DURHAM, N.C. Seven members of the Duke University faculty have been named Fellows of the American Association for the Advancement of Science (AAAS). Election as a AAAS Fellow is an honor bestowed upon AAAS members by their peers.

Dukes 2020 inductees are among 443 new fellows this year who are being recognized for scientifically or socially distinguished efforts to advance science or its applications. They are:

Ravi Bellamkonda, Ph.D., Vinik Dean of Engineering and Professor of Biomedical Engineering. For contributions to neural engineering through the use of materials for nerve and spinal cord repair and brain tumor therapies, and for innovations in engineering education.

Ashutosh Chilkoti, Ph.D., Alan L. Kaganov Professor and Chair of Biomedical Engineering. For distinguished contributions to field of biomedical engineering, particularly in the development of novel methods to deliver biotherapeutics and develop surfaces that resist protein interactions.

Tony Huang, Ph.D., William Bevan Professor of Mechanical Engineering and Mechanical Science. For distinguished contributions to the field of acoustofluidics, particularly for developing acoustic tweezers that are capable of precisely manipulating bioparticles in complex fluids.

Kevin LaBar, Ph.D., Professor of Psychology and Neuroscience in Trinity College of Arts & Sciences and associate director of the Center for Cognitive Neuroscience. For distinguished contributions to the study of the neuroscience of how emotional events modulate cognitive processes in the human brain.

Donald W. Loveland, Ph.D., Professor Emeritus of Computer Science in Trinity College of Arts & Sciences. For distinguished contributions to the field of automated deduction and development of the model elimination theorem-proving procedure. He is best known for the Davis-Putnam-Logemann-Loveland algorithm, a backtracking-based search algorithm.

Kenneth D. Poss, Ph.D., James B. Duke Professor of Cell Biology in the Medical School and Director of the Regeneration Next Initiative. For distinguished contributions to the field of organ regeneration, particularly using zebrafish as a model to study mechanisms underlying heart regeneration.

David M. Tobin, Ph.D., Associate Professor of Molecular Genetics and Microbiology in the Medical School. For distinguished contributions to the field of mycobacterial pathogenesis and host response, particularly using a zebrafish model to understand both bacterial and host contributions.

The new fellows will be presented with an official certificate and a gold and blue (representing science and engineering, respectively) rosette pin on February 15 during the 2020 AAAS Annual Meeting in Seattle.

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Seven From Duke Named Fellows of American Association for the Advancement of Science - Duke Today

The American Association for the Advancement of Science, which is the worlds largest scientific society, has named six UCLA faculty members as 2019 fellows. Since 1874, the AAAS, which publishes the journal Science, has chosen members for their distinguished efforts to advance science or its applications.

UCLAs new fellows are:

Paula Diaconescu, professor of chemistry and biochemistry. Diaconescus research focuses on the design of reactive metal complexes with applications to small molecule activation, organic synthesis and polymer formation. She is being honored for seminal contributions to the field of catalysis, particularly for applications of switchable catalytic systems to block copolymer synthesis.

David Glanzman, professor of integrative biology and physiology and of neurobiology. Glanzman studies the cell biology of learning and memory in marine snails and the zebrafish. He transferred a memory from one marine snail to another in 2018, thereby creating an artificial memory. Glanzman is being honored for his groundbreaking research on learning and memory, particularly on memory consolidation and erasure.

Margaret Jacob,distinguished professor emeritus of history. Jacobs expertise includes the history of science and intellectual history. She has played a critical role in shedding light on how the scientific and theoretical advancements of the Enlightenment worked their way into the mainstream of 17th- and 18th-century life. Jacob is being honored for distinguished and groundbreaking contributions to the cultural history of the Scientific Revolution, Newtonianism, and the Enlightenment, and effective communication of these to wider audiences.

Thomas Mason, professor ofphysical chemistry and professor of physics. Masons experimental research focuses on designing and studying new forms of soft matter that have innovative multi-scale dynamic micro- and nano-architectures and morphologies. He is being honored for distinguished contributions to the field of soft matter, particularly for creating and developing thermal-entropic passive microrheology, and for advances in emulsification and nanoemulsions.

Dr. Stephen Smale, vice dean for research at the at the David Geffen School of Medicine at UCLA and distinguished professor in the department of microbiology, immunology and molecular genetics. Smales research addresses the molecular mechanisms of gene regulation in cells of the immune system. He is being honored for distinguished contributions to the field of transcriptional regulation of eukaryotic gene expression, particularly in the immune system.

Yang Yang, professor of materials science and engineering, and the Carol and Lawrence E. Tannas, Jr. Professor of Engineering at the UCLA Samueli School of Engineering. Yangs research involves advanced technologies in thin film solar cells, transparent conductors, metal oxide transistors and other electronic devices, and has large potential for future applications at extremely low cost. He is being honored for extraordinary contributions to organic and hybrid electronic materials and interface processing, leading to highly efficient solar cells, digital memory, and organic displays.

A total of 443 scholars were selected as fellows this year. They will be honored Feb. 15, 2020, at the associations annual meeting in Seattle.

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Six professors named 2019 fellows of the American Association for the Advancement of Science - UCLA Newsroom

An intrinsically photosensitive retinal ganglion cell (ipRGC) as it would appear if you looked at a mouses retina through the pupil. The white arrows point to the many different types of cells with which it networks: other subtypes of ipRGCs (red, blue and green) and retinal cells that are not ipRGCs (red). The white bar is 50 micrometers long, approximately the diameter of a human hair. Credit: Franklin Caval-Holme, UC Berkeley

By the second trimester, long before a babys eyes can see images, they can detect light.

But the light-sensitive cells in the developing retina the thin sheet of brain-like tissue at the back of the eye were thought to be simple on-off switches, presumably there to set up the 24-hour, day-night rhythms parents hope their baby will follow.

University of California, Berkeley, scientists have now found evidence that these simple cells actually talk to one another as part of an interconnected network that gives the retina more light sensitivity than once thought, and that may enhance the influence of light on behavior and brain development in unsuspected ways.

In the developing eye, perhaps 3% of ganglion cells the cells in the retina that send messages through the optic nerve into the brain are sensitive to light and, to date, researchers have found about six different subtypes that communicate with various places in the brain. Some talk to the suprachiasmatic nucleus to tune our internal clock to the day-night cycle. Others send signals to the area that makes our pupils constrict in bright light.

But others connect to surprising areas: the perihabenula, which regulates mood, and the amygdala, which deals with emotions.

In mice and monkeys, recent evidence suggests that these ganglion cells also talk with one another through electrical connections called gap junctions, implying much more complexity in immature rodent and primate eyes than imagined.

Given the variety of these ganglion cells and that they project to many different parts of the brain, it makes me wonder whether they play a role in how the retina connects up to the brain, said Marla Feller, a UC Berkeley professor of molecular and cell biology and senior author of a paper that appeared this month in the journal Current Biology. Maybe not for visual circuits, but for non-vision behaviors. Not only the pupillary light reflex and circadian rhythms, but possibly explaining problems like light-induced migraines, or why light therapy works for depression.

The cells, called intrinsically photosensitive retinal ganglion cells (ipRGCs), were discovered only 10 years ago, surprising those like Feller who had been studying the developing retina for nearly 20 years. She played a major role, along with her mentor, Carla Shatz of Stanford University, in showing that spontaneous electrical activity in the eye during development so-called retinal waves is critical for setting up the correct brain networks to process images later on.

Hence her interest in the ipRGCs that seemed to function in parallel with spontaneous retinal waves in the developing retina.

We thought they (mouse pups and the human fetus) were blind at this point in development, said Feller, the Paul Licht Distinguished Professor in Biological Sciences and a member of UC Berkeleys Helen Wills Neuroscience Institute. We thought that the ganglion cells were there in the developing eye, that they are connected to the brain, but that they were not really connected to much of the rest of the retina, at that point. Now, it turns out they are connected to each other, which was a surprising thing.

UC Berkeley graduate student Franklin Caval-Holme combined two-photon calcium imaging, whole-cell electrical recording, pharmacology and anatomical techniques to show that the six types of ipRGCs in the newborn mouse retina link up electrically, via gap junctions, to form a retinal network that the researchers found not only detects light, but responds to the intensity of the light, which can vary nearly a billionfold.

Gap junction circuits were critical for light sensitivity in some ipRGC subtypes, but not others, providing a potential avenue to determine which ipRGC subtypes provide the signal for specific non-visual behaviors that light evokes.

Aversion to light, which pups develop very early, is intensity-dependent, suggesting that these neural circuits could be involved in light-aversion behavior, Caval-Holme said. We dont know which of these ipRGC subtypes in the neonatal retina actually contributes to the behavior, so it will be very interesting to see what role all these different subtypes have.

The researchers also found evidence that the circuit tunes itself in a way that could adapt to the intensity of light, which probably has an important role in development, Feller said.

In the past, people demonstrated that these light-sensitive cells are important for things like the development of the blood vessels in the retina and light entrainment of circadian rhythms, but those were kind of a light on/light off response, where you need some light or no light, she said. This seems to argue that they are actually trying to code for many different intensities of light, encoding much more information than people had previously thought.

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Reference: Gap Junction Coupling Shapes the Encoding of Light in the Developing Retina by Franklin Caval-Holme and Marla B. Feller, 7 November 2019, Current Biology.DOI: 10.1016/j.cub.2019.10.025

The research was supported by the National Institutes of Health (NIH F31EY028022-03, RO1EY019498, RO1EY013528, P30EY003176).

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Scientists Shocking Discovery That Babies in the Womb May See Much More Than We Thought - SciTechDaily

Hypoxia is a key factor that accompanies most brain pathologies, including ischemia and neurodegenerative diseases. Reduced oxygen concentration results in irreversible changes in nerve cell metabolism that entails cell death and destruction of intercellular interactions. Since neural networks are responsible for the processing, storage and transmission of information in the brain, the loss of network elements can lead to dysfunction of the central nervous system and, consequently, the development of neurological deficiency and the patient's severe disability.

This is the reason why the world's neurobiological community is currently involved in an active search for compounds that can prevent the death of nerve cells and support their functional activity under stress.

According to Maria Vedunova, Director of the Institute of Biology and Biomedicine at Lobachevsky University (UNN), the Institute's researchers propose to use the body's own potential to combat hypoxia and its consequences.

Our particular interest is in the glial cell line-derived neurotrophic factor (GDNF). These signal molecules take an active part in the growth and development of nerve cells in the embryonic period, and they are also involved in the implementation of protective mechanisms and adaptation of brain cells when exposed to various stressors in adulthood,"

Maria Vedunova, Director of the Institute of Biology and Biomedicine, Lobachevsky University

By applying advanced techniques for the study of the structure and functional activity of brain neural networks, a team of researchers from the Lobachevsky State University of Nizhny Novgorod and from the Institute of Cell Biology and Neurobiology at the Charit University Hospital in Berlin have shown that activation of the neurotrophic factor GDNF prevents the death of nerve cells and helps to maintain neural network activity after hypoxic injury. Of particular significance are the data that identify key players in the molecular cascades responsible for the implementation of the GDNF protective effect, namely, the RET, AKT1, Jak1 and Jak2t enzyme kinases.

"Thanks to the results already obtained, Lobachevsky University scientists have significantly advanced in developing the theoretical basis for a new method for correcting the hypoxic conditions of the central nervous system. The next stage of the work will be focused on studying the possibility of neurotrophic factor GDNF activation in experimental animals in a simulated hypoxic damage," continues Maria Vedunova.

It was shown by the researchers that activation of the glial cell line-derived neurotrophic factor helps protect brain cells from death during hypoxic damage and maintain the function of neural networks in the long term after the damaging effects.

A thorough understanding of the principles of work of neural networks subjected to hypoxic damage and of the protective action mechanisms of biologically active molecules of the body (the neurotrophic factor GDNF) can provide the basis for developing an effective method for correcting various CNS pathologies developing under oxygen deficiency.

The obtained results are of a fundamental nature, but they can be an important element in the comprehensive research aimed at developing new methods of diagnosis and treatment of CNS hypoxic conditions, which undoubtedly has great commercial potential.

Source:

Journal reference:

Mitroshina, E.V., et al. (2019) Intracellular Neuroprotective Mechanisms in Neuron-Glial Networks Mediated by Glial Cell Line-Derived Neurotrophic Factor. Oxidative Medicine and Cellular Longevity. doi.org/10.1155/2019/1036907.

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New method for correcting hypoxic conditions of the central nervous system - News-Medical.net

Applications are invited for the post of Research Associate at Prof. Kinya Otsus research group in the School of Cardiovascular Medicine and Sciences at King's College London. The postholder will focus on mechanisms of development of heart failure. We are utilizing integrated research approach including genetically engineered disease models, miniaturized physiological technology and a range of molecular and cell biological techniques and investigating the relationship among cell death including autophagy, inflammation and mitochondrial dynamics. Minimum qualifications are PhD and/or MD with strong expertise in molecular, cellular, biochemical biology and imaging. Excellent publication history is required. Candidates should be highly motivated individuals with excellent communication skills and have the ability to work independently. A contribution to undergraduate/postgraduate education will be part of the job, at an appropriate level as determined by the Head of Division.

This post will be offered on a fixed-term contract for 3 years.

This is a full-time role - 100% FTE.

For an informal discussion to find out more about the role please contact: Professor Kinya Otsu; kinya.otsu@kcl.ac.uk

To apply, please register with the Kings College London application portal and complete your application online.

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Research Associate in the School of Cardiovascular Medicine & Sciences job with KINGS COLLEGE LONDON | 187528 - Times Higher Education (THE)

Soft tissue sarcoma cells stop a key metabolic process which allows them to multiply and spread, and so restarting that process could leave these cancers vulnerable to a variety of treatments. The enzyme that controls the process is called FBP2, and researchers from the Abramson Cancer Center of the University of Pennsylvania, who detailed their findings in Cell Metabolism, also showed that manipulating sarcoma cells to ramp up FBP2 expression slows or even stops their growth entirely. This ultimately leaves them susceptible to targeted therapies and potentially takes away their ability to develop treatment resistance.

Soft tissue sarcoma is actually a collection of distinct, rare cancer types affecting tissues that connect and surround other parts of the body, including muscle, fat, tendons, nerves, and blood vessels. While they can grow anywhere, the arms, legs, chest, and stomach are the most common sites. Because these cancers appear in so many different places in the body, their biology is incredibly diverse, making it difficult to develop one targeted treatment that can be broadly effective for all patients. Currently, the best options for treatment are surgery - which may involve amputation - chemotherapy, and radiation.

"While other cancer types associated with high mutational burden have benefitted from the development of immunotherapies, the diversity and low frequency of genetic mutations in soft tissue sarcomas have made them more difficult to treat, which is why our identification of a broadly expressed metabolic approach is potentially so exciting," said the study's senior author M. Celeste Simon, PhD, the Arthur H. Rubenstein, MBBCh Professor of Cell and Developmental Biology in Penn's Perelman School of Medicine and scientific director of the Abramson Family Cancer Research Institute. The study's lead author is Peiwei Huangyang, who performed the work while obtaining her PhD in Simon's lab.

While FBP2 is broadly expressed in normal cells, soft tissue sarcomas have a way of dramatically suppressing it. Building on their previous work - published in Nature - showing a related pathway controlled by FBP1 serves a similar function in renal and liver cancer, Simon and her team used mouse models to show that causing soft tissue sarcoma cells to re-express FBP2 the way healthy cells do stops the cancer from growing, potentially making it more vulnerable to both targeted and immune-based therapies.

Essentially, once they start acting like normal cells, they don't hide and grow the way cancer normally does."

M. Celeste Simon, PhD, study's senior author

The team also found that the enzymes involved in this process are located in the cell's nucleus, meaning this pathway could stop cancer cells from adapting to their natural environment and becoming resistant to cytotoxic drugs. It's tied to the understanding of how cells respond to environmental stresses to alter their metabolism and survive, which is the work that received the 2019 Nobel Prize in Physiology or Medicine.

While this study shows the importance of FBP2, further research is needed to show that using drugs to manipulate cells to re-express FB2 will have the expected effect. Simon points out that these drugs already exist in other cancer treatments - specifically blood cancers - meaning the pipeline to translate this approach to patients should be relatively rapid if research proves it is effective.

Source:

Journal reference:

Huangyang, P., et al. (2019) Fructose-1,6-Bisphosphatase 2 Inhibits Sarcoma Progression by Restraining Mitochondrial Biogenesis. Cell Metabolism. doi.org/10.1016/j.cmet.2019.10.012.

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Broadly expressed metabolic approach could make sarcoma susceptible to targeted therapies - News-Medical.net

DALLAS Dr. Kathy Svoboda, Regents Professor in biomedical sciences at Texas A&M College of Dentistry, has been named assistant dean of the oral biology graduate program after serving as the director since 2009. Svoboda is a Hershey native.

Looking at Kathys background and expertise, I could think of no one better to serve in this capacity, said Dr. Lawrence Wolinsky, College of Dentistry dean. She is an asset to this institution and I am confident she will continue to move the oral biology graduate program in the right direction.

Svoboda was trained as a developmental biologist and anatomist at the University of Nebraska Medical Center. She continued her training in a postdoctoral position in the Department of Anatomy and Cellular Biology at Harvard Medical School.

Svoboda had an active research laboratory and taught gross anatomy, histology and human development at Harvard and Boston University School of Medicine before joining the College of Dentistry faculty in 1998.

She was promoted to professor, with tenure, in 2001 and named a Regents Professor in 2009. She has been a member of the Oral Biology Graduate Committee since 2003.

Svobodas research focuses on signal transduction pathways controlling developmental processes and cell biology of adult tissues. She currently serves as a guest editor for Anatomical Record, and on the editorial boards of Developmental Dynamics and FASEB BioAdvances. She has served on the executive board of the American Association of Anatomists, including the offices of program co-chair, vice president and president.

Svoboda also was named an AAA Fellow in 2009 and received the AJ Ladman Exemplary Service Medal in 2014. She served the Association for Research in Vision and Ophthalmology and received its Gold Fellow Award in 2014.

In 2017, Svoboda received the Institutional Service Award from the College of Dentistry for her leadership of the graduate program and other committees.

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Hershey native tapped for new administrative position at Texas A&M - North Platte Telegraph

By Paul Biegler

US scientists have overcome a major stumbling block in the creation of mini-organs, programming cells to take on the desired shape rather than relying on 3D printing or external scaffolds.

This inside out approach, described in a paper in the journal Cell Systems, could signal a paradigm shift in how mini-hearts, kidneys and brains are grown on the lab bench a technique used to study disease that may one day lead to personalised organ transplants.

The team, led by bioengineer Todd McDevitt at Gladstone Institutes in the US, was driven by an enduring issue with state-of-the-art ways of producing mini-organs such as 3D printing. The cells just wont stay put.

Making a mini-organ or organoid starts when scientists take a persons skin cell and, using the right mix of agents, turn it into an induced pluripotent stem cell. This IPS cell is the blank cheque of biology, capable of becoming almost any cell type.

Grow it into a mini-kidney, say, and you can reproduce kidney diseases and test treatments in a dish sitting on your lab bench. But how faithful that model is depends on the physical organisation of the cells; to mimic a real deal kidney, 3D printing is often used.

But cells, much like unruly teenagers, have a mind of their own and will often wander away from their printed position.

McDevitts team wanted to own those cellular minds and so took control of two genes that together make up something of a joystick that directs how the cells organise.

CDH1 and ROCK1 figure heavily in the complex moves that lead to the final configuration of a group of cells. The pair influences stickiness and repulsion between cells, the surface tension that makes them spherical and their overall speed of migration.

The researchers used the editing tool CRISPR to knock out the two genes at various stages in the evolution of a clump of cells. Their aim was to make a bulls eye pattern, a shape thats common in human development, including in early embryo formation.

To detect that aspirational pattern, they engineered another tweak making the cells fluoresce when CDH1 and ROCK1 were neutralised.

But there was a problem.

Factor in all the potential time points where the genes could be knocked out, the proportion of cells to be targeted, and a host of other variables, and the researchers calculated theyd need to do nearly 9000 trial-and-error experiments.

So they called on AI. They trained a machine learning model to compute the precise pattern of gene knockouts needed to realise their dream shape.

Machine learning can predict what movie you might like based on your viewing history, but it can also generate new insights into biological systems by mimicking them, says co-author Demarcus Briers, from the Boston University Bioinformatics Program.

Our machine-learning model allows us to predict new ways that stem cells can organise themselves, and produces instructions for how to recreate these predictions in the lab.

That model hit a bulls eye, quite literally, allowing the team to produce the concentric pattern of cells they were aiming at.

"We've shown how we can leverage the intrinsic ability of stem cells to organise," says McDevitt. "This gives us a new way of engineering tissues, rather than a printing approach where you try to physically force cells into a specific configuration."

Ultimately, that concrete target shape will give way to a target in the abstract, one with potential to shift the life course.

"We're now on the path to truly engineering multicellular organization, which is the precursor to engineering organs," McDevitt says. "When we can create human organs in the lab, we can use them to study aspects of biology and disease that we wouldn't otherwise be able to."

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AI helps cells pull themselves together - Cosmos

SAN DIEGO--(BUSINESS WIRE)--Boundless Bio, a company interrogating and targeting extrachromosomal DNA (ecDNA) in aggressive cancers, today announced that research describing new mechanisms by which ecDNA drive cancer growth, resistance, and recurrence has been published in the journal Nature. The manuscript, Circular ecDNA promote accessible chromatin and high oncogene expression, was co-authored by Boundless Bios scientific founders Paul Mischel, M.D., Distinguished Professor at the University of California San Diego (UC San Diego) School of Medicine and a member of the Ludwig Institute for Cancer Research; Vineet Bafna, Ph.D., Professor of Computer Science & Engineering, UC San Diego; Howard Chang, M.D., Ph.D., Virginia and D.K. Ludwig Professor of Cancer Genomics and Genetics, Stanford University; and Roel Verhaak, Ph.D., Professor and Associate Director of Computational Biology, The Jackson Laboratory. Boundless Bio scientists Kristen Turner, Ph.D. and Nam Nguyen, Ph.D. were co-lead authors on the manuscript as well.

The paper describes, for the first time, how ecDNA encode information not only in their sequence but also in their shape, enabling a new understanding of how ecDNA drive aggressive tumor growth. ecDNA differ profoundly in their shape from human chromosomal DNA in ways that have not been well-understood, and until now, the impact of the physical shape of ecDNA on cancer biology has remained a mystery. Mischel and his collaborators conducted an in-depth analysis of the structure of ecDNA in cancer, revealing a circular structure that is organized around protein cores in a different way than normal chromosomal DNA. They showed that ecDNA are wound around protein cores in a fashion that permits a far greater level of accessibility to the transcriptional machinery than occurs on chromosomes. As a result of this unique architecture, along with the very high number of ecDNA particles inside a tumor cell, oncogenes that are amplified on ecDNA are amongst the most highly transcribed genes in a tumor.

The researchers also showed that the circular architecture of ecDNA permits new regulatory interactions that might be important in controlling gene expression in cancer. These findings enabled the team to construct topologically informed circular maps of ecDNA that may potentially prove to be of value in guiding treatment for patients. These new findings build on and expand the impact of previous work from the team, which showed that ecDNA amplification is common in cancer and that it can drive aggressive growth and treatment resistance in part through the way that DNA is passed from mother cells to daughter cells (Turner et al., Nature, 2017; Verhaak et al., Nature Reviews Cancer, 2019; de Carvalho et al., Nature Genetics, 2018; Nathanson et al., Science, 2014).

The findings published in Nature represent a major leap forward in our understanding of both the structure of ecDNA and of the significant role that ecDNA play in promoting cancer growth and resistance, said Zachary Hornby, President and Chief Executive Officer of Boundless Bio. This new research arms us with essential knowledge that will enable our team at Boundless Bio to develop the first medicines capable of targeting the underlying biology that causes overexpressed oncogenes to develop and perpetuate in tumors that historically have been difficult-to-treat.

This new study sheds light on how the three-dimensional architecture of ecDNA plays a critical role in driving aggressive cancer growth and provides an important bridge between cancer genomics and epigenetics, said Dr. Mischel. These are exciting findings that we believe will propel Boundless Bios efforts to develop transformative new cancer medicines that eliminate cancer cells ability to employ ecDNA to drive cancer.

About ecDNA

Extrachromosomal DNA, or ecDNA, are large circles of DNA containing genes that are outside the cells chromosomes and can make many copies of themselves. ecDNA can be rapidly replicated within the cell, causing high numbers of oncogene copies, a trait that can be passed to daughter cells in asymmetric ways during cell division. Cells have the ability to upregulate or downregulate ecDNA and resulting oncogenes to ensure survival under selective pressures, including chemotherapy or radiation, making ecDNA one of cancer cells primary mechanisms of recurrence and treatment evasion. ecDNA are rarely seen in healthy cells but are found in many solid tumor cancers. They are a key driver of the most aggressive and difficult-to-treat cancers, specifically those characterized by high copy number amplification of oncogenes.

About Boundless Bio

Boundless Bio is a biotechnology company focused on interrogating a novel area of cancer biology, extrachromosomal DNA (ecDNA), to deliver transformative therapies to patients with previously intractable cancers. For more information, visit http://www.boundlessbio.com.

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Boundless Bio Announces Publication in Nature Elucidating the Role of Extrachromosomal DNA (ecDNA) Structure in Cancer Biology - Business Wire

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Newswise Eighteen scientists from St. Jude Childrens Research Hospital were recently named Highly Cited Researchers for 2019 by the Web of Science Group.

The annual list identifies scientists and social scientists who produced multiple papers ranking in the top 1% by citations for their field and year of publication. The ranking demonstrates significant research influence among their peers. The 2019 St. Jude Highly Cited Researchers are:

Kelly Caudle, PharmD, PhD, Pharmaceutical Sciences

James R. Downing, MD, St. Jude president and CEO

John Easton, PhD, Computational Biology

David Ellison, MD, PhD, Pathology chair

Amar Gajjar, MD, Pediatric Medicine chair

Douglas Green, PhD, Immunology chair

Thirumala-Devi Kanneganti, PhD, Immunology vice-chair

Richard Kriwacki, PhD, Structural Biology

Jing Ma, PhD, Clinical Application Core

Charles Mullighan, MBBS (Hons), MD, Pathology

Ching-Hon Pui, MD, Oncology chair

Mary Relling, PharmD, Pharmaceutical Sciences chair

Leslie Robison, PhD, Epidemiology and Cancer Control chair

Michael Rusch, Computational Biology

Paul Taylor, MD, PhD, Cell and Molecular Biology chair

ShengdarTsai, PhD, Hematology

Gang Wu, PhD, Center for Applied Bioinformatics

Jinghui Zhang, PhD, Computational Biology chair

The methodology that determines the whos who of influential researchers draws on the data and analysis performed by bibliometric experts from the Institute for Scientific Information at the Web of Science Group.

The data are taken from 21 broad research fields within Essential Science Indicators, a component of InCites. The fields are defined by sets of journals and, in the case of multidisciplinary journals such as Nature and Science, by a paper-by-paper assignment to a field based on an analysis of the cited references in the papers. This percentile-based selection method removes the citation advantage of older papers relative to recently published ones since papers are weighed against others in the same annual cohort.

The full 2019 Highly Cited Researchers list and executive summary can be found here, and the methodology can be found here.

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St. Jude researchers among the most highly cited in 2019 - Newswise