- Rita Allen Foundation

All Scholars

Since 1976, the Rita Allen Foundation has awarded millions of dollars in grants to early-career biomedical scholars. These grants allow Rita Allen Foundation Scholars to establish labs and pursue research directions with above-average risk and promise. See below for a full list of Scholars, or read more about the Rita Allen Foundation Scholars program.

2016

Steve Davidson +
University of Cincinnati College of Medicine

Steve Davidson

Steve Davidson (Award in Pain Recipient) earned a B.S. in psychology from the University of New Orleans and a Ph.D. in neuroscience from the University of Minnesota. He was a postdoctoral scholar in the Department of Anesthesiology at Washington University School of Medicine in St. Louis from 2009 to 2014, and in 2015 he joined the faculty of the University of Cincinnati College of Medicine. In 2010, Davidson received a Future Leader in Pain Research award from the American Pain Society.

Pain has long been recognized as a multidimensional experience. Yet research has focused almost exclusively on the sensory dimension, leaving the emotional and motivational components poorly understood and undertreated. The Davidson lab seeks to elucidate and control a neural circuit responsible for regulating the capacity for pain tolerance, an aspect of pain behavior dependent on emotional and motivational pain processing that occurs in the brain. Davidson’s research tests the main hypothesis that effective pain control can be achieved by manipulating neural activity in a thalamo-limbic pathway to enhance pain tolerance. His laboratory has developed a novel operant behavioral model in which rodents may obtain a reward by engaging with (tolerating) a noxious thermal stimulus. Using this approach, analgesics with efficacy for improving the affective measure of pain tolerance vs. reflexive withdrawal may be determined. To determine whether thalamo-limbic projection neurons control pain, virally infected posterior thalamic neurons containing optically gated ion channels will allow direct control of activity through an implanted light source while animals are tested for changes to pain tolerance and reflexive behaviors. Finally, the Davidson lab will test the hypothesis that chronic pain alters synaptic plasticity in the thalamo-limbic circuit. This will include examination of posterior thalamic projection neurons for altered excitability and synaptic plasticity at the posterior thalamus-insula synapse in rodent models of neuropathic and inflammatory chronic pain.
Camila dos Santos +
Cold Spring Harbor Laboratory

Camila dos Santos

Camila dos Santos completed undergraduate, master’s and doctoral studies at the University of Campinas in Brazil. She was a postdoctoral fellow at the Children’s Hospital of Philadelphia, as well as a postdoctoral fellow and research investigator at Cold Spring Harbor Laboratory with Gregory Hannon, a 2000 Rita Allen Foundation Scholar and a member of the Foundation’s Scientific Advisory Committee. She became an assistant professor at CSHL in 2015. In addition to the Rita Allen Foundation award, dos Santos has received a Glen Cove Cares Research Award, a Pershing Square Foundation Scholar Award and a research award from the Manhasset Women’s Coalition Against Breast Cancer.

The dos Santos laboratory aims to uncover the molecular basis of pregnancy-induced breast cancer protection. In humans, a full-term pregnancy before the age of 25 is known to reduce the risk of developing breast cancer by more than one-third. In rodents, pregnancy can decrease the frequency of carcinogen-induced mammary tumors by more than 60 percent. A recent study by dos Santos and colleagues has shown that transitions through pregnancy lead to massive and stable reorganization of DNA methylation in mammary epithelial cells. Now they propose to further characterize this phenomenon by mapping genome-wide enhancer activity in this system. They will test the hypothesis that the parous (post-pregnancy) epigenome modulates the effects of breast cancer oncogenes on epithelial cell oncogenesis. In addition, they will investigate pharmacological strategies that mimic these effects, which may provide a path toward strategies for breast cancer prevention.
Monica Dus +
University of Michigan

Monica Dus

Monica Dus (Milton E. Cassel Scholar) earned a B.S. in biology from the University of Redlands in Redlands, California, and a Ph.D. in the Watson School of Biological Sciences at Cold Spring Harbor Laboratory, where she worked with Gregory Hannon, a 2000 Rita Allen Foundation Scholar and a member of the Foundation’s Scientific Advisory Committee. After a postdoctoral fellowship in Greg Suh’s lab at the New York University School of Medicine, she became an assistant professor at the University of Michigan in 2015. In addition to being a Rita Allen Foundation Scholar, Dus has received a Pathways to Independence K99/R00 Award from the National Institute of Diabetes and Digestive and Kidney Diseases, a NARSAD Young Investigator Grant from the Brain and Behavior Research Foundation and a Klingenstein-Simons Fellowship Award in the Neurosciences.

One of the oldest debates in biology is that of nature versus nurture. Are our behaviors dictated by genes or by the environment? In the last decade it has become clear that neuroepigenetic processes play a key role in adult brain function by merging environmental information with ongoing brain processes to direct behavioral states. Disruption in these processes is linked to both normal and abnormal behaviors, such memory and addiction. However, the underlying mechanisms remain mysterious. In particular, we have no knowledge about the genetic loci of integration between the environment and behavior, or the identity of the neural pathways that control them in specific neural circuits. This presents a major roadblock to unlocking the molecular interface between brain and environment and the role it plays in brain function. To understand how the environment shapes and reprograms brain and behavior, the Dus lab exploits: 1) a simple behavior, eating, which is dependent on an experimentally controllable environment, diet; and 2) the fruit fly brain, which is orders of magnitude smaller than vertebrate brains, but shows conserved neurochemistry.
Katherine Hanlon +
Presbyterian College School of Pharmacy (University of New England College of Osteopathic Medicine)

Katherine Hanlon

Katherine Hanlon (Award in Pain Recipient) earned a B.S. in biochemistry and molecular biophysics and a Ph.D. in pharmacology from the University of Arizona, where she worked with Todd Vanderah. She went on to complete a postdoctoral fellowship in tumor immunology at the Mount Sinai Medical Center with Joshua Brody and Peter Heeger. In addition to her work in the lab, Hanlon currently teaches Biochemistry and Principles of Pharmacology in the School of Pharmacy at Presbyterian College and directs the College’s Office of Research. Her primary research interests include macrophage-neuron communication in pain processing and the role of tumor-associated macrophages in cancer development. She also studies the mechanisms of dysregulation of cannabinoid receptor signaling in tumor and immune cells in metastatic disease.

Studies in the Hanlon lab are carried out using multiple in vitro and in vivo models, including leukocytes and neurons isolated from dorsal root ganglia, leukocytes and tumor cells isolated from murine mammary tumors, leukocytes harvested from post-surgical peritoneal adhesions, and human blood monocyte primary cultures. With the support of the Rita Allen Foundation and the American Pain Society, the lab is able to explore the communication that occurs between sensory neurons and macrophages (innate immune cells that are critical in injury response) in dorsal root ganglia (DRG). Macrophages in the DRG are a unique population of cells that bear some resemblance to brain microglia, but are functionally distinct and exhibit specific phenotype differences. In response to peripheral injury, DRG macrophages respond to activity in the ascending pain pathways and may alter pain perception. By evaluating the phenotype and function of this unique population, Hanlon hopes to isolate novel and exploitable mechanisms that may be used to develop non-opioid therapeutics for the treatment of persistent pain.
Alex Kentsis +
Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College

Alex Kentsis

Alex Kentsis received undergraduate and master’s degrees from the University of Chicago, where he conducted research in the laboratory of Tobin Sosnick. He earned a Ph.D. from New York University, where he worked with Katherine Borden, and an M.D. from Mount Sinai School of Medicine, where his advisor was Roman Osman. He completed research and clinical fellowships at Boston Children’s Hospital and the Dana-Farber Cancer Institute, where he later became an attending physician, as well as an instructor at Harvard Medical School. He joined the faculties of Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College in 2013. In addition to being a Rita Allen Foundation Scholar, Kentsis has received a Damon Runyon Cancer Research Foundation Clinical Investigator Award, an American Society for Clinical Investigation Physician-Scientist Award, an American Society of Hematology Scholar Award and a Burroughs Wellcome Fund Career Award for Medical Scientists.

Genome sequencing efforts have revealed a surprising dearth of gene mutations in many human cancers, suggesting that alternative oncogenic mechanisms must be investigated to identify targets for improved therapy. Approximately half of the human genome originates from mobile DNA elements, or transposons, but their contributions to human disease and physiology remain almost completely unexplored. Kentsis aims to investigate mechanisms of tumorigenesis by a novel human DNA transposase in embryonal tumors, lethal childhood cancers that are refractory to intensive chemotherapy. Successful completion of proposed studies promises to transform our ability to identify the drivers of human cancer, thus leading to improved targeted therapies for these refractory pediatric tumors. This work will also establish powerful tools for the investigation of DNA transposition and genomic plasticity, with transformative applications in wide areas of human biology.
Bo Li +
The University of North Carolina at Chapel Hill

Bo Li

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Bo Li earned her B.S. in biological sciences from Beijing University and her Ph.D. in biochemistry from the University of Illinois at Urbana-Champaign. She was a postdoctoral fellow in the Department of Biological Chemistry and Molecular Pharmacology at Harvard Medical School, where she worked with Christopher T. Walsh. She has received a a Jane Coffin Childs Memorial Fund for Medical Research Fellowship and a National Institutes of Health Pathway to Independence Award.

Li’s lab identifies bioactive small molecules produced by bacteria—she and her colleagues explore the chemistry of their production and study the roles they play in the biology of bacteria and human hosts. Bacteria craft these gene-encoded molecules from primary metabolites using complex chemical transformations; the structures and activities of these small molecules have been optimized through millions of years of evolution and enable these molecules to mediate extensive microbe-microbe and microbe-host interactions. Li’s multidisciplinary research program uses bacterial genomics and metabolomics as enabling technologies to identify novel bacterial small molecules. First, her team is identifying small molecules from soil bacteria as novel antibiotics to combat multidrug-resistant pathogens; second, they are identifying metabolites produced by the human gut microbiota to unravel the chemical and molecular mechanisms of bacterial symbiosis and pathogenesis. Her work involves understanding fundamental biosynthetic mechanisms and extends to exploiting bacterial small molecules to improve human health and prevent disease.
Katharina Schlacher +
The University of Texas MD Anderson Cancer Center

Katharina Schlacher

Katharina Schlacher obtained her B.S. in microbiology at the Karl-Franzens University in Graz, Austria. For graduate studies, in 2003 she joined the lab of Myron Goodman at the University of Southern California, where she earned her Ph.D. While there, she discovered an unprecedented transactivation mechanism for mutagenic E. coli DNA polymerase V by proteobacter recombinase RecA, recognized by the USC College Doctoral Research Prize. In 2007, as a Damon Runyon Postdoctoral Fellow, Schlacher joined Maria Jasin at Memorial Sloan Kettering Cancer Center (MSKCC) and Hong Wu at the University of California, Los Angeles, to focus on her passion for mechanisms at the replication fork. She discovered a novel genomic instability and tumor suppressor mechanism at the DNA replication fork distinct from DNA repair. Specifically, Fanconi anemia proteins BRCA1/2 protect stalled DNA replication forks from degradation by MRE11. This replication fork protection discovery was recognized with the Parvin Foundation Award for academic excellence, the UCLA/Molecular Biology Institute Research Excellence Award and the MSKCC Postdoctoral Research Award. Schlacher received a National Cancer Institute K22 award and joined the faculty at MD Anderson Cancer Center in 2014.

Schlacher’s research focuses on developing an in-depth molecular and biological understanding of how replication fork protection suppresses cancer and disease to obtain biological insights suitable to develop disease prevention and treatment strategies.

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