School of Medicine


Showing 1-20 of 36 Results

  • Michitaka Nakano

    Michitaka Nakano

    Postdoctoral Research Fellow, Hematology

    Current Research and Scholarly Interests Understanding of tumor biology using cancer organoid from the clinical view point.

  • Yusuke Nakauchi

    Yusuke Nakauchi

    Postdoctoral Research Fellow, Stanford Cancer Center

    Current Research and Scholarly Interests From 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 the lives of patients. 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 PhD 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 current postdoctoral fellowship in the laboratory of Professor Ravindra Majeti, Department of Hematology at Stanford University.

    Many people suffer from leukemia each year, but we still don’t know how to completely cure it. Recent advances in sequencing technologies have tremendously improved our understanding of the underlying mutations that drive hematologic malignancies, although, the reality is that the majority of the mutations are not easily “druggable” and the discovery of these mutations has not yet made a significant impact in patient outcomes. I view this perhaps the most crucial challenges facing a translational cancer researcher like myself. My current research is a major step toward my long term goal to make personalized medicine a reality for patients with acute myeloid leukemia (AML) and other hematologic malignancies. Although my research is focused on targeting Ten-Eleven Translocation methylcytosine dioxygenase-2 (TET2) mutations, I anticipate it will lead to a better understanding of the cell context requirement for TET2 mutations in AML and help identify the critical cells to target to both prevent the development of de novo leukemia and halt relapse. It may also prove of value to understanding of the biology of a range of other cancers.

  • Manjari Narayan

    Manjari Narayan

    Postdoctoral Research Fellow, Psychiatry

    Bio Manjari Narayan is a postdoctoral research scholar at the Etkinlab. Her current research interests combine high dimensional statistics, graphical models, network science & statistical causal inference methods to analyze interventional neuroimaging experiments as well as precision psychiatry. She received a Ph.D in Electrical Engineering from Rice University in 2016 under the supervision of Dr. Genevera Allen and a B.S in Electrical Engineering from UIUC in 2007. Her dissertation work has been recognized by numerous student paper awards including the 2016 ENAR Distinguished Student Paper Award from the International Biometrics Society and the 2013 best paper travel award in Pattern Recognition in Neuroimaging.

  • Gernot Neumayer

    Gernot Neumayer

    Postdoctoral Research Fellow, Stem Cell Biology and Regenerative Medicine

    Current Research and Scholarly Interests My MSc project, carried out at the University of Salzburg in cooperation with the biotechnology company ProComCure, investigated the molecular interface between human cells and the bacterium Staphylococcus aureus. S. aureus exhibits a dramatic increase in resistance to antibiotics, thereby causing enormous challenges for health care. Using proteomics platforms, I identified numerous novel host-pathogen interactions. These findings are being developed further by ProComCure in order to design innovative therapies for S. aureus infections.

    My dissertation project, carried out at the University of Calgary, defined the functions of the human protein TPX2. TPX2 has been discovered over 17 years ago for its unique property to mediate cell division. However, when not involved in cell division TPX2 resides in the cell nucleus where its role had remained unknown. Building on my background in proteomics, I discovered a novel TPX2-containing protein complex that resides in the nucleus. Analysis of this complex unraveled a completely unexpected role for TPX2 in cellular reactions triggered by insults to DNA. To avoid cancers, cells respond to damaged DNA by either attempting its repair or, if this is not possible, by committing 'suicide'. My findings established that TPX2 impacts the molecular mechanisms that underlie these responses to DNA damage. More specifically, I found that TPX2 accumulates at DNA lesions and that the cellular levels of TPX2 negatively correlate with the ‘strength’ of the DNA damage response. Thus, TPX2 affects cellular proliferation, DNA repair, and survival upon genomic insult. This was the first function discovered for TPX2 in the cell nucleus. Since abnormally high levels of TPX2 are often found in human cancers, my discovery sheds light on the mechanistic implication of this protein in carcinogenesis. Furthermore, TPX2 is also a promising therapeutic target and my findings may advance novel cancer therapies. We propose that future treatments may attempt to reduce TPX2 levels in order to increase the strength of the DNA damage response. Subsequently, chemo- and radiotherapy doses may be lowered but still stay effective.

    In 2014, I joined the Wernig laboratory at Stanford University. Here, I capitalize on my expertise in mechanisms of DNA damage response to develop a pioneering technique capable of repairing pathogenic mutations in the genetic material of patients suffering from Epidermolysis Bullosa (a devastating and often lethal disease that causes chronic erosion of the skin). This novel technique, called CRISPR, introduces experimentally controlled and transient damage to the mutated DNA of patient cells and exploits naturally occurring DNA repair mechanisms to transform the disease-causing mutation to a normal state. I will combine development of CRISPR with Dr. Wernig’s expertise in regenerative medicine to generate patient derived stem cells with repaired (i.e. normal) genes. Subsequently, these stem cells will be employed to regenerate the skin of Epidermolysis Bullosa patients.