an amniocentesis. That procedure involves inserting a needle into the abdomen, and extracting some amniotic fluid.

Capello was nervous about it, because an amnio carries a small risk of miscarriage. Nonetheless, Capello and her husband needed to know what was up with their baby.

They soon found out. The test said the baby definitely had Down syndrome.

Capello: Basically, I just was frozen, I mean I just was in shock and very sad, and we cried a lot, because we were so, just fearful of what to expect, and you know, it wasn't something you plan or really think about.

Kim Capello and her husband had an agonizing decision to make. Should they terminate the pregnancy? Or, should they have the baby anyway, knowing it would likely be mentally retarded?

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Prenatal Genetic Tests Can Lead to Tough Choices

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April 29, 2013

Rayshell Clapper for redOrbit.com Your Universe Online

After learning about human genetic engineering, many readers might want to find out about some examples of genetic engineering. Both bizarre and beneficial, the following article highlights some truly fascinating and pragmatic examples of modern genetic engineering.

The Biotechnology Forums, a website for professionals and students in biotechnology (the area that studies genetic engineering) recently explained some of these examples. The first animal example of genetic engineering is the spider goat. Yes, you read that correctly. A spider goat is able to produce the strong, stretchable silk used by spiders to create their webs. This silk web is one of the strongest natural materials known to man, stronger even than steel.

Nexia Biotechnologies Company inserted the gene from a golden orb-weaver spider into the genome of goat in such a way that the goat secretes the protein of the spider web in its milk. The milk was then used to create a what Nexia called (and trademarked) BioSteel, a material with characteristics similar to spider webs.

Beyond goats capable of secreting spider webs in their milk, there are a number of other really cool examples of genetic engineering in animals. In one redOrbit blog, this author reported about a cat that glows in the dark. The glow-in-the-dark feline has a fluorescence gene that makes it glow under an ultraviolet light. As the Biotechnology Forum outlines, here is how South Korean scientists first created the glowing cat in 2007:

They took skin cells from Turkish Angora female cat (species that were originally tamed by Tatars, but was later transferred to Turkey and is now considered the countrys national treasure), and using the virus they inserted the genetic code for the production of red fluorescent protein. Then they put genetically modified nuclei into eggs for cloning and such cloned embryos are returned to the donor cat. It thus became the surrogate mothers own clones.

And why make a cat that glows in the dark? The researchers explained that this was no frivolous experiment and that potential benefits exist in medicine for treating and testing for human diseases caused by genetic disorders. And just today, researchers in Uruguay announced that they had successfully created a genetically modified glowing sheep. Though not directly applicable to medical technology, the researchers had this to say about the purpose of their research: Our focus is generating knowledge, make it public so the scientific community can be informed and help in the long run march to generate tools so humans can live better, but were not out in the market to sell technology.

Moving on, two other good example are the less-flatulent cow and the so-called Ecopig. As Mother Nature Network explains, cows produce a lot of methane gas, which is second only to carbon dioxide in contributing to the greenhouse effect. So scientists at the University of Alberta identified the bacteria responsible for producing methane and designed a breed of cows that create 25 percent less methane than the average cow. This is one genetic engineering example that directly and practically addresses one of the major problems facing modern man.

The Ecopig (aka enviropig or Frankenswine) is yet another of the many examples of genetic engineering that positively contribute to the environment. The Ecopig has been genetically altered to better digest and process phosphorus. The reason is that pig dung is high in phytate, a form of phosphorous that farmers use it as fertilizer but which over stimulates the growth of algae which can deplete oxygen in the watersheds and thus kill marine life. The Ecopig has been genetically modified by adding E. Coli and mouse DNA to the pig embryo, which reduce the pigs phosphorous output by about 70 percent.

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Examples Of Genetic Engineering: Bizarre Yet Beneficial Uses Of Modern Biotech

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SANTA MONICA, Calif.--(BUSINESS WIRE)--

For cancer patients, selecting a treatment plan can be a complex and difficult process. Often, understanding future medical breakthroughs that can provide hope remains a distant and incomprehensible proposition. This may be the case as the field of oncology races towards the era of precision medicine.

Now, a recently-released video interview featuring Mark Rubin, MD, director of the new Institute for Precision Medicine at Weill Cornell Medical College and New York-Presbyterian Hospital, provides simple understanding of precision oncology and what the future holds for cancer patients.

In the simplest of terms, the ability to map the genes of cancer patients tumors and determine their specific genotype (variety) is rapidly moving oncology into the practice of precision medicine where the right oncology treatment is delivered to the right patient for optimal outcome. Less effective treatments are bypassed and those that can best target specific tumor types and destroy them can be deployed sooner.

In the interview, Dr. Rubin says: The concept that prostate cancer is not one cancer, but rather many cancers, is important for patients and clinicians to think about. This is going to lead us in the direction of breast or lung cancer where there are very well-defined subtypes and known drugs that provide specific responses.

The 12-minute interview with Dr. Rubin was produced by the Prostate Cancer Foundation and is featured on the home page of http://www.pcf.org. The Foundation has funded game-changing research for new medicines to treat prostate cancer and the identification of more than 27 genetic varieties of prostate cancer. Together, these advances are helping to make precision oncology a reality for patients.

About the Prostate Cancer Foundation

The Prostate Cancer Foundation (PCF) is the worlds largest philanthropic source of support for accelerating the most promising research for better treatments and cures for prostate cancer. Founded in 1993, PCF has raised more than $530 million and provided funding to more than 1,600 research programs at nearly 200 cancer centers and universities in 16 countries. PCF advocates for greater awareness of prostate cancer and more efficient investment of governmental research funds for transformational cancer research. Its efforts have helped produce a 20-fold increase in government funding for prostate cancer. More information about the PCF can be found at http://www.pcf.org.

Originally posted here:
Genetic Screening of Tumors Paves Way for Precision Oncology

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Featured Article Academic Journal Main Category: Tropical Diseases Also Included In: Infectious Diseases / Bacteria / Viruses Article Date: 29 Apr 2013 - 4:00 PDT

Current ratings for: Genetic Fingerprints Track Drug-Resistant Malaria Parasites

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Senior author Dominic Kwiatkowski, from the University of Oxford and the Wellcome Trust Sanger Institute near Cambridge, and colleagues, discovered the new artemisinin-resistant strains in western Cambodia, a known hotspot for drug-resistance. They write about this, and how they were able to identify distinct genetic patterns for each of the strains, in the 28 April online issue of Nature Genetics.

Artemisinin is the key drug against malaria, which is caused when the parasite P. falciparum gets into the bloodstream through a mosquito bite. However, according to the World Health Organization (WHO), the emergence of drug-resistant strains of the parasite is weakening the impact of artemisinin, putting hundreds of thousands of lives at risk.

Co-author Nicholas White, a professor from the Centre for Tropical Medicine at the University of Oxford, says in a statement:

"Artemisinin resistance is an emergency which could derail all the good work of global malaria control in recent years. We desperately need methods to track it in order to contain it, and molecular fingerprinting provides this."

Using new genome sequencing technologies, the international group sequenced the entire DNA of 825 P. falciparum samples from South East Asia and Africa and found an "unusual pattern of parasite population structure at the epicenter of artemisinin resistance in western Cambodia".

The technologies enabled them to pick out genetic patterns or "fingerprints" for each of the artemisinin-resistant strains.

Kwiatkowski tells the press:

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Genetic Fingerprints Track Drug-Resistant Malaria Parasites

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The Genetics of Canine Morphology Part 1
A teaching project for the 2013 Bio Expo by Randee Zerger. This project was mainly about researching the evolution of dogs and what dogs had evolved from ove...

By: StudentBioExpo

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The Genetics of Canine Morphology Part 1 - Video

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