• Researcher Profile

    David Takeda, MD, PhD

     
    David Takeda, MD, PhD
     
    Physician

    Instructor in Medicine, Harvard Medical School

    Center/Program

    Genitourinary Oncology

    Office phone: 617-632-6328
    Fax: 617-632-2165

    Preferred contact method: office phone

    View Physician Profile
     
     

    Research Department

    Medical Oncology

    Interests

    Prostate cancer, Kidney cancer, Testicular cancer, Bladder cancer, Hormone and chemotherapy

    Area of Research

    Targeting the TMPRSS2-ERG Translocation in Prostate Cancer


    Dana-Farber Cancer Institute
    450 Brookline Avenue
    Dana 1230
    Boston, MA 02215

    Biography

    Harvard Medical School, MD PhD, 2007


    Internal Medicine Residency, Brigham and Women's Hospital, 2009


    Hematology/Oncology Fellowship, Dana Farber Cancer Institute, 2013


    Instructor in Medicine, Harvard Medical School, Dana Farber Cancer Institute

    Recent Awards

    • Prostate Cancer Foundation Young Investigator Award, 2012

    Research

    Targeting the TMPRSS2-ERG Translocation in Prostate Cancer

    Approximately half of all prostate cancers contain a translocation involving the transcription factor ERG with the androgen regulated gene TMPRSS2.  The TMPRSS2-ERG fusion results in androgen dependent overexpression of ERG which is not normally expressed in the prostate.  Several lines of evidence demonstrate that aberrant overexpression of ERG contributes to the development of prostate cancer making it an attractive therapeutic target.  However, transcription factors have historically been difficult to inhibit by conventional means.  Furthermore, identifying critical TMPRSS2-ERG dependent pathways to target is difficult as ERG regulates many cellular processes.  To address these challenges Dr. Takeda has developed a strategy to use gene expression signatures as a readout for TMPRSS2-ERG activity.  This novel gene expression signature assay was combined with recent advances in genetics, proteomics, and chemistry to identify genes and small molecules that modulate TMPRSS2-ERG activity in prostate cancer cells.  These findings will be important for understanding TMPRSS2-ERG function in prostate cancer and developing new therapeutics targeting its function.

    Select Publications

    • Kraemer FB, Takeda D, Natu V, and Sztalryd C. 1998. Insulin Regulates Lipoprotein Lipase Activity in Rat Adipose Cells via Wortmannin and Rapamycin Sensitive Pathways. Metabolism 47(5):555-559.
    • Nishiwaki H, Nakagawa Y, Takeda DY, Okazawa A, Akamatsu M, Miyagawa H, Ueno T, and Nishimura K. 2000. Binding activity of substituted benzyl derivatives of chloronicotinyl insecticides to housefly-head membranes, and its relationship to insecticidal activity against the housefly Musca domestica. Pest Management Science 56(10):875-881.
    • Takeda DY*, Wohlschlegel JA, and Dutta A. 2001. A Bipartite Recognition Motif for Cyclin Dependent Kinases. Journal of Biological Chemistry 276(3):1993-1997. (*co-first author)
    • Wohlschlegel JA, Dwyer BT, Takeda DY, and Dutta A. 2001. Mutational analysis of the Cy motif from p21 reveal sequence degeneracy and specificity for different cyclin dependent kinases. Molecular and Cellular Biology 21(15):4868-4874.
    • Saxena S, Yuan P, Dhar SK, Senga T, Takeda D, Robinson H, Kornbluth S, Swaminathan K, and Dutta A. 2004. A dimerized coiled-coil domain and an adjoining part of geminin interact with two sites on Cdt1 for replication inhibition. Molecular Cell 15(2):245-258.
    • Takeda DY*, Shibata Y, Parvin JP, and Dutta A. Recruitment of ORC or CDC6 to DNA is sufficient to create an artificial origin of replication in mammalian cells. 2005. Genes & Development 19(23):2827-2836. (*co-first author)
    • Takeda DY, Parvin JP, and Dutta A. Degradation of Cdt1 during S phase is Skp2-independent and is required for efficient progression of mammalian cells through S phase. 2005. Journal of Biological Chemistry 280(24):23416-23423.
    • Grisanzio C, Werner L, Takeda D, Awoyemi BC, Pomerantz MM, Yamada H, Sooriakumaran P, Robinson BD, Leung R, Schinzel AC, Mills I, Ross-Adams H, Neal DE, Kido M, Yamamoto T, Petrozziello G, Stack EC, Lis R, Kantoff PW, Loda M, Sartor O, Egawa S, Tewari AK, Hahn WC, Freedman ML. Genetic and functional analyses implicate the NUDT11, HNF1B, and SLC22A3 genes in prostate cancer pathogenesis. Proc Natl Acad Sci U S A. 2012 Jul 10;109(28):11252-7.
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