2008-12-07

The ASH Scholar Awards are highly competitive grants that provide partial salary support during the transitional period between completion of training and achievement of status as an independent investigator. The goal of the program is to encourage beginning hematologists to pursue a research career in either basic or clinical/translational research. ASH News Daily is proud to feature profiles of some of the current class of scholars in each issue of the paper at this year’s annual meeting.

Junping Wei, MD, PhD, a Basic Research Fellow Scholar, began her research career as a physician in China. Her research crosses multiple fields, such as molecular biology, cell biology, stem cell-based tissue regeneration, diabetes, cancer and cancer stem cell biology, signaling pathways, and cancer therapy. She earned her PhD at Shinshu University Graduate School of Medicine in Japan, where she successfully induced human amniotic epithelial stem cells to differentiate into insulin-producing cells, which could then correct the glucose level in diabetic mice. In 2004, she started her postdoctoral research at Cincinnati Children’s Hospital Medical Center. She has successfully immortalized human hematopoietic stem/progenitor cells (HSPCs) by using a self-renewal signal supplied by CBF fusion protein coupled with telomere maintenance. In addition, Dr. Wei has developed leukemia models based on a MLL-fusion gene, transduced primary human HSPC engrafted into NOD/SCID mice, and found that the lineage of the resulting leukemias can be readily manipulated by altering either the growth factors or the recipient strain of mouse. Using this model, she identified Rac GTPases as a key survival signal. Treatment with the Rac specific inhibitor, or knockdown of Rac expression by RNAi, induces cell cycle arrest and rapid apoptosis in MA9 cells. Her paper based on these findings was published in Cancer Cell.

Ethan Weiss, MD, a Basic Research Junior Faculty Scholar, joined the faculty at the University of California, San Francisco (UCSF) in 2003 as assistant professor of medicine. Dr. Weiss earned his medical degree from the Johns Hopkins University School of Medicine, and he completed his internship and residency at the John Hopkins Hospital. Dr. Weiss came to UCSF in 1998 as a cardiology fellow, where he spent three years under the scientific mentorship of Dr. Shaun Coughlin in the Cardiovascular Research Institute studying the effects of thrombin signaling in platelets. He then completed his clinical fellowship and served as chief cardiology fellow in 2002. Dr. Weiss’ clinical focus includes acute-care cardiology, coronary artery disease, and general cardiology with special interests in preventive cardiology, the genetics of atherothrombosis, and coronary disease in the young. Dr. Weiss now spends most of his time in the basic science laboratory where his group uses forward genetic models to enhance the understanding of mechanisms of hemostasis and thrombosis. His group is also working to understand mechanisms of sex differences in blood clotting.

Natalia Beglova, PhD, a Basic Research Junior Faculty Scholar, graduated with an MSc from the Moscow Physical and Technical Institute, in Moscow, Russia, and a PhD from McGill University in Montreal, Canada. At McGill University, she was trained by Kalle Gehring, PhD, to use solution NMR spectroscopy for protein characterization. Her doctoral thesis research focused on the solution structure and dynamics of bioactive peptides mimicking NGF. Since 1999, she has been a research fellow in the Department of Pathology, Brigham & Women’s Hospital, Harvard Medical School and has conducted mentored research in the laboratory of Stephen Blacklow, MD, PhD, on the molecular mechanisms of protein function. In this lab, Dr. Beglova learned x-ray crystallography and obtained extensive experience with both solution NMR and x-ray crystallography. She combined these methods of structural biology with biochemical studies to investigate the structure and function of the integrin and lipoprotein receptor families of the cell-surface receptors. In 2005, Dr. Beglova was promoted to instructor. In 2006, she joined Beth Israel Deaconess Medical Center, Harvard Medical School, and is assistant professor at the Division of Hemostasis and Thrombosis led by Drs. Bruce and Barbara Furie. Dr. Beglova’s research, supported by ASH, is focused on the structure and function of B2GPI complexes in antiphospholipid syndrome.

Silvia Buonamici, PhD, a Basic Research Fellow Scholar, works at New York University as research assistant professor in the Aifantis laboratory. She graduated from the University of Bologna in Italy where she decided to continue her PhD studies in the biology of acute myeloid leukemia at the L&A Seragnoli Institute. During this period, she had the opportunity to move to the University of Illinois at Chicago to study the role of Evi1 in myelodysplastic syndrome (MDS). After generating the first mouse model of MDS, she was certain that the study of a different leukemia, such as T-cell acute lymphoblastic leukemia (T-ALL), could help her to have a broader understanding of leukemia. She became interested in the pathogenesis of Notch1-induced T-ALL and its infiltration into the central nervous system (CNS), a process with devastating consequences to patients. She has found that activated Notch1 (a regulator of T-cell development) induces chemokines, which may be important in the migration of lymphoblasts into the CNS. She is working to define the role of these chemokines for future therapeutic use. She is planning on continuing her career in the study of leukemia with a particular interest in clinically relevant questions that could be used to develop new therapies.

Xuefang Cao, PhD, a Basic Research Fellow Scholar, received his medical degree in China and initially worked as a resident in internal medicine for two years. To pursue a research career in cancer-related research, he came to the United States for PhD training. As a PhD candidate, he was trained in W. Stratford May’s laboratory at the University of Florida Shands Cancer Center and studied the biochemical mechanisms and signal transduction pathways regulating apoptosis in the setting of hematologic malignancies. To gain experience in animal models of cancer, Dr. Cao moved to Washington University for postdoctoral work because of the strength of basic science in the Immunology and Oncology programs. In Timothy Ley’s laboratory, he was trained in molecular biology, genetics, genomics, and transgenesis technologies, as well as molecular imaging and preclinical animal models of tumor development and clearance. Based on Dr. Cao’s experience and interest, he is currently studying the mechanisms of regulatory T-cell (Treg) activation and function in the setting of primary tumor formation and progression. Dr. Cao is fully committed to pursuing a career as an independent investigator in academic medicine. His long-term goal is to develop immune-based therapies that are safe and effective for patients with various cancers, including solid tumors and hematologic malignancies.

L.R. Devireddy, DVM, PhD, a Basic Research Junior Faculty Scholar, obtained his DVM degree from A.P. Agricultural University in Hyderabad, India. He later attended Indian Institute of Science (IISC) in Bangalore to pursue a Master’s degree in Virology. He then enrolled in an interdisciplinary graduate program at University of Nebraska Medical Center studying the latency of herpes viruses under the guidance of Dr. Clinton Jones. After graduation, he joined Prof. Michael Green’s laboratory at the University of Massachusetts to study the transcriptional regulation of programmed cell death. His postdoctoral studies were funded by fellowships from the Leukemia and Lymphoma Society and the Howard Temin Award from NCI. In the fall of 2006, he accepted a faculty position in the Department of Pathology and Case Comprehensive Cancer Center at Case Western Reserve University. At Case, he studies regulation of apoptosis by newly discovered lipocalin. He is also interested in analyzing the role of lipocalin in normal physiology and myeloproliferative disease.

Kira Gritsman, MD, PhD, a Basic Research Fellow Scholar, completed the MD/PhD program at the New York University School of Medicine in New York in 2001. Her PhD thesis in the laboratory of Dr. Alexander Schier focused on the roles of One-eyed Pinhead (Oep), an essential cofactor for the TGF- family member Nodal, during mesoderm and endoderm development and left-right patterning in the zebrafish embryo. Dr. Gritsman received her training in Internal Medicine at Columbia University Medical Center in New York. She then moved to Boston to begin the Dana-Farber Cancer Institute/Partners Health Care fellowship program in hematology/oncology, which she completed in July 2008. For her postdoctoral research, she joined the laboratory of Dr. D. Gary Gilliland at Brigham and Women’s Hospital, where she has focused on PI3 kinase/AKT signaling, which is a pathway commonly dysregulated in leukemia. Dr. Gritsman has generated a murine bone marrow transplant model of disease using a constitutively activated myristoylated form of AKT to better understand the role of AKT pathway activation in the development and progression of acute myeloid leukemia. She is also studying mouse models with reduced PI3K/AKT signaling in hematopoietic stem cells to determine the roles of PI3K signaling during hematopoiesis, hematopoietic stem cell function, and leukemogenesis.

Jeanne Hendrickson, MD, a Basic Research Fellow Scholar, is a recipient of the 2008 ASH Scholar Award for her work on “Regulation of Red Blood Cell Alloimmunization by Different Subtypes of Recipient Inflammation.” Difficulty locating compatible units of RBCs for patients with sickle cell anemia and RBC allo-antibodies led Dr. Hendrickson into the laboratory. Her research, under the mentorship of Drs. James Zimring and Christopher Hillyer at Emory University, began during her Pediatric Hematology/Oncology and Transfusion Medicine fellowships. Utilizing the mHEL (membrane-bound hen egg lysozyme) system, Dr. Hendrickson has shown that inflammation with a viral-like stimulus (poly [I:C]) enhances alloimmunization to transfused mHEL RBCs, while inflammation with a bacteria-like stimulus (LPS) inhibits alloimmunization. Her research focuses on identifying the mechanistic differences seen following poly (I:C) and LPS treatment, from antigen presentation through antibody production. Ultimately, this knowledge may lead to the rational development of targeted immunomodulatory therapies to decrease rates of RBC allo-immunization. Dr. Hendrickson is an assistant professor in the Division of Pediatric Hematology/Oncology, AFLAC Cancer Center and Blood Disorders Service, with a secondary appointment in the Department of Pathology and Laboratory Medicine. She is a member of the Center for Transfusion and Cellular Therapies at Emory University and the assistant director of the Blood and Tissue Banks at Children’s Healthcare of Atlanta.

Elizabeth Hexner, MD, a Clinical/Translational Research Fellow Scholar, has a clinical and research interest in myeloproliferative disorders (MPDs) and experimental approaches to stem cell transplantation. She received her medical degree from the Columbia University College of Physicians and Surgeons, where she also completed her training in internal medicine. She completed her clinical fellowship training at the University of Pennsylvania and performed postdoctoral research in the laboratory of Stephen Emerson, where she focused on two preclinical projects: the role of T cells in umbilical cord blood transplantation (also an ASH Clinical Research Training Institute project) and the activity of JAK2 inhibitors in primary cells from patients with MPD. Both preclinical projects have moved into the clinical arena and are currently in phase I studies. Through the MPD research consortium, she is the study chair for a multicenter phase I/II study of CEP-701 in myelofibrosis; she has a particular interest in establishing reproducible bioassays from patient samples to evaluate for JAK2 activity and level of inhibition. She is currently assistant professor of medicine at the University of Pennsylvania and intends to continue her career such that it encompasses the areas of both late preclinical and early clinical testing of novel therapies in hematologic malignancies.

Heidi D. Klepin, MD, an Association of Specialty Professors (ASP)-ASH Clinical/Translational Research Junior Faculty Scholar, is working to become an independent clinician researcher integrating the fields of hematology/oncology and geriatrics, focusing on three themes: 1) the predictive value of baseline physical and cognitive function on treatment response and toxicity; 2) the impact of cancer therapy on physical and cognitive function; and 3) interventions to promote functional independence during treatment. She has completed specialty training in hematology, oncology, and geriatrics, as well as a master’s degree in health sciences research. Dr. Klepin’s current research focuses on acute myelogenous leukemia (AML) as the model of a disease for which optimal therapy for older adults remains unclear, partly due to increased toxicity with standard treatments. Supported by this Scholar Award, she aims to prospectively explore the predictive value of pretreatment self-report physical function and objective physical performance assessment on treatment-related mortality and overall survival, as well as the relationship between cytogenetic risk group and measures of physical function. Dr. Klepin is also collaborating on a pilot study which investigates the feasibility of an inpatient exercise intervention for older adults hospitalized for AML induction therapy. 

Han Liu, PhD, a Basic Research Fellow Scholar, is a postdoctoral research scholar in the Division of Molecular Oncology, at Washington University in St. Louis, MO. He received his BS degree in biotechnology and MS degree in biochemistry and molecular biology from the Peking University, China. Then, he joined Dr. Zhu Chen’s laboratory in Shanghai Institute of Hematology, Rui-Jin Hospital, affiliated with Shanghai Jiao Tong University, China. During that time, he began his research career in hematology. His graduate studies focused on the physiological function of proteins related to hematopoiesis and leukemia, with special emphasis on myeloid/lymphoid or mixed lineage leukemia (MLL) fusion proteins. He earned his PhD in genetics and trained as a postdoctoral researcher until 2005, when he joined Dr. James Hsieh’s laboratory at Washington University. Dr. Liu studies the molecular basis for MLL. His work focuses on the role of MLL in the cell cycle regulation. He discovered a biphasic expression of MLL through cell cycle, which is lost in MLLs. With the ASH Scholar Award, he is currently investigating the function of MLL in DNA damage checkpoint and how the MLL fusion proteins will cause checkpoint defects and contribute to the development of MLLs.

Takahiro Maeda, MD, PhD, a Basic Research Junior Faculty Scholar, received his medical degree from Nagoya University in 1994. After completing his internship, residency, and clinical training in the field of hematology/oncology at Konan Showa Hospital and Toyohashi Municipal Hospital, he returned to Nagoya University in 1999 to obtain a PhD degree with a keen interest in translational therapeutics. Dr. Maeda received a doctorate in hematology/oncology in 2002 and engaged in postdoctoral studies at Memorial Sloan-Kettering Cancer Center from 2001 to 2006. In 2007, Dr. Maeda accepted an assistant  professor position in the Department of Hematopoietic Stem Cell and Leukemia Research at City of Hope. Dr. Maeda wants to investigate the various mechanisms by which hematologic malignancies develop. His ultimate goal is to discover new therapeutic approaches for these diseases. During his postdoctoral fellowship, Dr. Maeda found that the transcription factor LRF is a proto-oncogene and a master regulator of hematopoietic cell development. Using state-of-the-art techniques in mouse genetics and molecular biology, Dr. Maeda will examine the role of LRF in normal B-cell development and elucidate how LRF exerts its oncogenic activity in lymphoma cells while maintaining a translational focus.

Shannon McKinney-Freeman, PhD, a Basic Research Fellow Scholar, developed her passion for hematologic research at the age of 16 when her father was treated for myelodysplasia with a bone marrow transplant. For the next 14 years, he struggled with and eventually succumbed to chronic graft-versus-host disease and immune suppression. Because of her personal experience, she has chosen to focus her research on hematopoietic stem cell (HSC) biology and the derivation of alternative sources of HSCs that might be exploited for bone marrow transplantation. Dr. McKinney-Freeman received her PhD from Baylor College of Medicine where she worked under Dr. Margaret Goodell studying adult stem cell trans-differentiation. Her doctoral work characterized the source of skeletal muscle-derived hematopoiesis and revealed that this phenomenon was due to circulating bone marrow HSCs taking up residence in skeletal muscle, rather than trans-differentiating skeletal muscle stem cells. Dr. McKinney-Freeman joined George Daley’s group at Children’s Hospital Boston as a postdoctoral fellow in 2003, where she pursues research aimed at achieving the derivation of definitive HSCs from embryonic stem cells. She is studying the role of the Cdx gene family in the specification of hematopoietic progenitors from differentiating embryonic stem cells and characterizing the cell surface phenotype and global gene expression patterns of hematopoietic repopulating cells from throughout development and engineered from murine embryonic stem cells by ectopic expression of the homeobox genes Cdx4 and HoxB4. She hopes that this work will allow for the refinement of current strategies to engineer hematopoietic repopulating cells from embryonic stem cells.

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