Squamous cell carcinoma (SCC) represents the second most frequent skin cancer with more than half million new patients affected every year in the world. Cancer stem cells (CSCs) are a population of cancer cells that have been described in many different cancers, including skin SCCs and that feed tumor growth, could be resistant to therapy thus being responsible for tumor relapse after therapy. However, still very little is known about the mechanisms that regulate CSCs functions.

In a new study published and making the cover of Cell Stem Cell, researchers led by Pr. Cdric Blanpain, MD/PhD, professor and WELBIO investigator at the IRIBHM, Universit libre de Bruxelles, Belgium, report the mechanisms regulating the different functions of Twist1 controlling skin tumour initiation, cancer stem cell function and tumor progression.

Benjamin Beck and colleagues used state of the art genetic mouse models to dissect, the functional role and molecular mechanisms by which Twist1 controls tumor initiation, cancer stem cell function and tumor progression. In collaboration with Dr Sandrine Rorive and Pr Isabelle Salmon from the department of Pathology at the Erasme Hospital, ULB and the group of Jean-Christophe Marine (VIB, KUL Leuven), they demonstrated that while Twist1 is not expressed in the normal skin, Twist1 deletion prevents skin cancer formation demonstrating the essential role of Twist1 during tumorigenesis. "It was really surprising to observe the essential role of Twist1 at the earliest step of tumor formation, as Twist1 was thought to stimulate tumor progression and metastasis" comments Benjamin Beck, the first author of this study.

The authors demonstrate that different levels of Twist1 are necessary for tumor initiation and progression. Low level of Twist1 is required for the initiation of benign tumors, while higher level of Twist1 is necessary for tumor progression. They also demonstrate that Twist1 is essential for tumor maintenance and the regulation of cancer stem cell function. The researchers also uncovered that the different functions of Twist1 are regulated by different molecular mechanisms, and identified a p53 independent role of Twist1 in regulating cancer stem cell functions.

In conclusion, this work shows that Twist1, a well-known regulator of tumor progression, is necessary for tumor initiation, regulation of cancer stem cell function and malignant progression. "It was really interesting to see that different levels of Twist1 are required to carry out these different tumor functions and that these different Twist1 functions are regulated by different molecular pathways. Given the diversity of cancers expressing Twist1, the identification of the different mechanisms controlled by Twist1 are likely to be relevant for other cancers" comments Cdric Blanpain, the last and corresponding author of this study.

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The above story is based on materials provided by Libre de Bruxelles, Universit. Note: Materials may be edited for content and length.

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Skin cancer: New mechanism involved in tumor initiation, growth and progression

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A new study identifies a gene that is especially active in aggressive subtypes of breast cancer. The research suggests that an overactive BCL11A gene drives triple-negative breast cancer development and progression.

The research, which was done in human cells and in mice, provides new routes to explore targeted treatments for this aggressive tumour type.

There are many types of breast cancers that respond differently to treatments and have different prognoses. Approximately one in five patients is affected by triple-negative breast cancer; these cancers lack three receptor proteins that respond to hormone therapies used for other subtypes of breast cancer. In recent years it has become apparent that the majority of triple-negative tumours are of the basal-like subtype.

Although new treatments are being explored, the prognosis for triple-negative cancer is poorer than for other types. To date, only a handful of genomic aberrations in genes have been associated with the development of triple-negative breast cancer.

The team looked at breast cancers from almost 3000 patients. Their search had a particular focus: they examined changes to genes that affect the behaviour of stem cells and developing tissues, because other work they have done suggests that such genes, when mutated, can often drive cancer development. Among these was BCL11A.

"Our understanding of genes that drive stem cell development led us to search for consequences when these genes go wrong," says Dr Pentao Liu, senior author on the study, from the Wellcome Trust Sanger Institute. "BCL11A activity stood out because it is so active in triple-negative cancers.

"It had all the hallmarks of a novel breast cancer gene."

Higher activity of the BCL11A gene was found in approximately eight out of ten patients with basal-like breast cancer and was associated with a more advanced grade of tumour. In cases where additional copies of the BCL11A gene were created in the cancer, the prospects for survival of the patient were diminished.

"Our gene studies in human cells clearly marked BCL11A as a novel driver for triple-negative breast cancers," says Dr Walid Khaled, joint first author on the study from the Wellcome Trust Sanger Institute and University of Cambridge. "We also showed that adding an active human BCL11A gene to human or mouse breast cells in the lab drove them to behave as cancer cells.

"As important, when we reduced the activity of BCL11A in three samples of human triple-negative breast cancer cells, they lost some characteristics of cancer cells and became less tumorigenic when tested in mice. So by increasing BCL11A activity we increase cancer-like behaviour; by reducing it, we reduce cancer-like behaviour."

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Novel breast cancer gene found: BCL11A is active in difficult-to-treat triple-negative breast cancer

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A collaborative research project between Australian and Chinese scientists has shown how soybean can be bred to better tolerate soil salinity.

The researchers, at the University of Adelaide in Australia and the Institute of Crop Sciences in the Chinese Academy of Agricultural Sciences in Beijing, have identified a specific gene in soybean that has great potential for soybean crop improvement.

"Soybean is the fifth largest crop in the world in terms of both crop area planted and amount harvested," says the project's lead, University of Adelaide researcher Associate Professor Matthew Gilliham. "But many commercial crops are sensitive to soil salinity and this can cause major losses to crop yields.

"On top of that, the area of salt-affected agricultural land is rapidly increasing and is predicted to double in the next 35 years. The identification of genes that improve crop salt tolerance will be essential to our efforts to improve global food security."

Professor Lijuan Qiu and Dr Rongxia Guan at the Institute of Crop Sciences pinpointed a candidate salt tolerance gene after examining the genetic sequence of several hundred soybean varieties. Researchers at the ARC Centre of Excellence in Plant Energy Biology at the University of Adelaide's Waite campus then investigated the function of this gene.

"We initially identified the gene by comparing two commercial cultivars," says Professor Qiu. "We were surprised and pleased to see that this gene also conferred salt tolerance in some other commercial cultivars, old domesticated soybean varieties and even wild soybean.

"It appears that this gene was lost when breeding new cultivars of soybean in areas without salinity. This has left many new cultivars susceptible to the rapid increases we are currently seeing in soil salinity around the world."

By identifying the gene, genetic markers can now be used in breeding programs to ensure that salt tolerance can be maintained in future cultivars of soybean that will be grown in areas prone to soil salinity.

"This gene functions in a completely new way from other salt tolerance genes we know about," says Associate Professor Gilliham. "We can now use this information to find similar genes in different crops such as wheat and grapevine, to selectively breed for their enhanced salt tolerance."

This research has received support from the Australian Research Council (ARC) and is a feature article in The Plant Journal.

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Salt tolerance gene in soybean found

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Story highlights Roughly two-thirds of cancers in adults can be attributed to random mutations, study says "The remaining third are due to environmental factors and inherited genes" Behaviors (e.g. smoking, excessive sun exposure) still strongly tied to some cancers

That's bad luck -- and it's the primary cause of most cancer cases, says a Johns Hopkins Medicine research study.

Roughly two-thirds of cancers in adults can be attributed to random mutations in genes capable of driving cancer growth, said two scientists who ran statistics on cancer cases.

That may sound jaw-dropping. And Johns Hopkins anticipates that the study will change the way people think about cancer risk factors.

They also believe it could lead to changes in the funding of cancer studies, with a greater focus on finding ways to detect those cancers attributed to random mutations in genes at early, curable stages.

Smoking can still kill you

But, no, that's not permission to smoke or to not use sunblock.

Some forms of cancer are exceptions, where lifestyle and environment play a big role. Lung cancer is one of them. So is skin cancer.

And, if cancer runs in your family, this unfortunately doesn't mean you're in the clear. Some cancers are more strongly influenced by genetic heritage than others.

"The remaining third (of cancer cases) are due to environmental factors and inherited genes," the Kimmel Cancer Center said in a statement on the study published Friday in the magazine Science.

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Gene mutations cause most cancers

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Perfect Genetics - Dual CAS!
Leaving a like on this video really helps guys, thanks Leave a comment below with name suggestions for these two ladies please!! First Name and Surname - Love you guys x I am a social...

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Perfect Genetics - Dual CAS! - Video

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Researchers at King's College London have identified a new mechanism by which skin damage triggers the formation of tumours, which could have important therapeutic implications for patients suffering with chronic ulcers or skin blistering diseases.

The study, published today in Nature Communications, highlights an innate sensing of bacteria by immune cells in the formation of skin tumours. This molecular process could tip the balance between normal wound repair and tumour formation in some patients, according to researchers.

Although an association between tissue damage, chronic inflammation and cancer is well established, little is known about the underlying cause. Epidermolysis Bullosa (EB), for instance, is one of several rare inherited skin conditions associated with chronic wounding and increased risk of tumours.

However, this study - funded primarily by the Medical Research Council (MRC) and the Wellcome Trust - is the first to demonstrate that bacteria present on the skin can contribute to the development of skin tumours.

Researchers found that when mice with chronic skin inflammation are wounded they develop tumours at the wound site, with cells of the immune system required for this process to take place. They discovered that the underlying signalling mechanism involves a bacterial protein, flagellin, which is recognised by a receptor (Toll-like receptor 5) on the surface of the immune cells.

Although the direct relevance to human tumours is yet to be tested, researchers have shown that a protein called HMGB1 - found to be highly expressed in mice with chronic skin inflammation - is increased in human patients with Epidermolysis Bullosa (EB). The study found a reduction in HMGB1 levels in mice when the TLR-5 receptor was removed from immune cells. This raises the possibility of future treatments aimed at reducing levels of the flagellin bacterial protein on the skin surface, or targeting the TLR-5 receptor.

Professor Fiona Watt, lead author and Director of the Centre for Stem Cells and Regenerative Medicine at King's College London, said: 'These findings have broad implications for various types of cancers and in particular for the treatment of tumours that arise in patients suffering from chronic ulcers or skin blistering diseases.

'In the context of chronic skin inflammation, the activity of a particular receptor in white blood cells, TLR-5, could tip the balance between normal wound repair and tumour formation.'

Professor Watt added: 'Our findings raise the possibility that the use of specific antibiotics targeting bacteria in wound-induced malignancies might present an interesting clinical avenue.'

###

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Bacteria could contribute to development of wound-induced skin cancer

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Stem-cell research by Colorado State University staffers using bone marrow from horses to heal joint injuries on the same animal is making strides, and researchers have great hope that the project will lead to human medical applications.

A team with CSU's Equine Orthopaedic Research Center reports that adding stem-cell therapy to traditional arthroscopic surgery on horses has significantly increased success rates.

Horses that had follow-up, stem-cell treatment were twice as likely to return to normal activity as those that did not, said David Frisbie, an associate professor of equine surgery with CSU and part of the research team.

"We've doubled it, conservatively," in treating cartilage damage in the knee, Frisbie said.

The team had results of its work published last year in the journal Veterinary Surgery.

Some lesions in the meniscus of horses that could not be treated by surgery have been successfully mended using stem cells alone.

"Western performance horses, reining and cutting horses, and barrel horses are very prone to meniscal injuries," Frisbie said.

Beyond meniscus damage, researchers also have focused on tendon lesions in the lower leg, which typically strike race horses.

Horses that suffered a tendon lesion had about a 66 percent chance of reinjury after surgery. Add stem-cell treatment and the reinjury rate drops to 21 percent, Frisbie said.

"It beats the old standards of therapies," which included cortisone and use of other steroids, Frisbie said.

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CSU research on horse injuries, stem-cell recovery, may help humans

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A new study identifies a gene that is especially active in aggressive subtypes of breast cancer. The research suggests that an overactive BCL11A gene drives triple-negative breast cancer development and progression.

The research, which was done in human cells and in mice, provides new routes to explore targeted treatments for this aggressive tumour type.

There are many types of breast cancers that respond differently to treatments and have different prognoses. Approximately one in five patients is affected by triple-negative breast cancer; these cancers lack three receptor proteins that respond to hormone therapies used for other subtypes of breast cancer. In recent years it has become apparent that the majority of triple-negative tumours are of the basal-like subtype.

Although new treatments are being explored, the prognosis for triple-negative cancer is poorer than for other types. To date, only a handful of genomic aberrations in genes have been associated with the development of triple-negative breast cancer.

The team looked at breast cancers from almost 3000 patients. Their search had a particular focus: they examined changes to genes that affect the behaviour of stem cells and developing tissues, because other work they have done suggests that such genes, when mutated, can often drive cancer development. Among these was BCL11A.

"Our understanding of genes that drive stem cell development led us to search for consequences when these genes go wrong," says Dr Pentao Liu, senior author on the study, from the Wellcome Trust Sanger Institute. "BCL11A activity stood out because it is so active in triple-negative cancers.

"It had all the hallmarks of a novel breast cancer gene."

Higher activity of the BCL11A gene was found in approximately eight out of ten patients with basal-like breast cancer and was associated with a more advanced grade of tumour. In cases where additional copies of the BCL11A gene were created in the cancer, the prospects for survival of the patient were diminished.

"Our gene studies in human cells clearly marked BCL11A as a novel driver for triple-negative breast cancers," says Dr Walid Khaled, joint first author on the study from the Wellcome Trust Sanger Institute and University of Cambridge. "We also showed that adding an active human BCL11A gene to human or mouse breast cells in the lab drove them to behave as cancer cells.

"As important, when we reduced the activity of BCL11A in three samples of human triple-negative breast cancer cells, they lost some characteristics of cancer cells and became less tumorigenic when tested in mice. So by increasing BCL11A activity we increase cancer-like behaviour; by reducing it, we reduce cancer-like behaviour."

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Novel breast cancer gene found

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Home News Stress News Sensitive Gene Plus Early Stress May Lead to Mental Health Disorders By Traci Pedersen Associate News Editor Reviewed by John M. Grohol, Psy.D. on January 8, 2015

Researchers from Duke University have identified a gene variant linked to extreme sensitivity in children. They found that children with this gene who also live in high-risk environments are far more likely to develop mental health disorders and substance abuse problems as adults.

Prior research has suggested that while some children thrive like dandelions in a variety of environments, others are more like orchids who wither or bloom depending on the circumstance. The new study shows that different levels of sensitivity are linked to differences in genomes.

The findings are a step toward understanding the biology of what makes a child particularly sensitive to positive and negative environments, said Dustin Albert, Ph.D., a research scientist at the Duke Center for Child and Family Policy. This gives us an important clue about some of the children who need help the most.

For the study, researchers analyzed two decades worth of data on high-risk first-graders from four locations across the country. They found that kids from high-risk backgrounds who also carried the sensitive gene variant (glucocorticoid receptor gene NR3C1) were extremely likely to develop serious problems as adults.

In fact, when left untreated, 75 percent of high-risk children with this gene variant developed psychological problems by age 25, including alcohol abuse, substance abuse, and antisocial personality disorder.

The good news is that these children are very responsive to help as well. Among sensitive, high-risk children who participated in an intensive social-services program called the Fast Track Project, only 18 percent developed psychopathology as adults.

Its a hopeful finding, Albert said. The children we studied were very susceptible to stress. But far from being doomed, they were instead particularly responsive to help.

Previous research has linked participation in Fast Track interventions to lower rates of psychiatric problems, substance abuse, and convictions for violent crime in adulthood. For the new study, researchers looked at the biology behind those responses.

Albert said these findings could one day lead toward personalized therapies for some of societys most troubled children, perhaps matching children with particular programs.

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Sensitive Gene Plus Early Stress May Lead to Mental Health Disorders

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IMAGE:Soft Robotics, a peer-reviewed journal published quarterly online with Open Access options and in print, combines advances in biomedical engineering, biomechanics, mathematical modeling, biopolymer chemistry, computer science, and tissue engineering... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, January 8, 2015-- By defining a set of key metrics to evaluate the fuel systems available to drive autonomous and wearable soft robots, a team of engineers and chemists are able to compare the advantages and limitations of current technology options. They assess various types of pneumatic energy sources and their benefits for specific applications in an article published in Soft Robotics, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Soft Robotics website.

Michael Wehner and coauthors from Harvard University (Cambridge and Boston, MA), Oregon State University (Corvallis, OR), Carnegie Mellon University (Pittsburgh, PA), Robot G and I Research (Bedford, MA), Worcester Polytechnic Institute (Worcester, MA), and Cornell University (Ithaca, NY), characterize the most advanced pneumatic energy systems designed to power untethered and wearable soft robots based on their energy density and flow capacity, as well as noise, toxic byproducts, application-specific requirements, and the time and additional parts needed for development. The goal of the study, entitled "Pneumatic Energy Sources for Autonomous and Wearable Soft Robotics," is to provide a framework for configuring fuel systems in soft robotics.

"As soft pneumatic systems start to gain acceptance in robotic applications, it is vital that the advantages and limitations of different energy systems are fully explored. This paper provides comparisons and analysis that will useful for anyone designing such systems," says Editor-in-Chief Barry A. Trimmer, PhD, who directs the Neuromechanics and Biomimetic Devices Laboratory at Tufts University (Medford, MA).

###

About the Journal

Soft Robotics, a peer-reviewed journal published quarterly online with Open Access options and in print, combines advances in biomedical engineering, biomechanics, mathematical modeling, biopolymer chemistry, computer science, and tissue engineering to present new approaches to the creation of robotic technology and devices that can undergo dramatic changes in shape and size in order to adapt to various environments. Led by Editor-in-Chief Barry A. Trimmer, PhD, and a distinguished team of Associate Editors, the Journal provides the latest research and developments on topics such as soft material creation, characterization, and modeling; flexible and degradable electronics; soft actuators and sensors; control and simulation of highly deformable structures; biomechanics and control of soft animals and tissues; biohybrid devices and living machines; and design and fabrication of conformable machines. Tables of content and a sample issue can be viewed on the Soft Robotics website.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including 3D Printing and Additive Manufacturing and Tissue Engineering. Its biotechnology trade magazine, Genetic Engineering News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 80 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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New study from Harvard compares design of fuel systems for soft robots

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GMO is an abbreviation for a genetically modified organism whose genome has been altered by the techniques of genetic engineering so that its DNA contains one or more genes not normally found there.

Eighty per cent of our food contains some sort of GMO that you buy at the grocery store, and proponents of the technology point out theres not one incidence of human health issue. The USDA, the FDA, the CDC, and the United Nations Food and Agricultural Organization have all concluded that the technology is safe, and agricultural producers maintain that this technology is an absolutely necessary tool for them to be able to feed a growing world population. Travis Miller is the Interim Associate Director for State Operations for the Texas A&M Agrilife Extension Service.

Id encourage people, I like to do a garden myself, and Id encourage people to grow a garden but you cant feed the 300 million people in the United States all with back yard gardens, plus the 50% or more of our crop that we send overseas to feed other people. And GMOs have provided the technology that has reduced the pesticide use, has reduced the insect damage to our crops, has improved the quality of our crops, so that we do have the, its one of the many technologies that were now using to get the kind of yields we have to have to continue to feed the world.

Genetically Modified Organism technology is invaluable to plant breeders. If you look at what crops used to look like when we first started cultivating crops, the dont even resemble what we have today. And that was through traditional breeding technology, pollen from one source and pollen from another source. Problems that have plagued agriculture for decades are being addressed.

Now GMO is another important tool that a plant breeder can put in his tool box and say, oh, well what about this plant disease that we have, well heres a gene that I can take from a spinach plant and put in in a grapefruit and solve a disease thats going to take the citrus industry out.

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From the Ground Up - GMOs Necessary To Feed The World

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PITTSBURGH, January 8, 2015 - Genetic mutations may link smoking and alcohol consumption to destruction of the pancreas observed in chronic pancreatitis, according to a 12-year study led by researchers at the University of Pittsburgh School of Medicine. The findings, published today in Nature Publishing Group's online, open-access journal Clinical and Translational Gastroenterology, provides insight into why some people develop this painful and debilitating inflammatory condition while most heavy smokers or drinkers do not appear to suffer any problems with it.

The process appears to begin with acute pancreatitis, which is the sudden onset of inflammation causing nausea, vomiting and severe pain in the upper abdomen that may radiate to the back, and is typically triggered by excessive drinking or gallbladder problems, explained senior investigator David Whitcomb, M.D., Ph.D., chief of gastroenterology, hepatology and nutrition, Pitt School of Medicine. Up to a third of those patients will have recurrent episodes of acute pancreatitis, and up to a third of that group develops chronic disease, in which the organ becomes scarred from inflammation.

"Smoking and drinking are known to be strong risk factors for chronic pancreatitis, but not everyone who smokes or drinks damages their pancreas," Dr. Whitcomb said. "Our new study identifies gene variants that when combined with these lifestyle factors make people susceptible to chronic pancreatitis and may be useful to prevent patients from developing it."

In the North American Pancreatitis Study II consortium, researchers evaluated gene profiles and alcohol and smoking habits of more than 1,000 people with either chronic pancreatitis or recurrent acute pancreatitis and an equivalent number of healthy volunteers. The researchers took a closer look at a gene called CTRC, which can protect pancreatic cells from injury caused by premature activation of trypsin, a digestive enzyme inside the pancreas instead of the intestine, a problem that has already been associated with pancreatitis.

They found that a certain variant of the CTRC gene, which is thought to be carried by about 10 percent of Caucasians, was a strong risk factor for alcohol- or smoking-associated chronic pancreatitis. It's possible that the variant fails to protect the pancreas from trypsin, leaving the carrier vulnerable to ongoing pancreatic inflammation and scarring.

"This finding presents us with a window of opportunity to intervene in the diseases process," Dr. Whitcomb said. "When people come to the hospital with acute pancreatitis, we could screen for this gene variant and do everything possible to help those who have it quit smoking and drinking alcohol, as well as test new treatments, because they have the greatest risk of progressing to end-stage chronic pancreatitis."

Whitcomb's team has been implementing more personalized approaches to pancreatic diseases in the Pancreas Center of Excellence within the Digestive Disorders Center at UPMC and hopes to learn whether use of genetic information can, in fact, reduce the chances of chronic disease in high-risk patients.

###

The study team includes Jessica LaRusch, Ph.D., Antonio Lozano-Leon, Ph.D., Kimberly Stello, Amanda Moore, Venkata Muddana, M.D., Michael O'Connell, Ph.D., Brenda Diergaarde, Ph.D., and Dhiraj Yadav, M.D., all of the University of Pittsburgh.

The project was funded by National Institutes of Health grants DK061451, DK077906 and DK063922, and the Conselleria de Industria e Innovacin, Xunta de Galicia, Spain.

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Smoking, alcohol, gene variant interact to increase risk of chronic pancreatitis

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Highlights

Washington, DC (January 8, 2015) -- New research provides insights into the ties between certain genetic variants and kidney disease in African Americans. The genetic association is one of the strongest ever reported for a common disease, and these latest findings may help improve diagnosis and treatment. The study appears in an upcoming issue of the Journal of the American Society of Nephrology (JASN).

African Americans have a 4-fold increased risk for chronic kidney disease compared with European Americans. Recent work from several research groups has shown that much of this risk is due to genetic variations in a gene called apolipoprotein L1 (APOL1), which creates a protein that is a component of HDL, or good cholesterol. These variants arose tens of thousands of years ago in sub-Saharan Africa, and so are present in individuals who have recent sub-Saharan African ancestry. Approximately 5 million African Americans carry APOL1 risk variants, placing them at increased risk for kidney disease.

Jeffrey Kopp, MD (National Institutes of Health) and his colleagues investigated the role of APOL1 variants in a particular form of kidney disease called focal segmental glomerulosclerosis (FSGS). The team studied information on 94 patients with FSGS and found that patients who had APOL1 variants tended to have more advanced disease when they were diagnosed, which fits with prior observations that this genetic form of FSGS progresses rapidly. Previous research has shown that patients with two APOL1 variants respond to glucocorticoids with reductions in urinary protein excretion, but they nonetheless may experience progressive loss of kidney function. The present study showed a similar pattern with cyclosporine and mycophenolate mofetil. "New therapies targeting APOL1 injury pathways are needed, as standard therapies do not work for many people with this gene variant," said Dr. Kopp.

The investigators also found that 72% of self-identified African Americans in the study had APOL1 risk variants, similar to earlier findings. "We also found the APOL1 risk genotype in 2 individuals of Hispanic descent, which is well known, and in 2 individuals who self-identified as White, or European American, which has not been reported before. This last finding suggests that APOL1 risk variants can be present in individuals who self-identify in various ways," said Dr. Kopp.

In an accompanying editorial, Christopher Larsen, MD (Nephropath) and Barry Freedman, MD, PhD (Wake Forest School of Medicine) write that "the report by Kopp et al. enhances our understanding of a common etiology of the FSGS lesion seen on kidney biopsy in African Americans." They note, however, that the findings from the trial, although informative, are not encouraging due to the poor outcomes that patients with APOL1 variants often ultimately experience.

###

Study co-authors include Cheryl Winkler, PhD, Xiongce Zhao, PhD, Milena Radea, PhD, Jennifer Gassman, PhD, Vivette D'Agati, MD, Cynthia Nast, MD, Changli Wei, MD, Jochen Reiser, MD, PhD, Lisa Guay Woodford, MD, Friedhelm Hildebrandt, MD, Marva Moxie-Mims, MD, Debbie Gipson, MD, Aaron Friedman, MD, and Frederick Kaskel, MD.

Disclosures: The authors reported no financial disclosures.

The article, entitled "Clinical Features and Histology of Apolipoprotein L1-Associated Nephropathy in the FSGS Clinical Trial," will appear online at http://jasn.asnjournals.org/ on January 8, 2015.

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Study provides insights into the role of genetic variants in kidney disease

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What: Shares of Seattle Genetics , a biotechnology company that utilizes its antibody-drug conjugate technology to develop therapies to fight cancer, dipped 12% in December, based on data from S&P Capital IQ , following the release of scientific data at the American Society of Hematology's annual meeting.

So what: Here's the interesting part: the study data presented by Seattle Genetics at ASH wasn't bad. The unfortunate part is the company was upstaged by cancer immunotherapies, and Wall Street is concerned about the long-term future of antibody-drug conjugates, or ADCs, in light of the recent success of these cancer immunotherapies that work with the body's immune system to identify and attack cancer cells.

For instance, Seattle Genetics presented four-year survival data on FDA-approved Adcetris in patients with relapsed or refractory systemic anaplastic large cell lymphoma at ASH. The company highlighted that an impressive 64% of patients were still alive, with half of the patients that achieved a complete response remaining disease-free. It also delivered positive phase 3 data with partner Takeda Pharmaceutical in the AETHERA trial for post-transplant Hodgkin lymphoma patients at risk for a relapse that were treated with Adcetris.

Source: Bristol-Myers Squibb.

The problem is that Seattle Genetics was upstaged by PD-1 inhibitors like Bristol-Myers Squibb 's Opdivo and Merck 'sKeytruda. Both showed remarkable efficacy in treating Hodgkin's lymphoma during ASH after patients had been treated with Adcetris and showed disease progression. The worry here is these PD-1 inhibitors may begin working their way up the scale to first- or second-line indications and push Adcetris and other ADCs out of the way.

Now what: This was a rough month for Seattle Genetics shareholders, and I suspect it could get rougher in 2015. While I'm a fan of ADCs in general and believe we'll see Adcetris' label expanded to new indications in the coming years, I also can't deny that immunotherapies are picking up steam, and that Seattle Genetics is accordingly looking very pricey.

Source: Seattle Genetics.

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Why Seattle Genetics, Inc. Stock Dove 12% in December

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Published 07 January 2015

Cellular Biomedicine Group, a biomedicine firm engaged in the development of effective treatments for degenerative and cancerous diseases, announced the initiation of patient recruitment to support a study of ReJoin human adipose derived mesenchymal progenitor cell (haMPC) therapy for Cartilage Damage (CD) resulting from osteoarthritis (OA) or sports injury.

The study is based on the same science that has shown tremendous progress in the treatment of Knee Osteoarthritis (KOA). Both arthroscopy and the use of magnetic resonance imaging (MRI) will be deployed to further demonstrate the regenerative efficacy of ReJoin on CD.

The decision to explore the efficacy of the company's proprietary ReJoin therapy on an additional orthopedic indication, Cartilage Damage (CD), follows the encouraging data readout from its Knee Osteoarthritis Phase IIa Clinical Trial, of which the twelve-month follow-up results were announced in December 2014.

"We anticipate patient treatment in this study to be completed by the end of Q2 2015, and to report the interim results in Q3 2015. We very much look forward to finding the promise of ReJoinTM therapy for further indications. The repair of damaged cartilage would fundamentally improve the quality of life for CD patients, allowing for greater mobility, flexibility and less pain," said Dr. William (Wei) Cao, Chief Executive Officer of the Company.

The Phase II clinical study is a single-blind, randomly assigned, controlled clinical research study that will enroll thirty patients with the purpose of evaluating the safety and efficacy of haMPCs combined with lavage, debridement, and/or microfracture under arthroscopy treatment for cartilage damage.

In addition, this study shall serve as a supporting study of ReJoin for the treatment of Knee Osteoarthritis (KOA) so as to bring additional clinical data to the protocol of future KOA trials.

The study is conducted by Shanghai Ninth People's Hospital, a leading teaching hospital affiliated with Shanghai Jiao Tong University School of Medicine. Professor Wang You, Director of the hospital's orthopedics department and Vice Chairperson of the Chinese Knee Society, will lead the study as Principal Investigator.

Currently in China KOA patients number over 57 million. The incidence of cartilage damage in routine knee arthroscopies has been reported to be almost 300,000 per year. (Source: Market analysis of Chinese arthroscopy, published on July 21, 2014 and "Advances in Orthopedics" Volume 2012, Article ID 528423) Similar to KOA, CD is an unmet orthopedic medical need.

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Cellular Biomedicine begins patient recruitment for cartilage damage stem cell therapy clinical research study

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Published 07 January 2015

Gamida Cell, a leader in cell therapy technologies and products for transplantation and adaptive immune therapy, announced that orphan drug designation has been granted by The US Department of Health and Human Services, The FDA Office of Orphan Products Development (OOPD) for the investigational medicinal product NiCord for the treatment of acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), Hodgkin lymphoma and myelodysplastic syndrome (MDS).

The FDA orphan drug designation coincides with the positive opinion of the European Medicines Agency's (EMA's) Committee for Orphan Medicinal Products (COMP) regarding NiCord as a treatment for AML. Gamida Cell intends to file for NiCord orphan drug status with the EMA for other indications as well.

"Receipt of orphan drug status for NiCord in the US and Europe advances Gamida Cell's commercialization plans a major step further, as both afford significant advantages. We very much appreciate the positive feedback and support of the FDA and EMA and look forward to continuing what has been a very positive dialogue with these important agencies," said Gamida Cell president and CEO Dr. Yael Margolin.

The FDA and EMA grant an orphan drug designation to promote the development of products that demonstrate promise for the treatment of rare diseases or conditions. Orphan drug designation provides for various regulatory and economic benefits, including seven years of market exclusivity in the U.S. and 10 years in the EU.

NiCord is derived from a single cord blood unit which has been expanded in culture and enriched with stem cells using Gamida Cell's proprietary NAM technology.

It is currently being tested in a Phase I/II study as an investigational therapeutic treatment for hematological malignancies such as leukemia and lymphoma. In this study, NiCord is being used as the sole stem cell source.

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Gamida Cell's NiCord gets FDA and EMA orphan drug status

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Boston, MA (PRWEB) January 08, 2015

James Sherley, Director of the new biotech start-up Asymmetrex, LLC (previously, the Adult Stem Cell Technology Center, LLC) says that he is looking forward to laboratories around the globe evaluating the companys most recent exciting new stem cell technology, which allows tissue stem cells to be counted for the first time. The new technology is reported online this week in Stem Cell Research.

With only the purchase of two commercially available antibodies, any basic cell biology lab can evaluate the new technology for counting its favorite adult tissue stem cells, which Asymmetrex also refers to as distributed stem cells. Asymmetrex scientists accomplished the essential proof of principle in the report with cultured mouse hair follicle stem cells. They also showed that cells with the specific detection criterion were found in mouse hair follicles themselves in regions known to contain the stem cells. With collaborator Dr. Jennifer Chen, they demonstrated that cells in experimental cultures enriched for human skeletal muscle stem cells had the criterion, too. The technology is predicted to be universally able to count adult tissue stem cells in many different tissue types and different vertebrate species, including most, if not all, human tissues.

To count tissue stem cells, the first antibody needed is one that identifies chromosomes found in all cells about an hour before they divide to become two cells. The second antibody needed is one that identifies a special set of chromosomes that is found specifically in adult tissue stem cells. Asymmetrexs Director Sherley spent the last 16 years defining properties of these unique chromosomes, which are called immortal chromosomes. By evaluating both of these antibodies cell detection patterns simultaneously, adult tissue stem cells can be identified with sufficient specificity to count them with a high degree of confidence.

The new report shows that getting to the new technology was a rather complicated business. The project started with the work of Dr. Minsoo Noh when he was a doctoral graduate student in Dr. Sherleys lab at the Massachusetts Institute of Technology. In his graduate studies, Dr. Noh applied a bioengineering-bioinformatics approach to identifying genes that were highly associated with the unique properties of adult tissue stem cells. To avoid the previously unsolved problem of impure tissue stem cells, Dr. Noh used a family of cells that were engineered to model the unique properties of tissue stem cells. He was successful in identifying a large number of cellular genes whose expression was highly specific for unique tissue stem cell properties.

With Dr. Nohs success, the research team now faced a common bioinformatics pitfall too many genes to know which to study next. Dr. David Winklers group at CSIRO in Australia, co-authors of the report, provided a solution. The new report details how Winklers team applied a newly emerging probabilistic approach to reduce a thousand-plus member gene set down to a single gene for interrogation, the histone H2A variant H2A.Z. Oddly, H2A.Z was reduced during adult tissue stem cell specific functions, which went against the conventional biomarker concept of being increased. Dr. Yang Hoon Huh, then a post-doctoral fellow with the Sherley team, undertook an intent investigation of H2A.Zs tissue stem cell-associated properties despite its non-conformist expression. Due to his persistent studies, H2A.Z emerged as the key target of the second antibody in the new technology.

The ability to identify adult tissue stem cells specifically means that now, for the first time, they can be counted. This long awaited capability will begin a new era of quantitative stem cell biology and stem cell medicine. Sherley predicts that, It will be as if tissue stem cell biology put on glasses for the first time. Previously, tissue stem cell research, existing stem cell medicine (e.g., bone marrow transplantation), and new regenerative medicine developments have operated in a blurry world of not knowing the actual number of the elusive tissue stem cells involved in experiments or transplantation treatments. The ability simply to count the critical cells will have a major impact on the quality and progress of these important applications for continuing advances in medicine and human health.

******************************************************************************************** Asymmetrex, LLC is a Massachusetts life sciences company. Asymmetrexs founder and director, James L. Sherley, M.D., Ph.D. is the foremost authority on the unique properties of adult tissue stem cells. The companys patent portfolio contains biotechnologies that solve the three main technical problems production, quantification, and monitoring that have stood in the way of successful commercialization of human adult tissue stem cells for regenerative medicine and drug development. In addition, the portfolio includes novel technologies for isolating cancer stem cells and producing induced pluripotent stem cells. Currently, Asymmetrex is employing its technological advantages to pursue commercialization of facile methods for monitoring adult tissue stem cell number and function.

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New Technology from Asymmetrex Promises to End the Era of Elusive Adult Tissue Stem Cells

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Dallas,TX (PRWEB) January 08, 2015

One of the major trends upcoming in this market is the automation of gene expression profiling. This helps reduce consumption of reagents, and enhances accuracy and productivity in research and drug discovery.

According to the report, one of the major drivers of the market is advances in the gene expression market. As a result of automation, accuracy, and sensitivity of gene expression, technology and products have improved. Advanced gene expression products such as DNA microarray chips, RT-PCR, and advanced NGS provide a high degree of accuracy, efficiency, and productivity in research and drug discovery.

Further, the report states that one of the major challenges in the market is intense competition among vendors. Numerous large and medium-scale companies in the market provide high-end gene expression products, including instruments and software.

Order a copy of this report at (Prices start at US $ 3000 for a single user PDF) http://www.reportsnreports.com/Purchase.aspx?name=322429 .

Key players in the Global Gene Expression Market are Affymetrix Inc., Agilent Technologies Inc., Bio-Rad Laboratories Inc., F. Hoffmann-La Roche Ltd., Illumina Inc., Qiagen NV and Thermo Fisher Scientific Inc.

Other Prominent Vendors in the market are Agena Bioscience, Applied Microarrays, Arrayit, AutoGenomics, BD, Beijing Genomics Institute, BioChain Institute, Biometrix Technology, Cepheid, CombiMatrix, Danaher, Danyel Biotech (a Part of Gamida for Life Group), EMD Millipore, Eppendorf, Exiqon, Fluidigm, GE Healthcare, Great Basin, LC Sciences, Luminex, Microarrays, Miltenyi Biotec, OriGene Technologies, Oxford Gene Technology, Oxford Nanopore Technologies, Partek, Perkin Elmer, Phalanx Biotech Group, Promega, Takara Bio, Tecan, Veredus Laboratories and Zyagen.

Market Driver

Market Challenge

Market Trend

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Gene Expression Market to Grow at a CAGR of 11.12% by 2019 a New Research Report at ReportsnReports.com

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1 hour ago Photo of a soybean salt-tolerant plant compared to a non-tolerant variety

A collaborative research project between Australian and Chinese scientists has shown how soybean can be bred to better tolerate soil salinity.

The researchers, at the University of Adelaide in Australia and the Institute of Crop Sciences in the Chinese Academy of Agricultural Sciences in Beijing, have identified a specific gene in soybean that has great potential for soybean crop improvement.

"Soybean is the fifth largest crop in the world in terms of both crop area planted and amount harvested," says the project's lead, University of Adelaide researcher Associate Professor Matthew Gilliham. "But many commercial crops are sensitive to soil salinity and this can cause major losses to crop yields.

"On top of that, the area of salt-affected agricultural land is rapidly increasing and is predicted to double in the next 35 years. The identification of genes that improve crop salt tolerance will be essential to our efforts to improve global food security."

Professor Lijuan Qiu and Dr Rongxia Guan at the Institute of Crop Sciences pinpointed a candidate salt tolerance gene after examining the genetic sequence of several hundred soybean varieties. Researchers at the ARC Centre of Excellence in Plant Energy Biology at the University of Adelaide's Waite campus then investigated the function of this gene.

"We initially identified the gene by comparing two commercial cultivars," says Professor Qiu. "We were surprised and pleased to see that this gene also conferred salt tolerance in some other commercial cultivars, old domesticated soybean varieties and even wild soybean.

"It appears that this gene was lost when breeding new cultivars of soybean in areas without salinity. This has left many new cultivars susceptible to the rapid increases we are currently seeing in soil salinity around the world."

By identifying the gene, genetic markers can now be used in breeding programs to ensure that salt tolerance can be maintained in future cultivars of soybean that will be grown in areas prone to soil salinity.

"This gene functions in a completely new way from other salt tolerance genes we know about," says Associate Professor Gilliham. "We can now use this information to find similar genes in different crops such as wheat and grapevine, to selectively breed for their enhanced salt tolerance."

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Research finds salt tolerance gene in soybean

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Since the discovery of how DNA encodes genetic information, most research on the evolution of life has focused on genes. According to the "selfish gene" theory, cells and organisms exist simply as packages to protect and transmit genes. New research challenges this idea, proposing instead that if anything is "selfish" it must be the ribosome. That up-ends everything we think we know about the evolution of life and, in fact, the function of ribosomes themselves.

What came first in the evolution of life? Until now, scientists have answered the question with three letters: DNA. But In a father-daughter collaboration published in Journal of Theoretical Biology, Dr. Meredith Root-Bernstein, Aarhus University, Denmark, and Dr. Robert Root-Bernstein, Michigan State University, USA, provide evidence that the question should rather be answered with the word: Ribosomes.

The ribosome is a large and complex molecule found in all living cells. It contains the machinery for translating the genetic information from DNA into the proteins that perform all the work of the cell and make up most of its structure.

"Ribosomes are made of three protein-encrusted RNA strands that textbooks tell us are purely structural, but we show that ribosomal RNA once acted as the genes, mRNAs and tRNAs required to make its own components -- and gave rise to these structures in modern cells," says Dr. Meredith Root-Bernstein.

What does DNA want?

The father-daughter research collaboration started when Meredith was re-reading her father Robert Root-Bernstein's 1989 book Discovering.

"Halfway through the book, inspired by the discovery strategies my father discusses there, I looked up and asked "what does DNA want?" It may sound strange to anthropomorphize a large molecule. However, the selfish gene theory is commonly expressed in a scientific short-hand as "DNA wants to replicate itself." But I wondered if this is really what DNA wants," Dr. Meredith explains.

When organic chemists anthropomorphize molecules, they say that molecules "want to be in their lowest energy conformation." This means that when they have energy molecules can move into different conformations, but they have a resting position that they come back to.

The resting position of DNA is very tightly curled up. It is so hard to unravel that researchers do not fully understand how the various helper molecules uncurl and unzip it for replication and translation.

Thus, as Meredith realized, from the organic chemistry point of view, the answer to "what does DNA want" is: It wants to sit curled up in a knot. DNA does not want to replicate or translate.

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Forget the selfish gene: Evolution of life is driven by the selfish ribosome, research suggests

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4.4 Genetic Engineering

By: Juliana Agostino

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4.4 Genetic Engineering - Video

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S033RS03 Science Topics Genetics and Genetic Engineering
Science Topics Genetics and Genetic Engineering #39;Science Topics #39; BBC schools programme. Series originally broadcast on BBC2 1983 - 1985. Repeated until 1992.

By: Lammas Science

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S033RS03 Science Topics Genetics and Genetic Engineering - Video

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Genetics Introduction
Introduction to the Genetics Playlist to be used for the introduction to a genetics unit.

By: Annie Gibson

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Genetics Introduction - Video

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PreAP Mendelian Genetics 5.1
This video screencast was created with Doceri on an iPad. Doceri is free in the iTunes app store. Learn more at http://www.doceri.com.

By: Jeana Gilbet

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PreAP Mendelian Genetics 5.1 - Video

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Stark B4 Biology Snowman Genetics
Stark B4 Biology Snowman Genetics.

By: Nicole Stark

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Stark B4 Biology Snowman Genetics - Video

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