Faculty

Bio

Dr. Boucher graduated from the University of Tennessee College of Medicine. He then completed his internal medicine/pediatrics residency at the University of Minnesota, followed by his pediatric hematology/oncology fellowship at the Cincinnati Children's Hospital Medical Center. He is a member of Alpha Omega Alpha, is board-certified in Internal Medicine, Pediatrics, and Pediatric Hematology/Oncology.

He joined the University of Minnesota faculty as Assistant Professor of pediatric hematology in the Department of Pediatrics in 2019. He holds a joint appointment in the Department of Medicine. His specific interests include inherited hemoglobinopathies, especially sickle cell disease (SCD) and thalassemia, and addressing diversity, equity, and inclusion (DEI) issues in clinical care. He sees pediatric patients with a wide range of hematologic disorders including red cell disorders, cytopenias, and marrow failure disorders.

In the Department of Medicine, he directs the SCD program with a focus on addressing care gaps for adolescents and young adults with SCD and other red cell disorders. In doing so, his goal is to build a lifespan approach to red cell disorders, particularly SCD, and strengthen our clinical care approach and research expansion.

Dr. Boucher's research includes improving patient-centered outcomes and community awareness for individuals with hemoglobinopathies like SCD and thalassemias. He also conducts research focused on addressing health inequities in clinical care, hematologic and otherwise. He is engaged in medical education for non-malignant hematology and in curriculum development around social determinants of health.

Research Summary

Bleed and Clotting Disorders Anemia Platelet disorders Sickle Cell Disorder Thalassemia

Clinical Summary

Bleed and Clotting Disorders; Anemia; Platelet disorders; Sickle Cell Disorder; Thalassemia

Bio

Throughout Dr. Galvin’s career pathway towards pediatric neuro-oncology, he developed a passion for the holistic care of patients and families affected by a brain tumor diagnosis. This encompasses compassionate and thorough high quality clinical care, engagement in research, and community advocacy. His research encompasses identifying new therapeutic opportunities to treat complications of Neurofibromatosis Type 1 and investigation of immunologic vulnerabilities of a subtype of glioblastoma, a malignant brain cancer, that affects children and young adults called diffuse hemispheric glioma, H3 G34-mutant. As a member of the Brain Tumor Program at the University of Minnesota, he strives to ensure availability of treatment options and clinical trial opportunities for those in need while working with the brain tumor community to continue making discoveries and advancements that will improve the lives of individuals affected by a brain tumor diagnosis.

Bio

Dr. Peter Gordon is an Associate Professor of Pediatrics in the Division of Hematology/Oncology at the University of Minnesota. Dr. Gordon received his MD/PhD from the University of Chicago in 2004. He completed his residency in Pediatrics in 2006 at Boston Children's Hospital and his fellowship in Pediatric Hematology, Oncology, and Bone Marrow Transplant in 2010 at Boston Children's Hospital/Dana Farber Cancer Institute. After completing his fellowship, Dr. Gordon served as an Instructor in Pediatric Hematology/Oncology until 2014. During his fellowship and time as an instructor, he completed post-doctoral research fellowships in the laboratories of Dr. David Fisher (Massachusetts General Hospital) and Dr. David Williams (Children's Hospital Boston) where his work focused on the role of the proto-oncogene c-KIT in cancer development.

Research Summary

Dr. Gordon's laboratory interests focus on how an improved understanding of leukemia development and maintenance at the molecular and cellular level can be leveraged into better therapies. A particular area of interest includes investigating how soluble factors that are secreted by different cell types within the bone marrow and extra-medullary environments impact leukemia development and response to therapy. An additional interest is in using pediatric bone marrow failure syndromes, which often have a significantly increased risk for leukemia development, as model systems for investigating how cooperativity amongst oncogenes leads to leukemia development.

Bio

Dr. Greengard is an Associate Professor of Pediatrics in the Division of Hematology/Oncology at the University of Minnesota. She is currently the Fellowship Director for Pediatric Hematology/Oncology.

Dr. Greengard received her medical degree in 2004 from Saint Louis University School of Medicine. She completed her residency in Pediatrics in 2007 at the Children's Memorial Hospital in Chicago, IL, and completed her fellowship in Pediatric Hematology-Oncology in 2010 at the Children's Hospital of Philadelphia. From 2007-2010, Dr. Greengard acted as an Instructor in Pediatrics at the University of Pennsylvania School of Medicine.

Dr. Greengard's research has focused on utilizing novel agents for the treatment of cancer in children. In 2010, she completed a project to develop a novel agent to treat pediatric malignancies. Within the arena of childhood cancers, she has specific interest in neuroblastoma and sarcomas. She also has a longstanding interest in pediatric palliative care.

Clinical Summary

Phase I clinical trials in pediatric cancer; Neuroblastoma; Sarcomas

Bio

David Largaespada, PhD, is a full professor in the Departments of Pediatrics and Genetics, Cell Biology, and Development and the Associate Director for Basic Research in the Masonic Cancer Center at University of Minnesota. He is an authority on mouse genetics, gene modification, and cancer genes. He received his BS in Genetics and Cell Biology from the University of Minnesota, Twin Cities in 1987 and his PhD in Molecular Biology with Dr. Rex Risser at the University of Wisconsin-Madison in 1992. He did a post-doctoral fellowship at the National Cancer Institute working with world-renowned geneticists Dr. Nancy Jenkins and Dr. Neal Copeland, where the Leukemia and Lymphoma Society of America awarded him a post-doctoral fellowship. He joined the faculty of the University of Minnesota in late 1996. Dr. Largaespada currently holds the Hedberg Family/Children's Cancer Research Fund Chair in Brain Tumor Research. He was awarded the American Cancer Society Research Professor Award in 2013, the highest award given by the ACS.

Research Summary

Cancer genetics, Neurofibromatosis type 1 (Nf1), RAS signaling, insertional mutagenesis, pediatric cancer, brain tumors, osteosarcoma, transposons, Sleeping Beauty

Dr. Largaespada's laboratory is working to exploit insertional mutagenesis, and other functional genomics methods (e.g. CRISPR/Cas9) to identify and understand genes and pathways that govern cancer cell behavior. The Largaespada lab pioneered the use of a vertebrate-active transposon system, called Sleeping Beauty (SB), for insertional mutagenesis in mouse somatic cells. SB is being used as a tool for forward genetic screens for cancer genes involved in sarcoma, hepatocellular carcinoma, and mammary, gastro-intestinal tract and NF1 syndrome-associated nervous system cancers. A special emphasis of this work is on genes that promote metastasis or govern treatment sensitivity. Also, novel mouse models are being used for preclinical evaluation of new drugs and drug combinations for cancer treatment.

The identity of the mutations and other changes that drive the development of cancer must be determined for developing molecularly targeted therapeutics. Studies on human cancer exon re-sequencing suggest that a large number of mutations are present in breast and colorectal tumors (Sjoblom et al., Science, 2006). But, the identification of those changes that are selected for is going to be difficult because the number of "passenger" alterations not selected for during tumorigenesis is very large. The human cancer genome project promises to help reveal the typical landscape of genomic changes in human cancer, but must be supplemented with complementary large-scale approaches for functional validation of targets and genetic screens that can identify cancer gene candidates. The Largaespada lab has developed approaches, using the SB transposon system, which can meet these needs. They have shown that SB transposon vectors can be mobilized in the soma of transgenic mice allowing forward genetic screens for cancer genes involved in sarcoma and lymphoma/leukemia to be performed in living mice (Collier et al., Nature, 2005; Dupuy et al., Nature, 2005). The system requires creating mice that harbor both a transposon array of the insertionally mutagenic SB vector, T2/Onc, and express the transposase enzyme in the target somatic tissue. If transposition can induce cancer, then tumor DNA is studied by cloning insertion sites. These insertion sites are analyzed and one looks for T2/Onc insertions at reproducibly mutated genes, called common insertion sites (CIS). The system has now been altered so that tissue-specific transposon mutagenesis for cancer gene discovery in various organs can be accomplished. In one illustrative project mice harboring mutagenic (SB) transposons were crossed to mice expressing SB transposase in gastrointestinal tract epithelium (Starr et al., Science, 2009). All mice developed intestinal lesions including intraepithelial neoplasia, adenomas, and adenocarcinomas. Analysis of over 95,000 transposon insertions from these tumors identified 77 candidate gastrointestinal tract cancer genes. These genes were then compared to those mutated in human cancer, including colorectal cancer (CRC), or amplified, deleted or misexpressed in CRC, which allowed us to generate an 18 gene list that is highly likely to contain driver mutations for CRC. These genes include many of the most commonly known genes mutated in human CRC, such as APC, BMPR1A, SMAD4 PTEN, FBXW7, DCC, MCC, in addition to several novel CRC candidate genes that function in pathways widely expected to participate in CRC such as the proliferation, adhesiveness and motility of epithelial cells. Similar work has revealed drivers for hepatocellular carcinoma development (Keng et al, Nature Biotech, 2009). These studies demonstrate the power of transposon-based mutagenesis when combined with human studies for identifying the driver mutations that cause cancer. Similar results are accumulating for hepatocellular carcinoma, brain tumors, sarcomas and several other types of cancer.

Dr. Largaespada is also using mouse models of murine leukemia virus induced acute myeloid leukemia (AML) to identify and characterize genes that have a role in leukemia progression after disease is initiated by mutations relevant to human AML. This work also includes genetic studies of myeloid leukemia chemotherapy resistance and relapse. AML is the most common adult leukemia. It is clear that genetically defined subsets of AML have varying prognoses. AML frequently harbor chromosomal translocations that create fusion oncoproteins that act as transcription factors or constitutively active kinases. These fusion genes are thought to be insufficient, by themselves, for AML induction. Instead, secondary mutations cooperate with them to produce AML. The full set of cooperating mutations and their usefulness as therapeutic targets are important unknown quantities. The lab is exploring these questions by using MuLV mutagenesis in mice carrying specific human translocation fusion oncogenes known to play a role in human AML. The lab has developed MuLV-accelerated models of AML initiated by expression of the MLL-AF9 and AML1-ETO fusion oncoproteins (Bergerson et al., In Preparation; Yin et al., In Preparation). We have cloned 4,731 unique proviral insertions from 89 MuLV accelerated Mll-AF9/+ leukemia and 79 control MuLV-induced leukemia. Preliminary analysis reveals ~90 common insertion sites with many showing strong bias for Mll-AF9+ leukemias. Comparisons to expression microarray data on human AML with MLL gene translocations are in progress. These data may help to distinguish between genes that are direct targets of MLL-AF9, those that are a cause of AML development and those that cooperate with MLL-AF9 to induce AML.

In another area of AML research, we have sought to address the role of the activated NRAS oncogene in AML maintenance. We therefore developed Vav-tTA (expressed in hematopoietic cells) and TRE-NRASG12V transgenic lines in FVB/n mice. Interestingly, the doubly transgenic Vav-tTA plus TRE-NRASG12V mice developed a myeloproliferative disease very similar to human aggressive systemic mastocytosis (ASM) without other detectable hematopoietic tumors (Wiesner et al., Blood, 2005). To determine the ability of NRASG12D to cooperate with a fusion oncogene encoding an altered transcription factor we created triple transgenic Vav-tTA; TRE-NRASG12V; Mll-AF9 lines in C57BL/6J X FVB/n F1 mice. AML were obtained in triple transgenic mice. When we transplanted triple transgenic Vav-tTA; TRE-NRASG12V; Mll-AF9 AML into SCID mice we found that doxycycline (DOX) treatment via the drinking water could prevent AML engraftment or eliminate AML cells after letting them grow to full-blown leukemia in recipients. However, at least some of these mice develop DOX-resistant AML, which do not re-express the NRASG12V (Kim et al., Blood, 2009). This suggests that RAS oncoproteins may be good therapeutic targets, even in complex tumors induced in cooperation with another strong oncogene. The mechanisms for oncogene addiction are not clearly understood. We are currently exploring the mechanism of AML cell death after NRAS oncogene suppression, the mechanism by which rare AML cells escape death in this context, and interactions between RAS targeted therapies and conventional chemotherapy.

Bio

Christopher Moertel is the Kenneth and Betty Jayne Dahlberg Professor of Pediatrics in the University of Minnesota School of Medicine. He is the Medical Director of the  Katie Hageboeck Children's Cancer Research Fund Clinic and leads the Pediatric Brain Tumor Program and the Comprehensive Neurofibromatosis Clinic. Dr. Moertel joined the University of Minnesota in 2007. Prior to that time, he was the lead physician of the Theodora Lang Pediatric Hematology/Oncology Clinic at Children's Hospital, St. Paul. He served in multiple leadership roles at Children's Hospitals of Minnesota, including Chief of Staff. Dr. Moertel's research interests include treatment of Neurofibromatosis-associated neoplasia, targeted therapy of pediatric brain tumors and immunotherapy of high grade glioma. He has sponsored at least 5 INDs and has conducted multiple investigator-initiated clinical trials. He has research collaborations in cancer genomics, cancer immunotherapy and cancer epidemiology, with a goal of bringing cutting edge discovery from the bench to the bedside. He has spoken at national and international medical conferences and participates in multiple national and international cooperative groups. Dr. Moertel also leads the pediatric neuro-oncology fellowship with the goal of educating future translational experts in neurofibromatosis and/or pediatric brain tumors.

Clinical Summary

Pediatric neuro-oncology; Rare pediatric tumors; Neurofibromatosis-associated neoplasia; Therapy of children with brain and spinal cord tumors

Bio

Dr. Branden Moriarity is currently an Associate Professor in the Department of Pediatrics, Division of Hematology/Oncology. He graduated from Saint Olaf College in 2007 with a BA in Biology, Chemistry, and Biomolecular sciences. He received his PhD in Molecular, Cellular, Developmental Biology & Genetics at the University of Minnesota in 2012. From 2012-2014 he was a post doctoral fellow in David Largaespda's lab, where he worked on identifying the genetics of pediatric sarcomas. He joined the Department of Pediatrics Faculty in 2014.

Dr. Moriarity runs a basic/translational research laboratory working to develop novel cellular therapeutics for gene therapy and cancer immunotherapy with the goal of translating new therapeutics to the clinic. To accomplish these goals, the Moriarity lab uses cutting edge genome engineering technologies, including CRISPR/Cas9, base editor technology, transposons, and rAAV. These tools allow for high frequency gene knockout, gene knock-in, induction of targeted sequence changes, and activation and/or repression of endogenous gene expression. Target cells for engineering include T cells, B cells, NK cells, Monocytes, and hematopoietic stem cells. In addition to developing cellular based therapeutics, the Moriarity lab also performs preclinical drug testing for pediatric cancers, such as osteosarcoma, in order to launch new clinical trials using antibody therapies rather than toxic chemotherapy.

Research Summary

Preclinical Drug Testing, Genome Engineering, Gene Therapy, and Cancer Immunotherapy.
Dr. Moriarity runs a basic/translational research laboratory working to develop novel cellular therapeutics for gene therapy and cancer immunotherapy with the goal of translating new therapeutics to the clinic. To accomplish these goals the Moriarity lab uses cutting edge genome engineering technologies including CRISPR/Cas9, base editor technology, transposons, and rAAV. These tools allow for high frequency gene knockout, gene knock-in, induction of targeted sequence changes, and activiation and/or repression of endogenous gene expression. Target cells for engineering include T cells, B cells, NK cells, Monocytes, and hematopoietic stem cells. In addition to developing cellular based therapeutics, the Moriarity lab also performs preclinical drug testing for pediatric cancers, such as osteosarcoma, in order to launch new clinical trials using antibody therapies rather than toxic chemotherapy. 

Bio

Dr. Joseph Neglia is the Head of the Department of Pediatrics at the University of Minnesota Medical School and the Physician-in-Chief of the M Health Fairview Masonic Children's Hospital. He holds the Ruben-Bentson Chair and a joint appointment as Professor in the Department of Pediatrics and in the Division of Epidemiology and Community Health in the School of Public Health.

Dr. Neglia's area of research involves the long-term effects of cancer therapy in cancer survivors and the occurrence of second malignancies following childhood cancer. He is nationally and internationally recognized for his contributions to the field of childhood cancer long-term effects. He currently is Principal Investigator at the Masonic Cancer Center, University of Minnesota for the Children's Oncology Group (COG), and the vice-chair of the Voting Body of the COG. Dr. Neglia is also Principal Investigator of an American Cancer Society Grant investigating neuro-behavioral outcomes of children recently treated for leukemia.

Dr. Neglia has been involved in numerous service activities both within and outside of the University of Minnesota. He is an active member of Children's Oncology Group, American Society of Pediatric Hematology/Oncology, and Masonic Cancer Center at the University of Minnesota. He regularly reviews manuscripts for numerous journals including the New England Journal of Medicine, the Journal of the National Cancer Institute, and Cancer among others. At the University level, he has been elected as an alternate member of the University Senate and developed and directed the original Cancer Center Database.

Bio

Dr. Lahn Nguyen is a Complex and Palliative care pediatrician. She received her DO from Des Moines University College of Medicine. After medical school she took a transitional year at Peconic Bay Medical Center in Riverhead. Dr. Nguyen completed her residency in Pediatrics in Brooklyn, NY at the Coney Island Hospital, SUNY Downstate Medical Center and Kings County Hospital in 2019. Dr. Nguyen graduated from one of the largest Pediatric Hospice and Palliative Care Fellowship programs in the USA at UTHSCSA in San Antonio, TX in the Summer of 2020.

Dr. Nguyen spent her formative years growing up in the Twin Cities of Minnesota before moving to Des Moines, IA where she received her BA in Biology and History from Drake University. Her professional interests are rooted in the cultural aspects of medical care, the exploration of successful medical education practices and a passion for ethics. In her downtime Dr. Nguyen enjoys reading, quilting projects, hiking, and time with family and friends. She added a new dog, Brady to her family in 2020.

Research Summary

Dr. Nguyen is interested in medical education and cultural aspects of care as it relates to complex care and chronic illness. 

Bio

Dr. Olin is Associate Professor in the Department of Pediatrics, Division of Hematology/Oncology.

Dr. Olin graduated from the University of Minnesota, Duluth, in 1995 with a BS in biochemistry and a BA in chemistry. After graduating, he worked in industry for 5 years before returning to the U of M to complete his PhD in Veterinary Medicine (Infectious Disease) in 2005. From 2006-2008 Dr. Olin did a postdoctoral fellowship with Dr. Philip Peterson studying the effects of opioids on tuberculosis meningitis, and from 2008-2011 he did a second post doctoral fellowship with Dr. John Ohlfest in brain tumor immunotherapy. Dr. Olin joined the Department of Pediatrics Faculty as an Assistant Professor in 2011.

Research Summary

Dr. Olin's scientific interest is defining the mechanism(s) of suppression inhibiting the ability to mount a tumoricidal response evident in the tumor draining lymph nodes and tumor environment and developed potential ways to modulate the immunosuppressive activity. Immunosuppressive tumor environment is a major hurdle for the immune system to overcome. Dr. Olin is focused on the development of inhibitors derived to overcome the suppressive tumor microenvironment.

Bio

Dr. Sadak received his medical degree from the George Washington University School of Medicine and Health Sciences in Washington, DC. He previously had received a Master's of Science in Engineering from the University of Pennsylvania in Biomedical Engineering. He completed his residency in Pediatrics at Inova Fairfax Hospital for Children in Falls Church, Virginia and his fellowship in Pediatric Hematology/Oncology at Children's National Medical Center in Washington, DC. During his fellowship, Dr. Sadak performed health services research in childhood cancer survivorship transition care and concurrently earned a Master's in Public Health in Epidemiology from the George Washington School of Public Health and Health Policy.

Dr. Sadak is currently the Director of the Childhood Cancer/BMT Survivor Program for the Division of Pediatric Hematology/Oncology in the Department of Pediatrics. His clinical and research expertise focuses on survivors of childhood cancer. He has particular interest in adolescent and young adult survivors and has performed research through mixed methodologies to identify facilitators of transition for childhood cancer survivors from pediatric- to adult-centered care.  Under his leadership, the Childhood Cancer/BMT Survivor Program has several clinical studies open to enrollment for childhood cancer survivors and has leveraged multi-disciplinary collaborations across the Cancer Center, the Academic Health Center, the University and beyond to obtain federal, institutional and foundation grants related to childhood cancer survivorship.

As Senior Medical Director of Pediatrics at the University of Minnesota Medical Center, Dr. Sadak provides operational leadership at M Health Fairview Masonic Children's Hospital related to its work in quality of care, patient/staff safety and patient experience.  His patient care quality improvement efforts have included reductions in hospital acquired conditions (e.g. central-line associated bloodstream infections) and serious safety events as well as improvements in patient flow, engagement in organizational safety culture and multi-disciplinary change management.

Research Summary

As Director of the Childhood Cancer/BMT Survivor Program, Dr. Sadak conducts health services research related to childhood cancer survivors of all ages.  His research focuses on survivors of childhood cancer/BMT and how to ensure that they have life-long survivor-focused care.  His research has helped inform program development specific to successfully transitioning the care of childhood cancer survivors from pediatric-centered care to adult-centered care ensuring that this vulnerable population does not slip through the cracks of our complex health systems. Through a mixed methods approach, including both quantitative and qualitative data, his research within a learning health system has resulted in rapid cycles of improvement in the care delivered to childhood cancer/BMT survivors and collaborative grant-funded research through institutional, federal and foundation awards.

Clinical Summary

Dr. Sadak delivers comprehensive and compassionate family-centered hematology/oncology care at the M Health Fairview Katie Hageboeck Children's Cancer Research Fund Clinic (formerly known as the Journey Pediatric Specialty Clinic), M Health Fairview Masonic Cancer Clinic, M Health Fairview Cancer Center Maple Grove Clinic and the M Health Fairview Masonic Children's Hospital.  

His focus is children, adolescents, and young adults that have been cured of childhood cancer or treated with a BMT to ensure they live the rest of their long lives with the highest quality of life possible.  He leads a team that delivers care to survivors of all ages and their families, performs research related to childhood cancer survivors and helps educate others on the care and needs of childhood cancer/BMT survivors.  This team includes nurse practitioners, nurses, social workers, neuropsychologists, several pediatric- and adult-subspecialists, complex schedulers, research personnel, medical providers and researchers.  

He believes each patient and family has a unique medical journey and therefore has unique medical needs that can be identified and then addressed together through patient-centered listening and teamwork that results in a patient-specific and personalized plan.

Specialties:

• Pediatric Hematology/Oncology
• Childhood Cancer/BMT Survivorship