Philadelphia, PA -
06/16/2009 - The Pew Charitable Trusts today named 17 early-career scientists as Pew Scholars in the Biomedical Sciences. Scholars receive a $240,000 award over four years to help support their work, which this year includes research related to cancer, Parkinson’s disease, birth defects and epilepsy. The Scholars also gain inclusion into a select community of scientists that includes Nobel Prize winners, MacArthur Fellows and recipients of the Albert Lasker Medical Research Award.
Now in its 25th year, the Program has invested more than $125 million to fund over 460 scholars.
The selection process for the Pew Scholars is rigorously competitive. Applicants must be nominated by an invited institution and must demonstrate excellence and innovation in their research. This year, 149 institutions were invited to nominate a candidate in basic biomedical research, and 111 eligible nominations were received.
“Pew is thrilled to celebrate 25 successful years for the Biomedical Scholars program,” said Rebecca W. Rimel, President and CEO of The Pew Charitable Trusts. “Not only does the program provide extraordinary scientists with the resources to carry out significant research early in their careers, it also offers them the opportunity to exchange ideas and foster relationships during the annual meetings and various networking activities. These gatherings have often led to collaborations that have resulted in significant scientific progress.”
“The Pew Biomedical Scholars are a synergistic community whose connections are reinforced over the years,” said Craig C. Mello, Ph.D., a 1995 Pew Scholar and a 2006 Nobel laureate in physiology or medicine, and the chair of the national advisory committee for the program. “I have no doubt that this immensely talented and diverse new class of Pew Scholars will have a major impact on biomedical research through their contributions as part of the Pew community and on science as a whole.”
Related Press Release: Ten Top Latin American Scientists Named 2009 Pew Fellows in the Biomedical Sciences
|The 2009 Pew Scholars in the Biomedical Sciences are:|
| || |
|Frank Alber, Ph.D.||University of Southern California|
|Diana M. Bautista, Ph.D.||University of California, Berkeley|
|Jon P. Boyle, Ph.D.||University of Pittsburgh|
|Zev D. Bryant, Ph.D.||Stanford University|
|Jennifer G. DeLuca, Ph.D.||Colorado State University|
|Qing R. Fan, Ph.D.||Columbia University|
|Kevin A. Janes, Ph.D.||University of Virginia|
|John K. Kim, Ph.D.||University of Michigan|
|Alexander Meissner, Ph.D.||Harvard University|
|Charles G. Mullighan, M.D.||St. Jude Children’s Research Hospital|
|Patrick J. Paddison, Ph.D.||Fred Hutchinson Cancer Research Center|
|Joseph R. Pomerening, Ph.D.||Indiana University|
|Nicholas J. Priebe, Ph.D.||University of Texas at Austin|
|Melissa M. Rolls, Ph.D.||The Pennsylvania State University|
|Joshua W. Shaevitz, Ph.D.||Princeton University|
|Ben Z. Stanger, M.D., Ph.D.||University of Pennsylvania|
|R. Grace Zhai, Ph.D.||University of Miami, Miller School of Medicine|
Frank Alber, Ph.D.
, received his doctorate from the Swiss Federal Institute of Technology in Zurich, Switzerland, in 1998. He conducted his postdoctoral work in computational structural biology at the International School for Advanced Studies in Trieste, Italy, and then did further postdoctoral training at the Rockefeller University and the University of California, San Francisco. In 2008, he joined the faculty of the University of Southern California, Los Angeles, as an assistant professor in the Department of Biological Sciences. Dr. Alber’s research is focused on the three-dimensional structure that occurs when the long strands of DNA are tightly packed to fit into the cell nucleus by nucleosomes, the repeating complexes that wind the DNA. When nucleosomes interact and fold, they form extremely compact structures that regulate expression of genes by allowing or blocking access to the DNA. This dynamic also makes it a difficult region to access in order to characterize it. Dr. Alber has developed a computational model for generating a structural description of this highly ordered DNA by merging multiple datasets from a range of experimental methodologies. His work will bridge the gap between genome sequencing, gene regulation and structural biology, and will provide insights to better understand many human diseases.Diana M. Bautista, Ph.D.
, earned her doctorate in neuroscience from Stanford University in 2002. She completed her postdoctoral work in neuroscience at the University of California, San Francisco, in the Department of Physiology. In 2008, she joined the faculty of the University of California, Berkeley’s Department of Molecular and Cell Biology. Dr. Bautista works in the field of sensory neuroscience. The ability to detect touch and pain rely on our somatosensory system and the somatosensory neurons that convey our senses. Dr. Bautista’s work centers on identifying the molecules that signal to neurons to convey these stimuli. She has developed experiments in a cell model to stimulate and detect responses in mammalian mechanosensensory neurons. In addition, she is using a novel model organism for touch reception: the star-nosed mole, whose nose is the most sensitive touch organ known due to its innervations by ~100,000 sensory neurons. Her efforts of understanding mechanosensory transduction in mammals will be highly relevant to the treatment of diseases such as AIDS and diabetes that impair the ability to detect feelings of pain and touch.Jon P. Boyle, Ph.D.
, received his doctorate in molecular parasitology from the University of Wisconsin-Madison in 2003. He conducted his postdoctoral research at Stanford University’s School of Medicine in molecular parasitology. He then joined the faculty of the University of Pittsburgh’s Department of Biological Sciences as an assistant professor in 2008. The main question that Dr. Boyle investigates is how virulence from a pathogen is determined not only by the host’s genetic factors, but more significantly by the genetic factors of the pathogen. For example, Dr. Boyle has identified virulence determinants, proteins expressed from the intracellular pathogen Toxoplasma gondii
, that when secreted can transform a benign strain of Toxoplasma
into a lethal one. He will determine at the molecular level how these proteins alter the virulence of Toxoplasma
by investigating their effects on the immune system and gaining insight to their structural properties, which will aid in the development of drug therapies against pathogens like Toxoplasma
.Zev D. Bryant, Ph.D.
, completed his doctorate at the University of California, Berkeley, in the Department of Molecular and Cell Biology in 2003. He continued his combined studies of biochemistry, bioengineering and biophysics at Stanford University during his postdoctoral fellowship. Dr. Bryant joined the faculty of the Department of Bioengineering at Stanford University as an assistant professor in 2007. The principal goal of Dr. Bryant’s research is to understand how a biological motor converts chemical energy into mechanical work. The fascinating part of this goal is that he is looking at nano-scale molecular motors that drive processes such as cell migration and DNA replication. He will test his hypothesis concerning how a molecular motor chooses its direction and speed by creating a molecular motor that can be signaled to change its direction while moving. This work may lead to long-term therapeutic applications by designing motors that could eventually be used for complicated processes such as genomic repair.Jennifer G. DeLuca, Ph.D.
, received her doctorate in 2000 from the Department of Molecular, Cellular & Developmental Biology of the University of California, Santa Barbara. She moved to the University of North Carolina, Chapel Hill, to do her postdoctoral work in cell biology and microscopy. In 2007, she joined the faculty of Colorado State University as an assistant professor in the Department of Biochemistry and Molecular Biology. Dr. DeLuca studies how chromosomes, long strands of DNA, are properly segregated during cellular division or mitosis. Chromosomes must attach to the cellular machinery responsible for their segregation, known as the microtubules of the mitotic spindle, during mitosis. Specifically, Dr. DeLuca explores how the chromosome attachment point of the mitotic spindle, a complex of proteins known as the kinetochore, is built and maintained. She uses a combination of biochemical, structural and cell-biological techniques to conduct her studies in living cells. An understanding of the molecular mechanisms that ensure proper chromosome segregation during mitosis will provide insight to multiple causes of birth defects and cancer that may eventually lead to innovative therapies.Qing R. Fan, Ph.D.
, received her doctorate in chemistry from Harvard University in 1999. She then changed fields to structural biology and completed her postdoctoral work at Columbia University. In 2007, she joined the faculty of Columbia University as an assistant professor in the Department of Pharmacology and Pathology. Dr. Fan’s work is focused on GABAB
receptors, trans-membrane proteins that act as receptors for gamma-aminobutyric acid (GABA). GABAB
receptors are found in the central and peripheral nervous system and act as inhibitory receptors to stop neurotransmitter release. GABAB
receptors play a critical role as gatekeepers to prevent signals from being improperly transmitted in the brain. Dr. Fan would like to combine her approaches of structural analyses with functional molecular studies to understand how this receptor recognizes and acts together with its sub-units to regulate signals properly. GABAB
receptors appear to be required for the prevention of numerous diseases, including epilepsy, therefore advancing our understanding of the molecular basis of GABAB
receptor action and activation will lead to the design of novel therapeutic treatments.Kevin A. Janes, Ph.D.
, received a doctorate in bioengineering from the Massachusetts Institute of Technology in 2005. He completed his postdoctoral work at Harvard Medical School and then joined the faculty at the University of Virginia as an assistant professor in the Department of Biomedical Engineering. Dr. Janes’ research focuses on the process of how cells take multiple signal inputs and interpret them to cause cell-fate decisions such as division, differentiation or death. Changes in cell fates, which can underlie complex diseases such as cancer, are usually the outcome of networks of signaling pathways that are interconnected. Instead of looking at a single pathway that directs cell fate changes, as is most commonly done, Dr. Janes uses a multipronged approach, combining quantitative biochemical techniques and statistical modeling. In addition, he performs experiments in cells that change more than one factor, or pathway, at a given time. By tracking changes in multiple signaling pathways during the transition of a cell into a new state, his studies contribute to the identification of optimal therapies for complex diseases like cancer that may require combinations of drug therapeutic approaches.John K. Kim, Ph.D.
, received his doctorate in biochemistry and molecular biology from the University of California, Davis, in 2000. He conducted his postdoctoral research in genetics at the Harvard Medical School and Massachusetts General Hospital. In 2006, he joined the faculty of the University of Michigan as an assistant professor in the Department of Human Genetics at the Life Sciences Institute. In the last decade, small RNAs have emerged as major regulators of gene expression, important for many processes in mammals. Dr. Kim studies the detailed steps of how small non-coding micro-RNAs (miRNAs) recognize the genes that they regulate and direct them to be turned off. His work centers on the identification of a new group of proteins that bind to these miRNAs and the genetic sequences they target in the model organism C. elegans
. By understanding the role that these newly identified proteins play in regulating known miRNA targets, his studies will provide crucial insights into what is now known to be a mode of gene regulation required for normal development and disease prevention.Alexander Meissner, Ph.D.
, received his doctorate in biology in 2006 from the Whitehead Institute for Biomedical Research at the Massachusetts Institute of Technology. He remained at the Whitehead Institute for his postdoctoral work in stem cell biology and epigenetics. In 2008, he moved to Harvard University, where he joined the Department of Stem Cell and Regenerative Biology as an assistant professor. Dr. Meissner studies how stem cells that can divide and become any cell type (known as pluripotency) are dynamically programmed through epigenetic changes, or chemical modifications to DNA and its associated proteins. Proteins that bind to specific DNA sequences and regulate gene expression, known as transcription factors, have recently been shown to change a specific cell type back to its un-programmed state with unlimited potential. Dr. Meissner would like to gain mechanistic insight into how specific transcription factors are involved in this process. His research is critical to illuminating the processes by which stem cells generate from already programmed specific cell types that will aid in the development of vital therapies for myriad diseases.Charles G. Mullighan, M.D.
, received his medical degree from the University of Adelaide, Australia. He then conducted his internship and residency at the Royal Adelaide Hospital in psychiatry and internal medicine, respectively. After clinical training in hematology at the Institute of Medicine and Veterinary Science in Adelaide, he shifted his career and began training as a postdoctoral fellow in studies of the molecular biology of acute leukemia at St. Jude Children’s Research Hospital in Memphis, TN. In 2008, he joined the staff at St. Jude Children’s Research Hospital as an assistant member of the department of pathology, where he is conducting research on acute lymphoblastic leukemia (ALL). Dr. Mullighan’s research is focused on the identification of genetic abnormalities that contribute to treatment failure in ALL. He has previously identified a gene that is a strong marker of adverse outcomes in different forms of ALL and is directing his efforts on expanding the targets of genetic alterations contributing to the recurrence of ALL. Together with mechanistic studies in a mouse model, his work will generate vital new therapeutic approaches for ALL patients.Patrick J. Paddison, Ph.D.
, received his doctorate from the Watson School of Biological Sciences at Cold Spring Harbor Laboratories in biological sciences in 2004. He continued at Cold Spring Harbor Laboratories to complete his postdoctoral fellowship in stem cell research in 2008, and then he joined the Fred Hutchinson Cancer Research Center as an assistant member in the Department of Human Biology. A common goal in biomedical research is to define how a cell maintains or alters its identity, which has implications in stem cell biology and human disease.Dr. Paddison’s work revolves around using functional genetic approaches to tease out the network of genes that regulate cell fate. Using a genome wide scale screening technique that he developed based on RNA interference (RNAi), he will compare the gene expression patterns from different in vitro
stem cell systems, to identify gene networks that regulate mammalian cell identity. His work will illuminate new gene networks to target for therapeutic purposes and will contribute to how RNAi itself may be used as a therapeutic agent for human diseases such as cancer.Joseph R. Pomerening, Ph.D.
, received his doctorate in molecular and cellular biology from the University of Illinois at Urbana-Champaign in 2000. He moved to Stanford University School of Medicine for his postdoctoral research in systems biology. In 2007, he became an assistant professor in the Department of Biology at Indiana University. Dr. Pomerening studies how the many stages required for cellular mitosis are regulated. His research takes advantage of single-cell approaches along with cell sorting and live cell imaging of mammalian cells. He is specifically investigating the role of cyclin-dependent kinases, proteins that modify other proteins to alter their expression, allowing for dynamic changes that ultimately direct the cell to progress in mitosis until the cell completes mitosis. Dr. Pomerening will merge both experimental and computational methods to create a big-picture, quantitative model of how kinase activity impacts cellular mitosis, which will increase our understanding of certain disease models with aberrant cell cycling progression such as cancer.Nicholas J. Priebe, Ph.D.
, received his doctorate in physiology from the University of California, San Francisco, in 2001. He completed his postdoctoral work at Northwestern University in the Department of Neurobiology and Physiology. In 2008, he joined the Department of Neurobiology at the University of Texas at Austin as an assistant professor. Dr. Priebe’s research is focused on understanding how cortical neurons in the brain translate their signals into a visual response. Specifically, he is investigating binocularity to determine how the brain integrates the inputs of signals to the cortical neurons from two eyes, and how different experiences alter this process. The goal of his research is to measure the synaptic inputs through in vivo
whole cell recordings of the cortical neurons in response to changes in the visual environment so that he can test how mechanisms, such as inhibition or excitation, lead to binocularity. This work will not only lead to an understanding of visual response and possible treatments for visual disorders, but also will increase our understanding of basic neuronal mechanisms related to learning and memory.Melissa M. Rolls, Ph.D.
, received her doctorate in biological and biomedical sciences from Harvard University in 2001. She moved to the University of Oregon to conduct her postdoctoral work in molecular biology and neuroscience. In 2007, she became an assistant professor in the Department of Biochemistry and Molecular Biology at the Pennsylvania State University. Dr. Rolls’ research is based on a little-studied field of investigation: dendrite degeneration. Neurons are comprised of dendrites, which receive and process signals—axons which send signals and cell bodies. Axons and dendrites extend long distances from the cell body, where they can be exposed to stress and damage independently of any other component of the neuron. It is known that axons have unique degeneration programs following injury; however, little is known about dendrite degeneration. Dr. Rolls will use the fruit fly as a model system to induce injury to dendrites and determine what mechanisms, including known degradation pathways and candidate genes, are activated to execute dendrite degeneration. Her work will advance our understanding of neuronal disorders such as seizures and stroke, and how the brain responds to these injuries.Joshua W. Shaevitz, Ph.D.
, earned his doctorate in biophysics from Stanford University in 2004. He then performed postdoctoral research in biophysics at the University of California, Berkeley, until he obtained his joint position as an assistant professor in the Department of Physics and the Lewis-Sigler Institute for Integrative Genomics at Princeton University. Dr. Shaevitz works on understanding the physical forces inside bacteria that regulate cellular organization and are required for bacterial function. Bacteria, like all cells, have mechanisms in place that allow for cell shape and motility and are required for processes such as chromosome segregation and cellular division. Dr. Shaevitz wants to understand these micron-scale physical mechanisms, and the forces they generate, by disturbing them mechanically and then using super resolution imaging in three-dimensions to watch the cellular response. Because most antibiotics rely on the disruption of normal bacterial processes such as cell growth and division, Dr. Shaevitz’s work of understanding bacteria at a mechanistic level never seen before will be directly linked to the creation of new classes of antibiotics to target major disease in humans.Ben Z. Stanger, M.D., Ph.D.
, received his medical degree and his doctorate in genetics from Harvard Medical School in 1997. He conducted his internship and residency at the University of California, San Francisco, in internal medicine and then did his clinical training in gastroenterology at Massachusetts General Hospital. He proceeded to do a postdoctoral fellowship in developmental biology at Harvard University. Dr. Stanger joined the faculty of the University of Pennsylvania as an assistant professor in 2006 in the Department of Medicine, where he studies how tissues know when to stop growing in order to reach the appropriate size in their own environment. He uses a mouse model to determine how specific genes regulate cell size, division and death through communication during development. It is likely that cellular growth-promoting signals require a population of cells signaling to one another to properly form an organ, like a liver, instead of cell-independent events. Dr. Stanger’s research will provide insights to develop therapies for cancer and other disease related to improper tissue growth.R. Grace Zhai, Ph.D.
, received her doctorate from the University of Alabama at Birmingham in neurobiology in 2001. She completed her postdoctoral studies at Baylor College of Medicine in genetics and, in 2007, she joined the University of Miami, Miller School of Medicine as an assistant professor in the Department of Molecular and Cellular Pharmacology. Dr. Zhai investigates how healthy neurons are able to live as long as we do and what mechanisms of protection and repair they use to achieve this long life-span. She takes advantage of the ease of Drosophila
genetics to uncover genes that normally protect neurons, or when their function is lost, cause neurodegeneration. Her efforts are focused on one of the genes she has identified, neuronal maintenance factor (NMNAT), whose loss of function induces rapid and severe neurodegeneration. She is identifying the molecular mechanisms that NMNAT uses to normally protect neurons in Drosophila
and then will apply these findings to the three NMNAT genes that are found in mammals to conduct similar functional studies. Through uncovering the genes that protect and maintain neurons, she will establish models to help promote the development of new drug therapies for neurodegenerative disorders.Photo on homepage:
From the lab of 2008 Pew Scholar Antonio Giraldez. Zebrafish embryos labeled with GFP mRNA that is repressed by microRNAs. Short embryos are mutants that lack miRNAs.