School of Medicine
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Bryson Nakamura
Director & Head Sport Scientist - Stanford Baseball Science Core, Orthopaedic Surgery
BioBryson Nakamura, PhD. is the Director & Head Sport Scientist for the Stanford Baseball Science Core. Nakamura will lead baseball sport science research efforts while also supporting the Stanford Baseball team.
Nakamura previously spent six seasons with the Milwaukee Brewers Baseball Club in various sport science and performance roles. In his years with the Brewers, Nakamura established the Integrative Sports Performance department, which aimed to leverage sport science processes and principles to help put the Brewers at the forefront of data-driven player development methods and to enhance and support all functions of baseball operations. In his final year with the club, he was also responsible for overseeing minor league strength and conditioning in his role as the Director of Player Performance.
Prior to joining the Brewers, Nakamura was a sport science intern with the Tampa Bay Rays while completing his doctorate at the University of Oregon in the Bowerman Sports Science Clinic. At Oregon, his primary research focused on gait characteristics of lower-extremity amputees, while his clinical work focused on the assessment of biomechanical and physiological performance factors for high-level distance runners. He graduated with a bachelor’s degree from the University of Puget Sound in Exercise Science where he played baseball and conducted research focused on balance and footwear product design.
Currently, Nakamura is a member of the American Society of Biomechanics, International Society of Biomechanics in Sport, American College of Sports Medicine, and is a founding member and Vice President of Conferences & Meetings for the American Baseball Biomechanics Society. -
Michitaka Nakano
Postdoctoral Scholar, Hematology
BioI am a MD/PhD postdoctoral fellow and medical oncologist with a long-standing interest in translational cancer research. My long-term goal is to be a lab-based physician-scientist and independent academic researcher, translating basic cancer research, and mentoring next-generation scientists. My thesis work in Japan focused on cancer stem cell equilibrium by uniquely applying organoid culture as a method to elucidate cancer stem cell dynamics, which was awarded in Japanese Cancer Association. Along with the development of the field represented by success in T cell checkpoint, my interest gradually shifted to immune oncology while I examined numerous numbers of cancer patients as a medical oncology fellow. My postdoctoral fellowship at Calvin Kuo Lab in Stanford (2019-present) focuses on tumor immune microenvironment. Kuo lab developed a unique 3D air-liquid interface (ALI) organoid system that cultures tumors while preserving their endogenous infiltrating immune cells (T,B ,NK, Myeloid cells). My postdoctoral work will prove the significance of organoids as a translational tool to discover tumor-immune interaction by novel checkpoint inhibitors for immune cells, which can be broadly applicable to basic cancer biology, precision medicine, therapeutics validation and biomarker discovery.
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Hiromitsu (Hiro) Nakauchi
Professor of Genetics (Stem Cell)
Current Research and Scholarly InterestsTranslation of discoveries in basic research into practical medical applications
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Yusuke Nakauchi
Instructor, Institute for Stem Cell Biology and Regenerative Medicine
Current Research and Scholarly InterestsFrom 2005 to 2010, my work as a clinical hematology fellow allowed me to experience first-hand how scientific advances that started in a laboratory can transform patients' lives. While many of my patients were cured of their disease with allogeneic hematopoietic stem cell transplantation, underscoring the importance of anti-tumor immunotherapy in eradicating leukemia, I witnessed face-to-face their suffering from the long-term consequence of graft-versus-host disease (GVHD). This experience was ultimately what drove me to engage in research to discover novel therapies. For this reason, I embarked on a Ph.D. program in 2010 to design antibody therapy to (i) target GVHD and (ii) target hematological malignancies. Under the mentorship of Professor Hiromitsu Nakauchi at the University of Tokyo, an international leader in hematopoiesis, I developed allele-specific anti-human leukocyte antigen (HLA) monoclonal antibodies for severe GVHD caused by HLA-mismatched hematopoietic stem cell transplantation (Nakauchi et al., Exp Hematol, 2015). This study was the first to find that anti-HLA antibodies can be used therapeutically against GVHD. That success gave me the motivation and confidence to further my research beyond targeting GVHD to targeting leukemic stem cells through my postdoctoral fellowship in the laboratory of Professor Ravindra Majeti here at Stanford University.
Many people suffer from leukemia each year, but we still don't know how to cure it completely. Recent advances in sequencing technologies have tremendously improved our understanding of the underlying mutations that drive hematologic malignancies. However, the reality is that most of the mutations are not easily "druggable," and the discovery of these mutations has not yet significantly impacted patient outcomes. This is perhaps the most crucial challenge facing a translational cancer researcher like myself. My current research is a major step toward my long-term goal of making personalized medicine a reality for patients with acute myeloid leukemia (AML) and other hematologic malignancies.
Since joining the Majeti lab, I have been targeting the ten-eleven translocation methylcytosine dioxygenase-2 (TET2) mutation, which is aberrant in leukemia at a high rate and has been studied using human-derived cells. TET2 is known to be involved in the clonal expansion of cells, and people with this mutation are more likely to suffer from hematologic malignancies. It is also known to be involved in the development of coronary artery disease, a gene that has attracted much attention in recent studies. In my field, it is an essential gene involved in the abnormal proliferation of hematopoietic stem cells. Focusing on this gene, I mapped TET2-dependent 5hmC, epigenetic and transcriptional programs matched to competitive advantage, myeloid skewing, and reduced erythroid output in TET2-deficient hematopoietic stem and progenitor cells (HSPC). Vitamin C and azacitidine restore the 5hmC landscape and phenotypes in TET2-mutant HSPCs. These findings offer a comprehensive resource for TET-dependent transcriptional regulation of human hematopoiesis and shed light on the potential mechanisms by which TET deficiency contributes to clonal hematopoiesis and malignancies. Of course, these findings would also be of value in understanding the biology of normal hematopoietic stem cells (HSCs) and various other TET2-related cancers.
And from now on, I would like to use the single-cell transplantation techniques mastered in the Majeti lab to study the behavior of normal and aberrant human HSCs using various new methods, ultimately preventing the progression of AML.
In my clinical experience, I have lost many AML patients. With the regret and sadness of losing these patients in my heart, I hope to one day contribute to developing treatments that will fundamentally change how the world treats leukemia.
