Alice Soragni and Paul Boutros of the UCLA Jonsson Comprehensive Cancer Center have received a five-year, $2.4 million award from the National Institutes of Health to study bone sarcomas at the molecular level, which is critical to understanding why treatment can either have a positive outcome or fail.
Bone sarcomas are rare tumors that are poorly characterized at the molecular and drug-resistance level, and clinical outcomes have not significantly improved over the past decade. Despite aggressive treatment, the overall five-year survival rate for the disease is 60%, and it drops to 30% if the cancer spreads to other parts of the body.
“Bone sarcomas are incredibly rare tumors overall; however, they are more commonly diagnosed in children and young adults,” said Soragni, an assistant professor of orthopedic surgery at the David Geffen School of Medicine at UCLA. “We still don’t have a complete understanding of how these tumors respond to therapy and how responses change as bone tumors evolve and metastasize to other organs. By developing tumor organoid models, we will investigate their drug sensitivity and resistance profiles. At the same time, we will uncover the molecular features of each bone tumor using whole genome sequencing.”
The collaborating labs of Soragni and Boutros established a pipeline to develop bone sarcoma organoids — tiny 3D tumor models grown in the lab using clinical samples — in order to screen hundreds of drugs, paired with whole genome sequencing to identify mutational correlates of drug sensitivity.
The grant will take advantage of this pipeline and help determine how the molecular and pharmacologic behavior of bone sarcomas differs spatially within a single patient and how sarcomas vary during the transition from a curable, primary disease to a lethal, metastatic disease.
“This study will allow us to define how bone sarcoma changes, metastases diverge and respond to therapy, and identify actionable drug sensitivities,” said Boutros, a professor of urology and human genetics who serves as associate director of cancer informatics at the UCLA Institute for Precision Health and director of cancer data science at the Jonsson Cancer Center. “This will create the first detailed portrait of how bone sarcomas evolve under therapeutic selective pressure, linked to clinical outcomes.”
Tracy Johnson, professor of molecular, cell, and developmental biology and holder of the Keith and Cecilia Terasaki Presidential Endowed Chair, has been named dean of the division of life sciences in the UCLA College, effective Sept. 1.
An award-winning scientist whose research focuses on understanding the mechanisms of gene regulation, particularly RNA splicing, chromatin modification and the intersection between these reactions, Johnson has been a member of the faculty since 2013 and has served as associate dean for inclusive excellence in the division of life sciences since January 2015.
“I am deeply humbled to serve as UCLA’s next dean of the division of life sciences. Our life sciences researchers and educators are consistently at the leading edge of scientific and educational innovation, and our international reputation for excellence has allowed the division to attract truly exceptional students,” said Johnson, who is also a Howard Hughes Medical Institute professor.
“These extraordinary times provide an opportunity for UCLA Life Sciences to exercise leadership in new and previously unimaginable ways across the UCLA campus, the city of Los Angeles, the state of California, the nation and beyond,” Johnson said. “I am honored to be a steward of these incredible opportunities to build on a foundation of excellence as we move forward into an exciting future.”
Prior to her appointment at UCLA, Johnson was a member of the UC San Diego biological sciences faculty from 2003 to 2013, and a Jane Coffin Childs postdoctoral research fellow at the California Institute of Technology.
Recognized for her scientific leadership and contributions to educational innovation, and as a champion of diversity, equity and inclusion, Johnson serves as a member of the UCLA Human Pluripotent Stem Cell Research oversight committee; chair and director of the biomedical research minor; co-director and steering committee member for the Bruins in Genomics summer program; and co-director/co-principal investigator for the National Institutes of Health–funded UPLIFT/IRACDA program, which supports postdoctoral researchers preparing for academic careers.
Johnson also started the UCLA-HHMI Pathways to Success program, which is funded through the Howard Hughes Medical Institute to support the success of students from diverse backgrounds in STEM fields. She is also the principal investigator for a second HHMI grant aimed at promoting greater access and success for students studying life sciences who transfer from community colleges.
Additionally, Johnson has served on numerous campus committees, including the faculty advisory committees for the Ralph J. Bunche Center for African American Studies and the UCLA Center for the Study of Women, the Moreno Report Implementation Committee, Jonsson Comprehensive Cancer Center executive committee, and diversity in research committee.
“Chancellor Block and I are confident that the division of life sciences will continue to thrive under Tracy’s capable leadership. Please join me in congratulating her and welcoming her to this new role,” said Emily Carter, UCLA executive vice chancellor and provost, who also thanked Dean Victoria Sork for her leadership of the division of life sciences.
Beyond UCLA, Johnson has served as chair of an NIH Molecular Genetics Study Section, the National Cancer Institute Board of Scientific Counselors, the executive committee for the Annual Biomedical Research Conference for Minority Students, and the executive board of the Society of Howard Hughes Medical Institute Professors.
She is the recipient of numerous awards, including the National Science Foundation CAREER Award; the Presidential Early Career Award for Scientists and Engineers; the UCLA Academic Senate Award for Career Commitment to Diversity, Equity and Inclusion; and the UCLA Life Sciences Award for Inclusive Excellence through teaching, mentorship, service and research.
Johnson earned her bachelor’s degree in biochemistry and cell biology at UC San Diego and her doctorate in biochemistry and molecular biology at UC Berkeley.
The study, published May 11 in the peer-reviewed journal Cell Stem Cell, identified various cell types present in skeletal muscle tissues, from early embryonic development all the way to adulthood. Focusing on muscle progenitor cells, which contribute to muscle formation before birth, and muscle stem cells, which contribute to muscle formation after birth and to regeneration from injury throughout life, the group mapped out how the cells’ gene networks — which genes are active and inactive — change as the cells mature.
The roadmap is critical for researchers who aim to develop muscle stem cells in the lab that can be used in regenerative cell therapies for devastating muscle diseases, including muscular dystrophies, and sarcopenia, the age-related loss of muscle mass and strength.
“Muscle loss due to aging or disease is often the result of dysfunctional muscle stem cells,” said April Pyle, senior author of the paper and a member of the Broad Stem Cell Research Center. “This map identifies the precise gene networks present in muscle progenitor and stem cells across development, which is essential to developing methods to generate these cells in a dish to treat muscle disorders.”
Researchers in Pyle’s lab and others around the world already have the capacity to generate skeletal muscle cells from human pluripotent stem cells — cells that have the ability to self-renew and to develop into any cell type in the body. However, until now, they had no way of determining where these cells fall on the continuum of human development.
“We knew that the muscle cells we were making in the lab were not as functional as the fully matured muscle stem cells found in humans,” said Haibin Xi, first author of the new paper and an assistant project scientist in Pyle’s lab. “So we set out to generate this map as a reference that our lab and others can use to compare the genetic signatures of the cells we are creating to those of real human skeletal muscle tissue.”
To create this resource, the group gathered highly specific data about two different groups of skeletal muscle cells: those from the human body, ranging from the fifth week of embryonic development to middle age, and those derived from human pluripotent stem cells the researchers generated in the lab. They then compared the genetic signatures of cells from both sources.
The group obtained 21 samples of human skeletal muscle tissue from their UCLA collaborators and from colleagues at the University of Southern California and the University of Tübingen in Germany. For the pluripotent stem cell–derived muscle cells, the group evaluated cells created using their own unique method and the methods of several other groups.
The Pyle lab collaborated with the lab of Kathrin Plath, a UCLA professor of biological chemistry and member of the Broad Stem Cell Research Center, to conduct high-throughput droplet-based single-cell RNA sequencing of all of the samples. This technology enables researchers to identify the gene networks present in a single cell and can process thousands of cells at the same time. Leveraging the power of this technology and the Plath lab’s bioinformatics expertise, the group identified the genetic signatures of various cell types from human tissues and pluripotent stem cells.
They next developed computational methods to focus on muscle progenitor and stem cells and mapped out their gene networks associated with every developmental stage. This enabled the group to match the genetic signatures found in the pluripotent stem cell–derived muscle cells with their corresponding locations on the map of human muscle development.
The group found that pluripotent stem cell–derived muscle cells produced by all the methods they tried resembled muscle progenitor cells at an early developmental state and did not align to adult muscle stem cells.
In addition to pinning down the true maturity of the lab-produced cells, this analysis also provided details about the other cell types present in skeletal muscle tissue across development and in populations derived from human pluripotent stem cells. These cells could play an essential role in muscle cell maturation and could be critical to improving methods to generate and support muscle stem cells in a dish.
“We found that some methods to generate muscle cells in a dish also produce unique cell types that likely support the muscle cells,” said Pyle, who is also a member of the UCLA Jonsson Comprehensive Cancer Center. “And so now our questions are, what are these cells doing? Could they be the key to producing and supporting mature and functional muscle stem cells in a dish?”
Moving forward, Pyle and her colleagues will focus on harnessing this new resource to develop better methods for generating muscle stem cells from human pluripotent stem cells in the lab. She hopes that by focusing on the stem cell–associated gene expression networks and supportive cell types they identified, they can produce high-powered muscle stem cells that can be useful for future regenerative therapies.
This research was supported by the California Institute for Regenerative Medicine; the National Institutes of Health; a UCLA Broad Stem Cell Research Center Rose Hills Foundation Innovator Grant; the David Geffen School of Medicine at UCLA; the UCLA Jonsson Comprehensive Cancer Center and UCLA Broad Stem Cell Research Center Ablon Scholars Program; the Howard Hughes Medical Institute; a UCLA Broad Stem Cell Research Center Rose Hills Foundation Graduate Scholarship; and the UCLA Tumor Cell Biology Training Program.
Sriram Sankararaman, assistant professor of computer science in the UCLA Samueli School of Engineering, has received a National Science Foundation CAREER award, the agency’s highest honor for faculty members at the start of their research and teaching careers.
The award includes a five-year, $686,000 grant to support his research to development of new computational tools to analyze very large datasets of genetic information. The tools will focus on understanding the larger picture of human traits and the genes that responsible for them.
This includes figuring out how particular traits are passed down across generations; how those genes are distributed across a population; relationships between multiple genes; and then what impact the environment may have on heredity.
The research funded by the study will bring researchers together from several fields, including computer science, statistics, bioinformatics and human genetics.
Sankararaman’s previous honors include a Sloan Research Fellowship, an Okawa Foundation Research Grant, and UCLA Samueli’s Northrop Grumman Excellence in Teaching award. He has UCLA faculty appointments in human genetics and computational medicine. A paper in Science Advances with Arun Durvasula, one of his graduate students, received global attention in February.
Sankararaman is the third computer science faculty member to receive the NSF CAREER Award this academic year, joining Guy Van den Broeck and Ravi Netravali.
UCLA computational biologists have discovered that four populations in West Africa can trace about 8% of their genetic ancestry to an archaic hominin, an extinct relative of humans that branched off from the hominid evolutionary tree more than 600,000 years ago — about 100,000 years earlier than Neanderthals did. The study is published in Science Advances.
Over the past decade, advances in computing, statistical analysis, molecular biology and genetics have revealed a richer picture of humans and their interactions with ancient relatives, such as Neanderthals. But research on the genetic ancestry of African populations has lagged behind discoveries about people with ancestral roots in Europe.
The researchers, from the UCLA Samueli School of Engineering, analyzed modern DNA obtained from an international repository of genomic data. In the past, researchers would have needed to compare the modern DNA to so-called “reference DNA” from ancient fossils to draw such conclusions. But the improved statistical techniques available today enabled them to look backward in time hundreds of thousands of years without fossil DNA.
“This opens a new path in understanding the complexity of human evolutionary history in Africa, where the picture hasn’t been as clear,” said Sriram Sankararaman, the study’s principal investigator, a UCLA assistant professor with appointments in computer science, human genetics and computational medicine.
The archaic hominin identified in the UCLA research is a close evolutionary relative of humans.
“There is not a lot known about these archaic hominins, which makes finding out how this ‘ghost population’ fits into human evolutionary history challenging. But our findings are very exciting,” said Sankararaman, who also is a member of UCLA’s Bioinformatics Interdepartmental Program.
Previous genomic studies have presented evidence that modern populations in Africa have complex genetic lineages, in which humans and close evolutionary relatives intermixed as recently as just a few thousand years ago. But this study may provide the strongest evidence yet that this intermixture took place.
The UCLA research reveals much more of that story for the four modern groups of people, the Yoruba of Nigeria, the Mende of Sierra Leone, the Esan of Nigeria and the Gambian in Western Divisions of Gambia.
“We don’t need reference DNA from fossils of the archaic hominin to confirm that, somewhere deep in our ancestry, humans intermixed with them,” Sankararaman said. “We can now see that such events took place by looking at our DNA itself.”
Segments of Neanderthal DNA extracted from fossils have been found in most modern populations outside of Africa. DNA has also been extracted and analyzed from the more recently discovered Denisovans, another extinct group of archaic humans, whose DNA is found in people living today in South Asia and Oceania.
Archaeological evidence shows that modern and archaic humans coexisted in Africa, and some fossils have features that suggest mixing between the two populations. However, usable DNA has not yet been extracted from archaic human fossils that have been found in that region — which is why the researchers’ ability to draw conclusions about evolution without reference DNA information could go such a long way toward solving previously unanswered questions.
Although the researchers found evidence of the archaic population’s DNA in modern humans, the findings are not clear enough to determine whether these two distinct populations intermixed just once or several times over hundreds of thousands of years.
Sankararaman and Arun Durvasula, a UCLA graduate student studying human genetics, used two new statistical methods that look for patterns in the genome that could reveal the presence of DNA from a distantly related unknown archaic population. They looked at genomic data of 405 people from the 1000 Genomes Project, an international public repository of genomic data from around the world. The results of both analyses were consistent.
The research was supported by the National Science Foundation, the National Institutes of Health, the Alfred P. Sloan Foundation and the Okawa Foundation.
Fifteen years later, neurologist Dr. S. Thomas Carmichael can still recall the patient who sparked his determination to find a cure for vascular dementia.
“She was a 55-year-old investment banker who couldn’t keep up with her spreadsheets and daily intellectual demands,” said Carmichael, co-director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. “As it turned out, she had vascular dementia. I found it just remarkable that there wasn’t anything we could do to help her get better. I’ve been studying the disease ever since.”
Unfortunately for patients, their families and clinicians like Carmichael, vascular dementia, and related diseases like Alzheimer’s and mixed dementia, have proven to be among the most intractable problems in medicine.
“To really get a handle on vascular dementia in humans is very demanding,” Carmichael said. “It requires an interdisciplinary team engaged in clinical contact with patients, brain tissue banking, sophisticated molecular biology, bioinformatics and an understanding of all the different cells and tissues within the brain.
“No one’s great at everything and the leading experts from the relevant fields aren’t commonly in the same room,” continued Carmichael, who is chair of the neurology department in the David Geffen School of Medicine at UCLA.
It took more than a dozen years, but last fall, Carmichael finally found himself in a room with the necessary experts — including stem cell researchers William Lowry and Kathrin Plath, vascular biologist Luisa Iruela-Arispe, neurobiologist Bennett Novitch and neuropathologist Dr. Inma Cobos.
This team of all-star researchers had been brought together to discuss an opportunity catalyzed by a gift from philanthropists David and Diane Steffy to the UCLA Broad Stem Cell Research Center.
“We approached the center with our interest in advancing brain aging research with the goal of improving quality of life,” said David Steffy, a business executive. “The medical field has made great strides in extending lifespans but these additional years will be marred by suffering if the problems of Alzheimer’s and other dementias remain unsolved.”
Around the world, nearly 50 million people are living with Alzheimer’s and other forms of dementia. The World Health Organization predicts this number will balloon to 152 million by 2050. Despite billions of dollars spent on research in the last few decades, there is no cure for Alzheimer’s, nor is there even a treatment available that slows its progression.
Seizing this opportunity, the center’s leadership convened the aforementioned team of UCLA researchers and invited them to use their varied expertise, repositories of donated human brain tissue and cutting-edge technologies to try to answer some of the biggest questions about Alzheimer’s and other dementias.
Novitch lab
Microscopic image of a mini brain organoid generated from human induced pluripotent stem cells.
.
At the time, only Cobos — who spent much of her career amassing a sizable bank of healthy and diseased frozen human brain tissue — was studying Alzheimer’s specifically. Carmichael was studying vascular dementia, Novitch was growing mini brain organoids, which are simplified human brain tissue grown in a lab dish from stem cells, Iruela-Arispe was studying blood vessels and Lowry was examining how neurons are born.
“Once we all started talking, it became clear how all of these component parts could come together to approach these diseases in a new and different way,” said Lowry, a professor of molecular, cellular and developmental biology.
Together, the group developed a plan to identify the myriad cellular processes that maintain brain health and examine what drives brain degeneration and repair in this devastating group of diseases.
First, they would conduct single-cell studies of frozen diseased and healthy human brain tissue from Cobos’ repository to identify the genes and cells that play a role in aging, disease progression and repair. Next, they would utilize both mouse models and mini brain organoids to further examine those genes and cells and identify potential drug targets.
To date, the vast majority of Alzheimer’s research has focused on one hallmark of the disease: how the buildup of a protein fragment called beta-amyloid affects neurons. The focus on beta-amyloid’s effect on neurons largely ignores the disease processes seen in all other cell types of the brain.
“Alzheimer’s and other dementias affect neurons, glial cells, blood vessels and immune cells simultaneously,” Lowry said. “Studies that focus only on how these diseases affect one cell type to the exclusion of others miss how the brain as a whole experiences and responds to damage.”
Not only is this focus on one cell type too narrow, there is increasing recognition in the field that Alzheimer’s researchers need to expand their scope and work toward understanding the link between all forms of dementia. Most people diagnosed with Alzheimer’s have a mixture of brain abnormalities.
“Most clinical dementia — like when your grandmother can’t remember where her keys are or where she parked her car — is now recognized to be mixed dementia,” Carmichael said. “Mixed dementia occurs when there is a component of Alzheimer’s on top of vascular dementia.”
Vascular dementia is caused by the accumulation of small strokes in the connecting areas of the brain, termed the “white matter.” Because these strokes occur in parts of the brain that do not control any vital functions, they typically don’t cause immediate noticeable effects. Instead, damage resulting from these repeated strokes accumulates over time, restricting blood flow to a larger area and causing noticeable neurological impairments.
It’s a vicious cycle: vascular dementia increases the incidence and progression of Alzheimer’s, and Alzheimer’s in turn increases the incidence and progression of vascular dementia.
“Vascular dementia is its own distinct entity but it’s also part of almost every case of Alzheimer’s,” Carmichael said, “so understanding vascular dementia is truly a critical element to understanding dementia as a whole.”
Efforts to understand vascular dementia using animal models have been hindered by the fact that it is a uniquely human disease. White matter accounts for 55% of the human brain and just 7% of the mouse brain — making it difficult to replicate the effects of white matter strokes in the laboratory.
Plath and Lowry labs
Microscopic image of neurons grown from human induced pluripotent stem cells.
“Vascular dementia is a disease that needs to be studied first and foremost in humans, which hasn’t historically been easy to do,” Carmichael said. “With this group’s resources and mastery of the latest technologies, we’re able to root our studies in human tissue.”
The Broad Stem Cell Research Center team is leveraging each scientist’s expertise and avoiding two of the key pitfalls of past Alzheimer’s and dementia research. The group’s studies are beginning in healthy and diseased human (rather than mouse) brain tissue and they are utilizing (and in some cases developing) technologies to study the effects of Alzheimer’s and dementia on all of the cell types found in the brain.
“Our study is not just examining how a dementia brain is different from a healthy brain, but how every one of the different cell types in the brain is affected by this disease, which is a huge distinction,” Lowry said. “With our combined expertise and enthusiasm, a lot of things would have to go wrong for us to not learn a whole lot about dementias.”
Though careful to caution that the project is at an early stage, Lowry is optimistic that the group’s open collaboration, cutting-edge technologies and human-tissue first approach will yield findings that will advance the field.
“We all have someone in our lives who has been affected by these diseases and we’re so grateful the Steffys’ gift brought us together to work on this problem,” Lowry said. “If not for their forward-thinking philanthropy, this group never would’ve come together in the way it did.”
This year, Bioinformatics IDP PhD students Jesse Garcia, Brian Nadel, and Harry Yang organized the retreat at the University of Southern California’s Wrigley Marine Science Center in Two Harbors, 20 miles offshore from Los Angeles.
During the 3-day retreat, Bioinformatics IDP graduate students presented research papers and had their student meeting on applying for fellowships, writing letters of intent, managing graduate school funding packages, creating handbook, and using campus mental health resources. In addition to science, faculty and students enjoyed hiking the chaparral hills, kayaking in the bay, snorkeling in the kelp forest, and enjoying dinner overlooking the beach in Two Harbors.
A team of researchers from UCLA’s Jonsson Comprehensive Cancer Center, Cedars-Sinai Cancerand Dana-Farber Cancer Institute has identified 34 genes that are associated with an increased risk for developing the earliest stages of ovarian cancer. The findings, published today in the journal Nature Genetics, will both help identify women who are at highest risk of developing ovarian cancer and pave the way for identifying new therapies that can target these specific genes.
The study was co-led by Simon Gayther, director of the Center for Bioinformatics and Functional Genomics at Cedars-Sinai; Bogdan Pasaniuc, associate professor of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA; Alexander Gusev, assistant professor of medical oncology at Dana-Farber; and Kate Lawrenson, assistant professor of obstetrics and gynecology at Cedars-Sinai.
“If you detect ovarian cancer really early, then the survival rate is very high, nearly 90 percent,” said Pasaniuc, who is also a member of the UCLA cancer center. “But that doesn’t happen often. Most cases are found at a later stage and survival drops dramatically. That’s why we want to understand the genetics behind it — so we can do a better job at predicting who is at a higher risk of developing this cancer.”
The current study builds on previous research of large-scale genetic data gathered over more than a decade by the Ovarian Cancer Association Consortium. Those researchers compared the genetic profiles of about 25,000 women with ovarian cancer and 45,000 women without the disease. The investigators found more than 30 regions in the genome that are associated with ovarian cancer.
Weizhe Hong, an assistant professor of biological chemistry and neurobiology at the David Geffen School of Medicine at UCLA, has been honored by The McKnight Endowment Fund for Neuroscience.
Hong was one of six scientists chosen for a 2019 McKnight Scholar Award for his research project titled, “Neural Circuit Mechanisms of Maternal Behavior.” The central goal of his lab is to provide a deeper understanding of the neural circuit mechanisms underlying social behaviors and how they malfunction in psychiatric disorders.
The three-year grant awards $225,000 to advance his research. The McKnight Scholar Awards are granted to young scientists in the early stages of establishing their research careers and who have demonstrated a commitment to neuroscience.
UCLA computer scientists and their collaborators have devised a plan for the use of cloud computing and big data analysis to allow scientists in developing countries to jumpstart bioinformatics research programs.
Bioinformatics is the computational analysis of biological data. Research in this emerging area has broad applications for diagnosing and treating diseases and preventing their spread; and in developing public health strategies and new drugs. The team’s proposal was published in Nature Biotechnology. The scientists have also created an online educational resource guide.
“A computer and a high-speed internet connection are all the infrastructure that’s required for good bioinformatics studies, and these resources are often already at universities in lower-income countries,” said study co-author Serghei Mangul, a UCLA postdoctoral scholar in computer science who specializes in biosciences.
That investment is much cheaper, Mangul said, than building a state-of-the-art life sciences lab, often called a “wet” lab because of chemicals and fluids that are used and analyzed. The cost of those facilities can start at hundreds of thousands of dollars to set up and maintain. There are also safety regulations and policy issues to consider, he added.
A startup bioinformatics program doesn’t necessarily have to gather the data.
“There is already a lot of publicly available data in genomics and in related fields that could yield impactful insights that would be locally relevant,” Mangul said.
For example, existing bioinformatics research on tropical countries could lead to new ways to prevent the spread of malaria, dengue fever, Chagas disease and other diseases that are prevalent in those regions, he said. Additionally, previously published bioinformatics data may offer more insight on a “second pass,” something that trained bioinformatics researchers could do.
“I really believe in the secondary analysis of the data; it can be just as important as the first pass,” said Mangul, who is also a fellow in The Collaboratory at UCLA’s Institute for Quantitative and Computational Biosciences.
Mangul was born and raised in Moldova, a lower-middle-income country in Eastern Europe. He came to the U.S. for his doctoral studies. He said that helping developing countries, such as his own, is a particular passion for him.
The same is true for Lana Martin, the study’s other co-author and the programs manager at the UCLA institute. She said working on this idea was partly motivated by growing up in a lower-income region of Texas, and partly by experiences conducting field research in Panama while completing her doctorate in anthropology at UCLA.
“There are already good scientists in those regions that only need some training to quickly get them up to speed on state-of-the-art data analysis techniques,” Martin said.
Their online educational resource guide, which is available at the software platform site GitHub, includes examples of bioinformatics codes and datasets, as well as a way to access datasets; and cloud computing-based resources. Mangul and Martin are working with one of their co-authors in Panama to build a strong bioinformatics research program there.
The researchers plan to develop university-level curricula and build a networking platform to connect bioinformatics scientists around the world.
“There will be an even greater demand for analysis of bioinformatics data in coming years,” Martin said. “With that in mind, we believe that establishing a global bioinformatics training and support consortium, with unified platforms and materials, will encourage scientists in lower-income countries and institutions to participate in cutting-edge, and more importantly, locally beneficial STEM research.”
“Ultimately, this would increase domestic scientific research and publication productivity,” she added.
Eleazar Eskin, a UCLA professor of computer science and human genetics, was also an author of the paper. Other authors are from Johns Hopkins University, Technological University of Panama, the George Washington University School of Medicine and Health Sciences, and UC San Diego.
The study was primarily supported by the National Institutes of Health, with additional support from the National Science Foundation and other educational and scientific organizations.
