The focus of my academic training has been on immune cell therapies for the treatment of ovarian cancer, meduloblastoma, and neuroblastoma with special attention given to therapies for breast cancer. My experience includes syngeneic and xenograph cancer models, murine models of orthotopic breast cancer including pre-clinical studies for the advancement of small molecule drugs and combined immune cell therapies. I am currently developing a combination therapy for the treatment of metastatic and minimal residual disease in breast cancer. The therapy seeks to combine the approved chemotherapy, bortezomib, with the much-studied immune cell therapy of cytokine-induced killer cells. While unsuccessful in clinical studies for the treatment of breast cancer, bortezomib has been shown to cause cellular stress in cancer cells leading to the upregulation of surface molecules such as MICA/B. The cytokine-induced killer (CIK) cells are an oncolytic population of NKT cells that recognize and mediate cell killing through the NKG2D receptor for which MICA/B is a ligand. In vitro studies of breast cancer cells treated with bortezomib have shown promising results in that NKG2D ligand expression can be modulated and that this modulation improves CIK cell efficacy. By using bortezomib in combination with the CIK cells we believe that the treatment of metastatic breast cancer can be improved.

Boards, Advisory Committees, Professional Organizations

  • Associate Member, AACR (2011 - Present)
  • Member, ASM (2014 - Present)
  • Member, AAAS (2013 - Present)

Professional Education

  • Bachelor of Science, Notre Dame de Namur University, Biology (1997)
  • Doctor of Philosophy, Stanford University, MI-PHD (2010)

Stanford Advisors

Community and International Work

  • Educational Outreach

    Partnering Organization(s)

    Susan G. Komen Foundation


    Bay Area

    Ongoing Project


    Opportunities for Student Involvement



Journal Articles

  • Monitoring Dynamic Interactions Between Breast Cancer Cells and Human Bone Tissue in a Co-culture Model. Molecular imaging and biology Contag, C. H., Lie, W., Bammer, M. C., Hardy, J. W., Schmidt, T. L., Maloney, W. J., King, B. L. 2014; 16 (2): 158-166


    Bone is a preferential site of breast cancer metastasis, and models are needed to study this process at the level of the microenvironment. We have used bioluminescence imaging (BLI) and multiplex biomarker immunoassays to monitor dynamic breast cancer cell behaviors in co-culture with human bone tissue.Femur tissue fragments harvested from hip replacement surgeries were co-cultured with luciferase-positive MDA-MB-231-fLuc cells. BLI was performed to quantify breast cell proliferation and track migration relative to bone tissue. Breast cell colonization of bone tissues was assessed with immunohistochemistry. Biomarkers in co-culture supernatants were profiled with MILLIPLEX(®) immunoassays.BLI demonstrated increased MDA-MB-231-fLuc cell proliferation (p < 0.001) in the presence vs. absence of bones and revealed breast cell migration toward bone. Immunohistochemistry illustrated MDA-MB-231-fLuc cell colonization of bone, and MILLIPLEX(®) profiles of culture supernatants suggested breast/bone crosstalk.Breast cell behaviors that facilitate metastasis occur reproducibly in human bone tissue co-cultures and can be monitored and quantified using BLI and multiplex immunoassays.

    View details for DOI 10.1007/s11307-013-0685-0

    View details for PubMedID 24008275

  • Definition of an Enhanced Immune Cell Therapy in Mice That Can Target Stem-Like Lymphoma Cells CANCER RESEARCH Contag, C. H., Sikorski, R., Negrin, R. S., Schmidt, T., Fan, A. C., Bachireddy, P., Felsher, D. W., Thorne, S. H. 2010; 70 (23): 9837-9845


    Current treatments of high-grade lymphoma often have curative potential, but unfortunately many patients relapse and develop therapeutic resistance. Thus, there remains a need for novel therapeutics that can target the residual cancer cells whose phenotypes are distinct from the bulk tumor and that are capable of reforming tumors from very few cells. Oncolytic viruses offer an approach to destroy tumors by multiple mechanisms, but they cannot effectively reach residual disease or micrometastases, especially within the lymphatic system. To address these limitations, we have generated immune cells infected with oncolytic viruses as a therapeutic strategy that can combine effective cellular delivery with synergistic tumor killing. In this study, we tested this approach against minimal disease states of lymphomas characterized by the persistence of cancer cells that display stem cell-like properties and resistance to conventional therapies. We found that the immune cells were capable of trafficking to and targeting residual cancer cells. The combination biotherapy used prevented relapse by creating a long-term, disease-free state, with acquired immunity to the tumor functioning as an essential mediator of this effect. Immune components necessary for this acquired immunity were identified. We further demonstrated that the dual biotherapy could be applied before or after conventional therapy. Our approach offers a potentially powerful new way to clear residual cancer cells, showing how restoring immune surveillance is critical for maintenance of a disease-free state.

    View details for DOI 10.1158/0008-5472.CAN-10-2650

    View details for Web of Science ID 000285045900033

    View details for PubMedID 20935221

  • Targeting Localized Immune Suppression Within the Tumor Through Repeat Cycles of Immune Cell-oncolytic Virus Combination Therapy MOLECULAR THERAPY Thorne, S. H., Liang, W., Sampath, P., Schmidt, T., Sikorski, R., Beilhack, A., Contag, C. H. 2010; 18 (9): 1698-1705


    A major limitation to the use of immunotherapy in the treatment of cancer has been the localized immune suppressive environment within the tumor. Although there is evidence that tumor-selective (oncolytic) viruses may help to overcome this immune suppression, a primary limitation to their use has been limited systemic delivery potential, especially in the face of antiviral immunity. We recently demonstrated that tumor-trafficking immune cells can efficiently deliver oncolytic viral therapies to their tumor targets. These cells act as both a therapeutic agent and also a carrier vehicle for the oncolytic virus. Here, we demonstrate that such delivery is also possible in the face of pre-existing antiviral immunity, so overcoming the limited systemic delivery of naked, cell-free virus. It was also found that treatment of previously immunized mice or repeat treatments leading to immunization resulted in a switch from a primarily oncolytic to an immunotherapeutic mechanism of action. Furthermore, repeat cycles of treatment with combination immune cell-viral therapy resulted in increased tumor infiltration of effector T-cells and a general reduction in the levels of known immune suppressive lymphocyte populations. This therefore represents a novel and effective means to overcome localized immune suppression within the tumor microenvironment.

    View details for DOI 10.1038/mt.2010.140

    View details for Web of Science ID 000281502300017

    View details for PubMedID 20606649

  • Characterization of the rhesus cytomegalovirus US28 locus JOURNAL OF VIROLOGY Penfold, M. E., Schmidt, T. L., Dairaghi, D. J., Barry, P. A., Schall, T. J. 2003; 77 (19): 10404-10413


    Human cytomegalovirus (CMV) US28 (and the related open reading frame [ORF] US27) are G-protein-coupled receptor homologs believed to play a role in viral pathogenesis. In vitro, US28 has been shown to bind and internalize ligands, as well as activate intracellular signaling in response to certain chemokines, and to initiate the migration of smooth muscle cells to chemokine gradients. To assess the role of US28 in vivo, we examined the rhesus model and sequenced and characterized the rhesus CMV US28 locus. We found that rhesus CMV carries five tandem homologs of US28, all widely divergent from US28 and from each other. By reverse transcription-PCR and Northern analysis, we demonstrated expression of these ORFs in infected cells. With stable cell lines expressing these ORFs, we analyzed the homolog's binding and signaling characteristics across a wide range of chemokines and found one (RhUS28.5) to have a ligand binding profile similar to that of US28. In addition, we localized US28 and the rhesus CMV homolog RhUS28.5 to the envelope of infectious virions, suggesting a role in viral entry or cell tropism.

    View details for DOI 10.1128/JVI.77.19.10404-10413.2003

    View details for Web of Science ID 000185400400023

    View details for PubMedID 12970425

Stanford Medicine Resources: