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Wen-Kai Weng, MD, PhD

Academic Appointments

Key Documents

Contact Information

  • Clinical Offices
    Blood & Marrow Transplantation 875 Blake Wilbur Dr Clinic C MC 5820 Stanford, CA 94305
    Tel Work (650) 498-6000 Fax (650) 725-8950
  • Academic Offices
    Personal Information
    Email Tel (650) 723-7689
    Alternate Contact
    Janice Smith Administrative Associate Tel Work 650-724-4155
    Not for medical emergencies or patient use

Professional Overview

Clinical Focus

  • Cancer> Blood and Marrow Transplant
  • Cancer> Lymphoma
  • Cutaneous T-Cell Lymphoma
  • Medical Oncology
  • Myeloma

Administrative Appointments

  • Scientific Advisory Board, Lymphoma Research Foundation (2011 - present)

Honors and Awards

  • ITI Seed Grant Award, Institute for Immunity, Transplantation and Infection, Stanford University (2011-2012)
  • Division Teaching Award, BMT, Stanford University (2010)
  • Developmental Research Award, Stanford University Cancer Center (2009-2010)
  • Division Teaching Award, BMT, Stanford University (2009)
  • K08 Clinical Scientist Career Development Award, NIH/NCI (2005-2009)
View all 9honors and awards of Wen-Kai Weng

Professional Education

Board Certification: Medical Oncology, American Board of Internal Medicine (2008)
Board Certification: Internal Medicine, American Board of Internal Medicine (2007)
Fellowship: SUMC - Graduate Medical Education CA (2002)
Residency: University of Texas Medical School TX (1999)
Internship: University of Texas Medical School TX (1997)
View All 7

Graduate & Fellowship Program Affiliations

Scientific Focus

Current Research Interests

My clinical focus is non-Hodgkin's lymphoma (NHL) and am currently conducting clinical trials with novel therapies on these patients. My basic research interest is immunotherapy for cancer, with two components: monoclonal antibody therapy and tumor vaccines. On the antibody therapy end, I have studied the mechanism of an anti-CD20 antibody, rituximab, in treating B cell NHL. I found that the main anti-tumor action of rituximab is through Antibody-dependent Cellular Cytotoxicity (ADCC) and the poperty of Fc receptor on the killer cells (NK and Macrophages) is the predictive factor of clinical response. I also found that tumor-specific cytotoxic T cells were generated after rituximab therapy probably due to dendritic cell activation by Fc receptor/rituixmab interaction and cross-presentation of tumor antigens to the T cells. Based on the importance of interaction between the Fc of therapeutic antibodies and FcR on killer cells, I am designing the next generation of monoclonal antibodies with higher affinity to various FcR. The goal is to make an antibody with more efficient ADCC ability to overcome resistance in patients who did not response to treatment.

For the tumor vaccine end, I am conducting clinical trials using a tumor-specific antigen (idiotype) as a vaccine in patients with follicular NHL after induction thearpy. I also recently found out that the clinical benefit from this idiotype vaccination was associated with anti-idiotype antibody induction after vaccination and with the poperty of FcR on killer cells. This result supports the model that anti-tumor antibodies are critical part of this tumor vaccine therapy. Currently, I am developing a novel strategy to use rituximab-coated tumor cells/dendrtic cells as a therapeutic vaccine.

Publications

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