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Our world seems to grow smaller by the day as biodiversity rapidly dwindles, but Mother Earth still has a surprise or two up her sleeve. An international team of researchers were the first to investigate a never before studied species -- a giant, black, mud dwelling, worm-like animal. The odd animal doesn't seem to eat much, instead it gets its energy from a form of sulfur. The findings, led by scientists at the University of Utah, Northeastern University, University of the Philippines, Sultan Kudarat State University and Drexel University, will be published online in the Apr. 17 issue of the Proceedings of the National Academy of Sciences. People have known about the existence of the creature for centuries. The three- to five-foot long, tusk-like shells that encase the animal were first documented in the 18th century. "The shells are fairly common," begins lead investigator Daniel Distel, Ph.D., a research professor and director of the Ocean Genome Legacy Center at Northeastern University, "But we have never had access to the animal living inside." The animal's preferred habitat was unclear, but the research team benefitted from a bit of serendipity when one of their collaborators shared a documentary that aired on Philippine television. The video showed the bizarre creatures planted, like carrots, in the mud of a shallow lagoon. Following this lead, the scientists set up an expedition and found live specimens of Kuphus polythalamia. With a live giant shipworm finally in hand, the research team huddled around Distel as he carefully washed the sticky mud caked to the outside of the giant shipworm shell and tapped off the outer cap, revealing the creature living inside. "I was awestruck when I first saw the sheer immensity of this bizarre animal," says Marvin Altamia, researcher at the marine sciences institute, University of the Philippines. "Being present for the first encounter of an animal like this is the closest I will ever get to being a 19th century naturalist," says the study's senior author Margo Haygood, a research professor in medicinal chemistry at the University of Utah College of Pharmacy. Because the animal had never been studied rigorously, little was known about its life history, habitat, or biology. "We suspected the giant shipworm was radically different from other wood-eating shipworms," says Haygood. "Finding the animal confirmed that." Altamia continues, "Frankly, I was nervous. If we made a mistake, we could lose the opportunity to discover the secrets of this very rare specimen." The scientists were then faced with an interesting dilemma explain why Kuphus is so unusual. The answer may lie in the remote habitat in which it was found, a lagoon laden with rotting wood. The normal shipworm burrows deep into the wood of trees that have washed into the ocean, munching on and digesting the wood with the help of bacteria. Unlike its shipworm cousins, Kuphus lives in the mud. It also turns to bacteria to obtain nourishment, but in a different way. Kuphus lives in a pretty stinky place. The organic-rich mud around its habitat emits hydrogen sulfide, a gas derived from sulfur, which has a distinct rotten egg odor. This environment may be noxious for you and me, but it is a feast for the giant shipworm. And yet Kuphus themselves don't eat, or if they do, they eat very little. Instead, they rely on beneficial bacteria that live in their gills that make food for them. Like tiny chefs, these bacteria use the hydrogen sulfide as energy to produce organic carbon that feeds the shipworm. This process is similar to the way green plants use the sun's energy to convert carbon dioxide in the air into simple carbon compounds during photosynthesis. As a result, many of Kuphus's internal digestive organs have shrunk from lack of use. The giant shipworm's lifestyle lends support to a hypothesis proposed by Distel almost two decades ago. Acquiring a different type of beneficial bacteria could explain how shipworms transition from a wood-eating organism to one that uses a noxious gas in mud to survive. The research team will continue to examine the role wood plays in the unique transition between the normal shipworm and the giant shipworm. "We are also interested to see if similar transitions can be found for other animals that live in unique habitats around the world," said Distel. The discovery of this flagship creature expands on our understanding of biodiversity in the Indo-Pacific region, which was made possible through collaborative nature of this interdisciplinary, international research group. This work is an important component of research grants provided by the International Cooperative Biodiversity Groups program. The program helps researchers conduct projects in developing countries to identify unique, novel compounds for future drug development, while building research capacity and conserving biodiversity in the host country. Distel and Haygood collaborated with colleagues from University of Utah, Drexel University, Second Genome in San Francisco, Ecole Normale Superieure, France and the University of the Philippines, the Sultan Kudarat State University and the Philippine Genome Center in the Philippines. The research was funded by National Institutes of Health, National Science Foundation and U.S Department of Energy, Joint Genome Institute.


News Article | May 1, 2017
Site: www.prweb.com

A novel gene therapy using CRISPR genome editing technology effectively targets cancer-causing “fusion genes” and improves survival in mouse models of aggressive liver and prostate cancers, University of Pittsburgh School of Medicine researchers report in a study published online today in Nature Biotechnology. “This is the first time that gene editing has been used to specifically target cancer fusion genes. It is really exciting because it lays the groundwork for what could become a totally new approach to treating cancer,” explained lead study author Jian-Hua Luo, M.D., Ph.D., professor of pathology at Pitt’s School of Medicine and director of its High Throughput Genome Center. Fusion genes, which often are associated with cancer, form when two previously separate genes become joined together and produce an abnormal protein that can cause or promote cancer. Luo and his team had previously identified a panel of fusion genes responsible for recurrent and aggressive prostate cancer. In a study published earlier this year in the journal Gastroenterology, the team reported that one of these fusion genes, known as MAN2A1-FER, also is found in several other types of cancer, including that of the liver, lungs and ovaries, and is responsible for rapid tumor growth and invasiveness. In the current study, the researchers employed the CRISPR-Cas9 genome editing technology to target unique DNA sequences formed because of the gene fusion. The team used viruses to deliver the gene editing tools that cut out the mutated DNA of the fusion gene and replaced it with a gene that leads to death of the cancer cells. Because the fusion gene is present only in cancer cells, not healthy ones, the gene therapy is highly specific. Such an approach could come with significantly fewer side effects when translated to the clinic, which is a major concern with other cancer treatments such as chemotherapy. To conduct the study, the researchers used mouse models that had received transplants of human prostate and liver cancer cells. Editing the cancer fusion gene resulted in up to 30 percent reduction in tumor size. None of the mice exhibited metastasis and all survived during the eight-week observation period. In contrast, in control mice treated with viruses designed to cut out another fusion gene not present in their tumors, the tumors increased nearly 40-fold in size, metastasis was observed in most animals, and all died before the end of the study. The new findings suggest a completely new way to combat cancer. “Other types of cancer treatments target the foot soldiers of the army. Our approach is to target the command center, so there is no chance for the enemy’s soldiers to regroup in the battlefield for a comeback,” said Luo. Another advantage over traditional cancer treatment is that the new approach is very adaptive. A common problem that renders standard chemotherapies ineffective is that the cancer cells evolve to generate new mutations. Using genome editing, the new mutations could be targeted to continue fighting the disease, Luo noted. In the future, the researchers plan to test whether this strategy could completely eradicate the disease rather than induce the partial remission observed in the current study. This work was supported by National Institutes of Health grant RO1 CA098249, Department of Defense grant W81XWH-16-1-0364 and a grant from the University of Pittsburgh Cancer Institute. Additional authors include: Zhang-Hui Chen, Ph.D., Yan Yu, M.D., Ph.D., Ze-Hua Zuo, Ph.D., Joel Nelson, M.D., George Michalopoulos, M.D., Ph.D., Satdatshan Monga, M.D., Silvia Liu, B.S., and George Tseng, Sc.D., all of Pitt. About the University of Pittsburgh School of Medicine As one of the nation’s leading academic centers for biomedical research, the University of Pittsburgh School of Medicine integrates advanced technology with basic science across a broad range of disciplines in a continuous quest to harness the power of new knowledge and improve the human condition. Driven mainly by the School of Medicine and its affiliates, Pitt has ranked among the top 10 recipients of funding from the National Institutes of Health since 1998. In rankings recently released by the National Science Foundation, Pitt ranked fifth among all American universities in total federal science and engineering research and development support. Likewise, the School of Medicine is equally committed to advancing the quality and strength of its medical and graduate education programs, for which it is recognized as an innovative leader, and to training highly skilled, compassionate clinicians and creative scientists well-equipped to engage in world-class research. The School of Medicine is the academic partner of UPMC, which has collaborated with the University to raise the standard of medical excellence in Pittsburgh and to position health care as a driving force behind the region’s economy. For more information about the School of Medicine, see http://www.medschool.pitt.edu.


News Article | May 1, 2017
Site: www.eurekalert.org

PITTSBURGH, May 1, 2017 - A novel gene therapy using CRISPR genome editing technology effectively targets cancer-causing "fusion genes" and improves survival in mouse models of aggressive liver and prostate cancers, University of Pittsburgh School of Medicine researchers report in a study published online today in Nature Biotechnology. "This is the first time that gene editing has been used to specifically target cancer fusion genes. It is really exciting because it lays the groundwork for what could become a totally new approach to treating cancer," explained lead study author Jian-Hua Luo, M.D., Ph.D., professor of pathology at Pitt's School of Medicine and director of its High Throughput Genome Center. Fusion genes, which often are associated with cancer, form when two previously separate genes become joined together and produce an abnormal protein that can cause or promote cancer. Luo and his team had previously identified a panel of fusion genes responsible for recurrent and aggressive prostate cancer. In a study published earlier this year in the journal Gastroenterology, the team reported that one of these fusion genes, known as MAN2A1-FER, also is found in several other types of cancer, including that of the liver, lungs and ovaries, and is responsible for rapid tumor growth and invasiveness. In the current study, the researchers employed the CRISPR-Cas9 genome editing technology to target unique DNA sequences formed because of the gene fusion. The team used viruses to deliver the gene editing tools that cut out the mutated DNA of the fusion gene and replaced it with a gene that leads to death of the cancer cells. Because the fusion gene is present only in cancer cells, not healthy ones, the gene therapy is highly specific. Such an approach could come with significantly fewer side effects when translated to the clinic, which is a major concern with other cancer treatments such as chemotherapy. To conduct the study, the researchers used mouse models that had received transplants of human prostate and liver cancer cells. Editing the cancer fusion gene resulted in up to 30 percent reduction in tumor size. None of the mice exhibited metastasis and all survived during the eight-week observation period. In contrast, in control mice treated with viruses designed to cut out another fusion gene not present in their tumors, the tumors increased nearly 40-fold in size, metastasis was observed in most animals, and all died before the end of the study. The new findings suggest a completely new way to combat cancer. "Other types of cancer treatments target the foot soldiers of the army. Our approach is to target the command center, so there is no chance for the enemy's soldiers to regroup in the battlefield for a comeback," said Luo. Another advantage over traditional cancer treatment is that the new approach is very adaptive. A common problem that renders standard chemotherapies ineffective is that the cancer cells evolve to generate new mutations. Using genome editing, the new mutations could be targeted to continue fighting the disease, Luo noted. In the future, the researchers plan to test whether this strategy could completely eradicate the disease rather than induce the partial remission observed in the current study. This work was supported by National Institutes of Health grant RO1 CA098249, Department of Defense grant W81XWH-16-1-0364 and a grant from the University of Pittsburgh Cancer Institute. Additional authors include: Zhang-Hui Chen, Ph.D., Yan Yu, M.D., Ph.D., Ze-Hua Zuo, Ph.D., Joel Nelson, M.D., George Michalopoulos, M.D., Ph.D., Satdatshan Monga, M.D., Silvia Liu, B.S., and George Tseng, Sc.D., all of Pitt. About the University of Pittsburgh School of Medicine As one of the nation's leading academic centers for biomedical research, the University of Pittsburgh School of Medicine integrates advanced technology with basic science across a broad range of disciplines in a continuous quest to harness the power of new knowledge and improve the human condition. Driven mainly by the School of Medicine and its affiliates, Pitt has ranked among the top 10 recipients of funding from the National Institutes of Health since 1998. In rankings recently released by the National Science Foundation, Pitt ranked fifth among all American universities in total federal science and engineering research and development support. Likewise, the School of Medicine is equally committed to advancing the quality and strength of its medical and graduate education programs, for which it is recognized as an innovative leader, and to training highly skilled, compassionate clinicians and creative scientists well-equipped to engage in world-class research. The School of Medicine is the academic partner of UPMC, which has collaborated with the University to raise the standard of medical excellence in Pittsburgh and to position health care as a driving force behind the region's economy. For more information about the School of Medicine, see http://www. .


News Article | May 3, 2017
Site: www.medicalnewstoday.com

A novel gene therapy using CRISPR genome editing technology effectively targets cancer-causing "fusion genes" and improves survival in mouse models of aggressive liver and prostate cancers, University of Pittsburgh School of Medicine researchers report in a study published online in Nature Biotechnology. "This is the first time that gene editing has been used to specifically target cancer fusion genes. It is really exciting because it lays the groundwork for what could become a totally new approach to treating cancer," explained lead study author Jian-Hua Luo, M.D., Ph.D., professor of pathology at Pitt's School of Medicine and director of its High Throughput Genome Center. Fusion genes, which often are associated with cancer, form when two previously separate genes become joined together and produce an abnormal protein that can cause or promote cancer. Luo and his team had previously identified a panel of fusion genes responsible for recurrent and aggressive prostate cancer. In a study published earlier this year in the journal Gastroenterology, the team reported that one of these fusion genes, known as MAN2A1-FER, also is found in several other types of cancer, including that of the liver, lungs and ovaries, and is responsible for rapid tumor growth and invasiveness. In the current study, the researchers employed the CRISPR-Cas9 genome editing technology to target unique DNA sequences formed because of the gene fusion. The team used viruses to deliver the gene editing tools that cut out the mutated DNA of the fusion gene and replaced it with a gene that leads to death of the cancer cells. Because the fusion gene is present only in cancer cells, not healthy ones, the gene therapy is highly specific. Such an approach could come with significantly fewer side effects when translated to the clinic, which is a major concern with other cancer treatments such as chemotherapy. To conduct the study, the researchers used mouse models that had received transplants of human prostate and liver cancer cells. Editing the cancer fusion gene resulted in up to 30 percent reduction in tumor size. None of the mice exhibited metastasis and all survived during the eight-week observation period. In contrast, in control mice treated with viruses designed to cut out another fusion gene not present in their tumors, the tumors increased nearly 40-fold in size, metastasis was observed in most animals, and all died before the end of the study. The new findings suggest a completely new way to combat cancer. "Other types of cancer treatments target the foot soldiers of the army. Our approach is to target the command center, so there is no chance for the enemy's soldiers to regroup in the battlefield for a comeback," said Luo. Another advantage over traditional cancer treatment is that the new approach is very adaptive. A common problem that renders standard chemotherapies ineffective is that the cancer cells evolve to generate new mutations. Using genome editing, the new mutations could be targeted to continue fighting the disease, Luo noted. In the future, the researchers plan to test whether this strategy could completely eradicate the disease rather than induce the partial remission observed in the current study. This work was supported by National Institutes of Health grant RO1 CA098249, Department of Defense grant W81XWH-16-1-0364 and a grant from the University of Pittsburgh Cancer Institute. Article: Targeting genomic rearrangements in tumor cells through Cas9-mediated insertion of a suicide gene, Luo, Jian-Hua et al. Nature Biotechnology, doi: 10.1038/nbt.3843, published 1 May, 2017.


News Article | April 17, 2017
Site: www.eurekalert.org

Today (April 12), UC Davis researchers announced in Nature Communications that they have unlocked a treasure-trove of genetic information about lettuce and related plants, releasing the first comprehensive genome assembly for lettuce and the huge Compositae plant family. Garden lettuce, or Lactuca sativa, is the plant species that includes a salad bar's worth of lettuce types, ranging from iceberg to romaine. With an annual on-farm value of more than $2.4 billion, it is the most valuable fresh vegetable and one of the 10 most valuable crops, overall, in the United States. Lettuce is a member of the huge Compositae family, which includes the good, the bad, and the ugly of the plant world, from the daisy and sunflower to ragweed and the dreaded star thistle. The genome assembly -- a compilation of millions of DNA sequences into a useful genetic portrait -- provides researchers with a valuable tool for exploring the Compositae family's many related plant species. "This genome assembly provides the foundation for numerous further genetic, evolutionary and functional studies of this whole family of plants," said Sebastian Reyes-Chin-Wo, the lead author and a graduate student in the laboratory of plant geneticist Richard Michelmore. "This is particularly significant because Compositae is the most successful family of flowering plants on earth in terms of the number of species and environments inhabited," said Richard Michelmore, who directs the UC Davis Genome Center. The researchers found that specific genes in the lettuce genome were consistent with certain physical traits -- like the production of a rubber-containing milky sap -- that have also been found in taxonomically distinct species, such as the rubber tree. The study also provided evidence that somewhere during the evolution of lettuce about 45 million years ago, its genome was "triplicated." As a result, one-fourth of the genome -- including about 30 percent of all of its identified genes -- now appears in multiple related regions. Because such genomic duplications may give plant species an advantage in colonizing new environments, the ancient triplication event might, in part, explain the success of the Compositae plant family. Michelmore noted that this is the first reported genome assembly of a plant species resulting from use of a new technology that gives information about the physical proximity of the DNA sequences to which proteins are bound. The new approach, developed by Dovetail Genomics, a company spun out from UC Santa Cruz, resulted in a more contiguous and accurate genome assembly, even though lettuce has one of the larger plant genomes sequenced to date, he said. The sequencing was done in collaboration with the genomics firm BGI. Funding was provided by 10 plant breeding companies through the Lettuce Genomics Sequencing Consortium, UC Davis Genome Center, National Science Foundation and U.S. Department of Agriculture.


News Article | May 1, 2017
Site: www.futurity.org

Using CRISPR to edit the “fusion genes” that can cause or worsen cancer reduced the size of tumors and improved survival in mice, report researchers. “This is the first time that gene editing has been used to specifically target cancer fusion genes. It is really exciting because it lays the groundwork for what could become a totally new approach to treating cancer,” explains lead study author Jian-Hua Luo, professor of pathology at University of Pittsburgh’s School of Medicine and director of its High Throughput Genome Center. Fusion genes, which often are associated with cancer, form when two previously separate genes become joined together and produce an abnormal protein that can cause or promote cancer. Luo and his team had previously identified a panel of fusion genes responsible for recurrent and aggressive prostate cancer. In a study published earlier this year in the journal Gastroenterology, the team reported that one of these fusion genes, known as MAN2A1-FER, also is found in several other types of cancer, including that of the liver, lungs, and ovaries, and is responsible for rapid tumor growth and invasiveness. In the current study, published online in Nature Biotechnology, the researchers employed the CRISPR-Cas9 genome editing technology to target unique DNA sequences formed because of the gene fusion. The team used viruses to deliver the gene editing tools that cut out the mutated DNA of the fusion gene and replaced it with a gene that leads to death of the cancer cells. Because the fusion gene is present only in cancer cells, not healthy ones, the gene therapy is highly specific. Such an approach could come with significantly fewer side effects when translated to the clinic, which is a major concern with other cancer treatments such as chemotherapy. To conduct the study, the researchers used mouse models that had received transplants of human prostate and liver cancer cells. Editing the cancer fusion gene resulted in up to 30 percent reduction in tumor size. None of the mice exhibited metastasis and all survived during the eight-week observation period. In contrast, in control mice treated with viruses designed to cut out another fusion gene not present in their tumors, the tumors increased nearly 40-fold in size, metastasis was observed in most animals, and all died before the end of the study. The new findings suggest a completely new way to combat cancer. “Other types of cancer treatments target the foot soldiers of the army. Our approach is to target the command center, so there is no chance for the enemy’s soldiers to regroup in the battlefield for a comeback,” says Luo. Another advantage over traditional cancer treatment is that the new approach is very adaptive. A common problem that renders standard chemotherapies ineffective is that the cancer cells evolve to generate new mutations. Using genome editing, the new mutations could be targeted to continue fighting the disease, Luo notes. In the future, the researchers plan to test whether this strategy could completely eradicate the disease rather than induce the partial remission observed in the current study. Grants from the National Institutes of Health, the Department of Defense, and the University of Pittsburgh Cancer Institute supported this work.


News Article | May 5, 2017
Site: www.prweb.com

Although more remains to be learned, great advances have recently been made in the understanding of the molecular and genetic bases of disease resistance in plants. It is now time to deploy this knowledge to provide more durable disease resistance. Much of these advances have been enabled by improvements in analytical technologies. In particular, high-throughput DNA sequencing enable detailed analysis of food crops and their pathogens. It is now possible to characterize the resistance gene repertoires of plants and variability in pathogen populations. This information can be used as the foundation for rational deployment of resistance genes to maximize the evolutionary hurdle for pathogens to become virulent. In this webinar, sponsored by Dovetail Genomics, participants will learn about the genetic basis for disease resistance in plants and the value of high-quality reference genomes in crop research and improvement. In addition, participants will take away an understanding of how genomics is speeding up crop breeding programs. The speaker for this event will be Dr. Richard Michelmore of the University of California, Davis. Dr. Michelmore currently is a professor of Genetics in the Departments of Plant Sciences, Molecular & Cellular Biology, and Medical Microbiology & Immunology; and Director of the Genome Center at UC-Davis. He earned his doctorate in natural science from the University of Cambridge. Dr. Michelmore’s research focuses on pathogens, genetic changes resistance in plants and development of disease resistance in crops. LabRoots will host the event May 31, 2017, beginning at 9:00 a.m. PDT, 12:00 p.m. EDT. To read more about this event, learn about the continuing education credits offered, and to register for free, click here. About Dovetail Genomics Dovetail Genomics LLC is transforming genomics by making long-range information readily accessible to all. The company enables researchers and clinicians to solve complex problems involving de novo assembly, structural variation, microbiome analysis, cancer research, phasing analysis and more by providing them a more comprehensive view of the genome. Its proprietary in vitro proximity ligation approach simplifies genomic discovery by integrating the highest quality long-range genomic information with next-gen sequencing output. Dovetail is based in Santa Cruz, California. For more information on Dovetail, its technology, and service offerings, visit dovetailgenomics.com. Follow Dovetail on Twitter @DTGenomics. About Labroots LabRoots is the leading scientific social networking website, which provides daily scientific trending news, as well as produces educational virtual events and webinars, on the latest discoveries and advancements in science. Contributing to the advancement of science through content sharing capabilities, LabRoots is a powerful advocate in amplifying global networks and communities. Founded in 2008, LabRoots emphasizes digital innovation in scientific collaboration and learning, and is a primary source for current scientific news, webinars, virtual conferences, and more. LabRoots has grown into the world’s largest series of virtual events within the Life Sciences and Clinical Diagnostics community.


News Article | February 28, 2017
Site: www.prnewswire.co.uk

SHANGHAI, CAMBRIDGE, Mass. and REYKJAVIK, Iceland, Feb. 28, 2017 /PRNewswire/ -- WuXi NextCODE, a WuXi AppTec group company and the contract genomics organization enabling precision medicine worldwide, today announced that the company's chief operating officer Hannes Smarason has been appointed as the company's chief executive officer, and WuXi AppTec senior vice presidents John Long and Alex Fowkes have been named chief financial officer and chief operating officer, respectively. "WuXi NextCODE is executing on its vision to enable anyone to use the genome to advance health and wellness worldwide," said Dr Ge Li, founder and chairman of WuXi AppTec group and chairman of WuXi NextCODE. "It is also positioning itself as the data management platform at the heart of the genomics revolution and what may become the world's largest data ecosystem. Hannes, John and Alex have the breadth of vision and proven executive capabilities to carry out this strategy and advance the company to the next level." "This is an exciting time at WuXi NextCODE, as we work on leading projects in every facet of genomics and advance a global standard for the way genomic data is organized, mined and shared," said Mr Smarason. "John and Alex's leadership and experience in life sciences finance and operations, and in the recent independent listing of other WuXi AppTec companies, will be invaluable as we grow our business and forge our own strategic path. We are very pleased to have them join our team and offer them a warm welcome to WuXi NextCODE." Hannes Smarason co-founded NextCODE Health in 2013 as a spinout from deCODE genetics. He oversaw NextCODE's acquisition by WuXi AppTec in 2015 and its merger with the WuXi Genome Center to create WuXi NextCODE. He served as COO until January 2017 and as CEO will lead the company's overall business and corporate strategy. John Long has served as WuXi AppTec's senior vice president of finance since 2013. He was actively involved in WuXi AppTec's privatization from NYSE in 2015 and played important roles in WuXi AppTec's subsequent corporate restructuring, supporting WuXi Biologics's recent IPO filing process in Hong Kong as well as private placements in the China capital market. John has over twenty years' experience in financial management, investment and operations in the US, China and Singapore, and prior to joining WuXi AppTec served in senior roles at Willis Group, Tyco International and Lucent Technologies. In addition to finance and operations leadership, he will provide WuXi NextCODE with global expertise in governance, reporting, strategic planning, treasury and tax. John holds a bachelor's degree in economics from the University of International Business and Economics in Beijing and received his MBA from Wharton School of Business at University of Pennsylvania. Alex Fowkes has twenty years experience in the life science industry in operations, business development, strategy and legal roles. He joined WuXi AppTec in 2012 initially to lead corporate development and then most recently serving as senior vice president of commercial operations. Prior to WuXi Alex served in a variety roles for Pfizer in the US, UK, Australia and China over 14 years. About WuXi NextCODE WuXi NextCODE is a fully integrated global contract genomics organization. With offices in Shanghai; Kendall Square in Cambridge, Massachusetts; and Reykjavik, Iceland, we offer comprehensive services that enable population, precision medicine, diagnostics and wellness initiatives and enterprises to use the genome to improve health around the world. Our capabilities span study design, sequencing, secondary analysis, storage, and interpretation and scalable analytics – all backed by the most proven and widely used technology for organizing, mining and sharing genome sequence data. We are also applying the same capabilities to advance a growing range of sequence-based tests and scans in China. WuXi NextCODE is a WuXi AppTec Group company. Visit us on the web at wuxinextcode.com.


News Article | March 2, 2017
Site: www.eurekalert.org

Humanity may soon generate more data than hard drives or magnetic tape can handle, a problem that has scientists turning to nature's age-old solution for information-storage--DNA. In a new study in Science, a pair of researchers at Columbia University and the New York Genome Center (NYGC) show that an algorithm designed for streaming video on a cellphone can unlock DNA's nearly full storage potential by squeezing more information into its four base nucleotides. They demonstrate that this technology is also extremely reliable. DNA is an ideal storage medium because it's ultra-compact and can last hundreds of thousands of years if kept in a cool, dry place, as demonstrated by the recent recovery of DNA from the bones of a 430,000-year-old human ancestor found in a cave in Spain. "DNA won't degrade over time like cassette tapes and CDs, and it won't become obsolete--if it does, we have bigger problems," said study coauthor Yaniv Erlich, a computer science professor at Columbia Engineering, a member of Columbia's Data Science Institute, and a core member of the NYGC. Erlich and his colleague Dina Zielinski, an associate scientist at NYGC, chose six files to encode, or write, into DNA: a full computer operating system, an 1895 French film, "Arrival of a train at La Ciotat," a $50 Amazon gift card, a computer virus, a Pioneer plaque and a 1948 study by information theorist Claude Shannon. They compressed the files into a master file, and then split the data into short strings of binary code made up of ones and zeros. Using an erasure-correcting algorithm called fountain codes, they randomly packaged the strings into so-called droplets, and mapped the ones and zeros in each droplet to the four nucleotide bases in DNA: A, G, C and T. The algorithm deleted letter combinations known to create errors, and added a barcode to each droplet to help reassemble the files later. In all, they generated a digital list of 72,000 DNA strands, each 200 bases long, and sent it in a text file to a San Francisco DNA-synthesis startup, Twist Bioscience, that specializes in turning digital data into biological data. Two weeks later, they received a vial holding a speck of DNA molecules. To retrieve their files, they used modern sequencing technology to read the DNA strands, followed by software to translate the genetic code back into binary. They recovered their files with zero errors, the study reports. (In this short demo, Erlich opens his archived operating system on a virtual machine and plays a game of Minesweeper to celebrate.) They also demonstrated that a virtually unlimited number of copies of the files could be created with their coding technique by multiplying their DNA sample through polymerase chain reaction (PCR), and that those copies, and even copies of their copies, and so on, could be recovered error-free. Finally, the researchers show that their coding strategy packs 215 petabytes of data on a single gram of DNA--100 times more than methods published by pioneering researchers George Church at Harvard, and Nick Goldman and Ewan Birney at the European Bioinformatics Institute. "We believe this is the highest-density data-storage device ever created," said Erlich. The capacity of DNA data-storage is theoretically limited to two binary digits for each nucleotide, but the biological constraints of DNA itself and the need to include redundant information to reassemble and read the fragments later reduces its capacity to 1.8 binary digits per nucleotide base. The team's insight was to apply fountain codes, a technique Erlich remembered from graduate school, to make the reading and writing process more efficient. With their DNA Fountain technique, Erlich and Zielinski pack an average of 1.6 bits into each base nucleotide. That's at least 60 percent more data than previously published methods, and close to the 1.8-bit limit. Cost still remains a barrier. The researchers spent $7,000 to synthesize the DNA they used to archive their 2 megabytes of data, and another $2,000 to read it. Though the price of DNA sequencing has fallen exponentially, there may not be the same demand for DNA synthesis, says Sri Kosuri, a biochemistry professor at UCLA who was not involved in the study. "Investors may not be willing to risk tons of money to bring costs down," he said. But the price of DNA synthesis can be vastly reduced if lower-quality molecules are produced, and coding strategies like DNA Fountain are used to fix molecular errors, says Erlich. "We can do more of the heavy lifting on the computer to take the burden off time-intensive molecular coding," he said. The Data Science Institute at Columbia University is training the next generation of data scientists and developing innovative technology to serve society. http://datascience. Columbia Engineering is one of the top engineering schools in the U.S. and one of the oldest in the nation. Based in New York City, the School offers programs to both undergraduate and graduate students who undertake a course of study leading to the bachelor's, master's, or doctoral degree in engineering and applied science. Columbia Engineering's nine departments offer 16 majors and more than 30 minors in engineering and the liberal arts, including an interdisciplinary minor in entrepreneurship with Columbia Business School. With facilities specifically designed and equipped to meet the laboratory and research needs of faculty and students, Columbia Engineering is home to a broad array of basic and advanced research installations, from the Columbia Nano Initiative and Data Science Institute to the Columbia Genome Center. These interdisciplinary centers in science and engineering, big data, nanoscience, and genomic research are leading the way in their respective fields while our engineers and scientists collaborate across the University to solve theoretical and practical problems in many other significant areas. The New York Genome Center is an independent, nonprofit academic research organization at the forefront of transforming biomedical research and clinical care with the mission of saving lives. A collaboration of renowned academic, medical and industry leaders across the globe, the New York Genome Center's goal is to translate genomic research into development of new treatments, therapies and therapeutics against human disease. Its member organizations and partners are united in this unprecedented collaboration of technology, science and medicine, designed to harness the power of innovation and discoveries to advance genomic services.


News Article | February 14, 2017
Site: www.rdmag.com

Scientists have discovered a new “mastermind fusion gene” may be associated with a rare cancer-causing tumor – pheochromocytomas (“pheo”) and paragangliomas, according to a study published Feb. 13 in Cancer Cell, by researchers at the Uniformed Services University (USU) and the National Cancer Institutes’ The Cancer Genome Atlas. This breakthrough discovery could lead to more precise treatment as well as a better understanding of cancer itself. These adrenal gland tumors are often benign, but they can become malignant, and in some cases lead to life-threatening hypertension, arrhythmia, and stroke, but it’s not clear which tumors will become metastatic because of the disease’s rarity and complex biology. Therefore, patients with the metastatic disease have few treatment options and poor prognosis. To help detect genetic mutations and better understand this disease, a group of researchers at USU and the nationwide Cancer Genome Atlas Research Network examined 173 tumors, performing six genomic tests, such as DNA and RNA sequencing. The researchers found what they refer to as the mastermind fusion gene – the first fusion gene associated with this type of tumor. This hybrid gene forms from two previously separate genes and only occurs in a new subtype of this disease. The researchers suggest this disrupts the normal biology of the cell and thus producing tumor cells. The researchers believe this mastermind fusion gene will help describe for some patients why the tumor has developed, and better predict patient outcome. The fusion gene may also lead to future targeted therapy and have implications for other cancers. Additionally, the researchers found 18 “driver” genes in this type of tumor, meaning there are 18 different ways this tumor could become cancerous. This is an unusually large amount of drivers, not typical for many other tumor types, according the study’s senior author Dr. Matthew Wilkerson, associate professor and Bioinformatics Director of The American Genome Center and the Collaborative Health Initiative Research Program at USU. This finding allowed their team to classify tumors into four major molecular subtypes, which could also lead to developing new therapies. “For patients who have this diagnosis, surrounded by its uncertainties, this new discovery sheds light on the disease. We think these results will ultimately lead to individuals and their families having a better understanding of their prognosis and more precise treatment,” Wilkerson said. The paper’s co-senior authors are Dr. Katherine Nathanson, a professor in the division of Translational Medicine and Human Genetics at the University of Pennsylvania’s Abramson Cancer Center, and Dr. Karel Pacak, chief of the section on Medical Neuroendocrinology at the Eunice Kennedy Shriver National Institute of Child Health and Human Development at the National Institutes of Health.

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