Targeting MLL in Acute Myeloid Leukemia
Yali Dou, Ph.D., is an assistant professor in the department of pathology and holds a joint appointment in the department of biological chemistry at the University of Michigan.
Dou received a bachelor’s degree in medicine from Beijing Medical University (now Peking University Health Center), Beijing, China in 1996, and a master’s degree in biology in 1998 and a doctorate in biology in 2000 both from the University of Rochester, New York. She completed postdoctoral training at the University of Rochester, followed by postdoctoral training at The Rockefeller University.
She possesses more than 10 years of experience researching histone biology and biochemistry. Her broad research objectives are to understand the mechanisms for chromatin modifying enzymes to regulate various cellular processes. Dou is also exploring how disruption of their functions leads to carcinogenesis.
Targeting Genetic and Metabolic Networks in T-ALL
Adolfo A. Ferrando, M.D., Ph.D., is assistant professor of pediatrics and pathology at Columbia University.
He earned his medical doctorate in 1994 and his doctor of philosophy in 1999 from the University of Oviedo, Spain. Ferrando conducted postdoctoral research at Dana-Farber Cancer Institute in Boston.
Ferrando’s work focuses on the molecular basis of T-cell lymphoblastic leukemia. His research elucidates the molecular mechanisms that promote and sustain the malignant proliferation and survival of leukemic cells using a combination of genomic technologies, biochemical and genetic analysis.
Targeting Protein Quality Control for Cancer Therapy
Estela Jacinto, Ph.D., is assistant professor in the department of physiology and biophysics at the University of Medicine & Dentistry of New Jersey - Robert Wood Johnson Medical School.
Jacinto earned a bachelor’s degree in zoology in 1986 from the University of the Philippines, and her doctor of philosophy in biomedical sciences in 1997 from the University of California, San Diego. She conducted postdoctoral work at the University of Basel in Switzerland.
Jacinto’s research is focused on the TOR signaling pathway, which is critical for the regulation of cell growth and size. TOR is a protein kinase that regulates cell growth in response to the presence of nutrients or energy sources. Her research objective is to determine how the TOR pathway can link nutrient signals to other extracellular or environmental signals to promote growth, and provide insights on growth-regulatory mechanisms that could be targeted for development of drugs.
Targeting PP2A and the Glutamine-Sensing Pathway as Cancer Treatment
Mei Kong, Ph.D., is assistant professor in the division of tumor cell biology at Beckman Research Institute of City of Hope in Duarte, Calif.
Kong earned a bachelor’s degree in biology 1994 from East China Normal University, a Master of Science in 1997 from the Shanghai Institute of Cell Biology of the Chinese Academy of Sciences, and a doctor of philosophy in 2003 from McGill University. She conducted postdoctoral work at Abramson Family Cancer Research Institute at the University of Pennsylvania, under the tutelage of Craig B. Thompson, M.D.
Kong studies the oncogenic signal transduction pathways, focusing on the cellular functions of protein phosphatases. She researches cell metabolism, cell death, immunology, biochemistry and molecular biology. Specifically, her current work focuses on PP2A in regulation of cell apoptosis and cell metabolism.
Chimeric RNAs Generated by Trans-splicing and Their Implications in Cancer
Hui Li, Ph.D., is assistant professor of pathology at the University of Virginia in Charlottesville, Va.
Li earned a bachelor’s degree in chemical physics in 1998 from the University of Science and Technology of China, and a doctorate in microbiology and molecular biology in 2003 from Case Western Reserve University. He conducted postdoctoral work at Yale University.
Li researches gene fusions, which have been viewed as unique features of cancer and result from chromosomal translocation. Li has shown that the fusion products can be present in normal cells and they can be made through a mechanism that doesn’t require DNA translocation. His lab is now working on finding more examples of “trans-splicing.”
Exome Sequencing of Melanomas with Acquired Resistance to BRAF Inhibitors
Roger S. Lo, M.D., Ph.D., is assistant professor in the division of dermatology/department of medicine and the department of molecular and medical pharmacology at the David Geffen School of Medicine at the University of California.
Lo earned his bachelor’s degree in biology in 1994 from Stanford University, his medical doctorate and doctorate in philosophy (Howard Hughes Medical Institute) in 2002 from Weill Cornell, Memorial Sloan-Kettering Cancer Center and Rockefeller University. He conducted a residency in dermatology and postdoctoral work at UCLA Medical Center and Howard Hughes Medical Institute.
Lo’s laboratory is focused on melanoma research. He studies somatically mutated genes in melanoma pathogenesis. He also researches the mechanisms of primary and acquired resistance to targeted therapies using integrated genomic technologies.
Identification and Targeting of Novel Rearrangements in High-risk ALL
Charles G. Mullighan, M.D., is assistant member in the department of pathology at St. Jude Children’s Research Hospital.
He earned a Bachelor of Medicine and a Bachelor of Surgery in 1993 from the University of Adelaide in South Australia, a Master of Science in medical immunology in 1997 from the University of London, and a medical doctorate in 1998 from the University of Adelaide. Mullighan trained as a hematologist at the Royal Adelaide Hospital and performed postdoctoral studies in leukemia biology at St. Jude Children’s Research Hospital.
Mullighan is an academic hematologist and hematopathologist dedicated to using genomic approaches and experimental modeling to understand the genetic factors driving the pathogenesis and outcome of acute leukemia. He has expertise in genomic profiling of genetic alterations in acute leukemia, and translating the findings from these studies into experimental mouse models and the diagnostic arena.
A Systems Approach to Understanding Tumor Specific Drug Response
Dana Pe’er, Ph.D., is assistant professor in the biological sciences department at Columbia University in New York.
Pe’er earned her bachelor’s degree in mathematics in 1995, her master’s degree in 1999 and her doctorate in machine learning and computational biology in 2003, all from Hebrew University in Jerusalem. She conducted postdoctoral work in systems biology at Harvard Medical School.
Pe’er’s research is focused on elucidating tumor-specific molecular networks, working towards personalized cancer care. Her lab focuses on the integration and analysis of high-throughput data toward understanding how molecular networks process signals. Pe’er pioneered the use of Bayesian networks for analysis of molecular networks and has demonstrated the success of this approach in a broad number of applications spanning diverse types of biological data.
Targeting Sleeping Cancer Cells
Sridhar Ramaswamy, M.D., is assistant professor of medicine at Harvard Medical School and Massachusetts General Hospital Cancer Center, and associate member of the Broad Institute, and a principal member of the Harvard Stem Cell Institute.
He earned his bachelor’s degree in biochemistry from Williams College in 1987, and his medical doctorate in 1993 from Boston University. He obtained his medical training and conducted postdoctoral work at the Columbia-Presbyterian Medical Center, Dana-Farber Cancer Institute, Brigham & Women’s Hospital, Massachusetts General Hospital, National Institutes of Health, Harvard Medical School and Massachusetts Institute of Technology.
Ramaswamy studies the molecular basis of cancer drug resistance, to inform the development of new cancer biomarkers and drugs. His experimental approach integrates molecular and cell biology, genomic, proteomic and chemical screening, live cell imaging, animal modeling, molecular pathology and computational biology.
Inhibiting Innate Resistance to Chemotherapy in Lung Cancer Stem Cells
Eric Alejandro Sweet-Cordero, M.D., is assistant professor of pediatrics at Stanford University School of Medicine. Sweet-Cordero earned bachelor’s degrees in anthropology and biology from Stanford University in 1989, and his medical doctorate in 1995 from the University of California, San Francisco. He conducted a pediatric residency at UCSF; was a clinical fellow in pediatric hematology/oncology at Children’s Hospital Boston/Dana-Farber Cancer Institute of Harvard Medical School; and was a postdoctoral fellow at the Center for Cancer Research at MIT, under Tyler Jacks, Ph.D.
Sweet-Cordero’s laboratory identifies novel therapeutic approaches for cancer that target the altered signaling networks that are specific to cancer cells. He leverages genetically engineered mouse models of cancer as well as human cell lines and the analysis of primary human tissue samples to dissect the response to therapeutic agents. His research is focused on identifying and characterizing “synthetic lethal” interactions that alter the outcome of oncogenic Kras activation.
Developing New Therapeutic Strategies for Soft-tissue Sarcoma
Amy J. Wagers, Ph.D., is associate professor in the department of stem cell and regenerative biology at Harvard University and Harvard Medical School, and is a Howard Hughes Medical Institute early-career scientist.
Wagers earned her bachelor’s degree in biological sciences from Northwestern University in 1994, and her doctorate in immunology and microbial pathogenesis from Northwestern University Medical School in 1999. She conducted her postdoctoral work in stem cell biology at Stanford University.
Wagers has worked to develop and optimize sensitive cell sorting approaches that allow direct isolation of mouse and human muscle satellite cells, and to assess their phenotype and function in normal and pathological conditions. She applies these unique approaches to reveal the molecular underpinnings of soft-tissue sarcoma and to evaluate candidate therapeutic approaches for these tumors.
Framing Therapeutic Opportunities in Tumor-activated Gametogenic Programs
Angelique W. Whitehurst, Ph.D., is assistant professor in the department of pharmacology and Lineberger Comprehensive Cancer Center at the University of North Carolina at Chapel Hill.
Whitehurst earned her bachelor’s degree in chemistry and biochemistry from Virginia Polytechnic Institute in 1997, and her doctorate in cell and molecular biology in 2004 from University of Texas Southwestern Medical Center, where she conducted postdoctoral work.
Whitehurst’s research characterizes the components that permit uncontrolled growth of tumor cells. She has developed an RNAi-based functional genomics approach to identify genes that modulate paclitaxel sensitivity in lung tumor cells. This strategy revealed many unanticipated proteins that play critical roles in modulating the response of tumor cells to a first line chemotherapeutic.
Coupled Genetic and Functional Dissection of Chronic Lymphocytic Leukemia
Catherine J. Wu, M.D., is assistant professor of medicine at Harvard Medical School and Dana-Farber Cancer Institute. She is staff physician at Brigham & Women’s Hospital and Dana-Farber Cancer Institute.
Wu earned her bachelor’s degree in biochemistry from Harvard University in 1988, and her medical doctorate from Stanford University School of Medicine in 1994. She conducted a residency in internal medicine at Brigham & Women’s Hospital, and a fellowship in hematology-oncology at Dana-Farber Cancer Institute.
Wu’s research focuses on understanding the biology and on developing effective therapies for the treatment of CLL. She is leveraging the recent availability of next-generation massively parallel sequencing technologies to comprehensively identify and assess the potential functional effects of genetic mutations within CLL cells. She uses this information to identify novel and patient tumor-specific antigens that can be targeted immunologically, and to develop global understanding of the mutational landscape of CLL and how this relates to clinical heterogeneity.