Division Faculty Labs
Larry Anderson, M.D., Ph.D.
My lab is interested in finding targets for T cell therapy of Multiple Myeloma and other Monoclonal Gammopathies, such as Waldenstrom’s Macroglobulinemia. The ultimate goal of this research is to translate findings from tissue culture and mouse studies into immunotherapies for Myeloma patients. Thus far we have identified 2 potentially relevant peptides from the candidate myeloma antigen MAGE-C1 (CT-7), a cancer testis antigen, and we are also looking for epitopes from other candidate antigens. We are using various methods including reverse immunology as well as vaccination of HLA-A2 transgenic mice with gene-modified cellular vaccines to elicit T-cell responses. Another goal of the lab is to identify the targets recognized by T-cells in the setting of Graft versus Myeloma responses and Graft versus Waldenstrom’s following Allogeneic Stem Cell Transplantation.
Theodora Ross, M.D., Ph.D.
Website: Ross Lab
Our laboratory is interested in understanding mechanisms of transformation of normal cells to cancer cells and the use of that understanding in the clinic. Our focus is on three areas. First, we are interested in receptor tyrosine kinases and their connection to an endocytic protein called Huntingtin Interacting Protein 1 (HIP1) in cancer biology. Second, the role(s) of tyrosine kinase oncogenes in cancer initiation, maintenance and drug resistance are being studied using humanized knock-in mouse models of leukemia. Finally, we are defining the molecular and cellular biology of families with a high risk for cancer in hopes that we can use this information in the general management of cancer prone families.
Pier Paolo Scaglioni, M.D.
Website: Scaglioni Lab
We are interested in gaining insights into the processes that underlie tumor initiation, progression and maintenance. To achieve these goals, we utilize a broad array of technologies that include cellular and molecular biology techniques mouse genetics and novel targeted drugs. We focus our interests on the promyelocytic leukemia tumor suppressor and oncogenic K-RAS. These genes control processes that are key in oncogenesis. We expect that their study will reveal the critical molecular pathways that drive tumor formation and maintenance revealing novel targets that can be exploited in cancer therapy.
Nima Sharifi, M.D.
Website: Sharifi Lab
This laboratory is focused on steroid metabolism and androgen receptor (AR) function as it relates to prostate cancer. The first line of therapy for metastatic prostate cancer is androgen deprivation therapy (ADT), often with gonadotropin-releasing hormone agonists (GnRH-A), which block the release of gonadal testosterone (see figure below). Almost all prostate cancers express AR and require AR for survival, growth and disease progression, which is why the majority of patients initially respond well to ADT. However, metastatic disease eventually becomes resistant to ADT. Prostate cancer that progresses in the face of ADT is termed castration-resistant prostate cancer (CRPC). Several laboratories have shown that AR is somehow reactivated by a gain-of-function in CRPC and is often driven by these tumors making their own androgens. Therefore, compounds that block the synthesis of androgens or antagonize AR with novel mechanisms should be useful for the treatment of CRPC.