Michael Yi Bonner

Michael Yi Bonner

Besöksadress: Solnavägen 9, 3A, 17177 Stockholm
Postadress: C2 Medicinsk biokemi och biofysik, 171 77 Stockholm

Om mig

  • My long-term goal is to become an academic investigator and establish my own
    research group, which will focus on advancing our understanding of cancer
    biology. In the short term, I am focused on cultivating the necessary skills,
    knowledge, and networks that will help me succeed. The laboratory of Prof.
    Jack L. Arbiser, MD, PhD, a pupil of the late Judah Folkman, MD, has a long
    history developing small molecules as antiangiogenic and antitumor therapies.
    The lab has both discovered natural products and synthesized novel small
    molecules. I have spent the past ten years learning the scientific techniques
    used in his research. Prior to joining the Arbiser group, I obtained a BA
    degree in Chemistry at Emory University, and I have since assisted in the
    discovery of the antiangiogenic and/ in vivo/ antitumor properties of
    honokiol, a natural product from the Magnolia tree. I have also synthesized
    honokiol analogs. In addition, I have helped synthesize and test Imipramine
    Blue, a novel NADPH oxidase inhibitor with systemic availability and
    antitumor efficacy. I have helped pioneer a novel synthesis of Solenopsin A
    (ant venom) and Solenopsin A analogs, which has been demonstrated to act as
    ceramide analogs with tumor suppressive activity. Finally, I have helped
    reveal the antitumor properties of palladium complexes, including Tris DBA
    Palladium, for clinical development.
    My previous experience with the Arbiser group has given me broad knowledge in
    biochemistry, cancer biology, and organic chemical synthesis focused towards
    pre-clinical therapeutic research. Most importantly, it has given me the
    poise and skills to pursue a professional education and career as an
    independent academic scientist. Currently I have co-authored a number of
    peer-reviewed publications, a testament to my dedication to scientific
    scholarship.
    I have since joined Prof. Rikard Holmdahl’s group at the Karolinska
    Institute in Stockholm, Sweden as a PhD candidate. I have found a Thesis
    project entitled "*Redox Modulation- Impact on Tumor Growth & Therapeutic
    Anticancer Efficacy"* that expands on my experience in angiogenesis and
    cancer biology, as well as offer new opportunities to further develop in
    Redox biology, immunology, and proteomics.
    *2022 Robert Lundberg Memorial Foundation*
    The purpose of the foundation is to promote scientific research in the field
    of tumour diseases, especially cancer.
    *2018 SWIMM Travel Award*
    Swedish Society of Immunology SWIMM
    SWIMM is a part of the Scandinavian Society for Immunology (SSI), which also
    comprises of the Danish, Finnish, Norwegian and Icelandic National Societies.
    The main goal for the society is to assemble immunologists in Sweden and work
    for the progress of basic and applied immunology. SSI award travel grants to
    applicants who fulfill our eligibility criteria.
    https://swimm.se/ [1]
    *2017 Ruth L. Kirschstein Predoctoral Individual National Research Service
    Award (4 years + 1 year)*
    NIH: National Cancer Institute
    The purpose of the Kirschstein-NRSA program is to enable promising
    predoctoral students with potential to develop into a productive, independent
    research scientists, to obtain mentored research training while conducting
    dissertation research.
    https://www.cancer.gov/about-nci/budget/fact-book/extramural-programs/nrsa
    [1] https://swimm.se/

Forskningsbeskrivning

  • My current project focuses on changes in the REDOX environment of leukocytes
    that stem from the Nox2 complex in murine cancer models. Specifically, I am
    focused on understanding how murine cancer models develop slower in mice
    carrying mutations in the Ncf1 (p47-phox) gene, a key component of the Nox2
    complex controlling for production of superoxide /hydrogen peroxide in
    leukocytes which is also mutated in approximately 23% of patients diagnosed
    with chronic granulomatous disease (CGD).

Artiklar

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