ROBERT K. BRIGHT
- : (806) 743-4592
Fax: (806) 743-2334
- DEPARTMENTDepartment of Immunology and Molecular Microbiology
Texas Tech University Health Sciences Center
Extensive studies over the past few decades have established that cancer patients can mount immune responses against their own tumor(s), and that these responses can be effectively manipulated to treat patients with cancer by using defined targets isolated from the tumor cells, known as tumor associated antigens as vaccines. Recently the National Cancer Institute sponsored a pilot project to prioritize cancer vaccine target antigens for translational research. The study involved developing a set of nine “ideal” cancer antigen criteria/ characteristics, with 1) therapeutic function, 2) immunogenicity and 3) a role in oncogenicity deemed as having the greatest importance. From a growing but representative list of antigens, a group defined as over-expressed self-proteins stands out as the group with the largest number of potentially important target antigens. My research at present has focused on tumor immunology and cancer vaccines, which can be categorized by work in: a) the discovery and validation of novel tumor associated antigens using genomics and proteomics, b) the design of vaccine strategies and c) the study of mechanisms that impede effective vaccine induced immunity to include CD4+ and CD8+ regulatory T cells. Our systems biology efforts along these lines have led to the discovery of a novel cancer over-expressed self onco-protein, Tumor Protein D52, which is an active focus of our research. Tumor protein D52 (D52) is involved in cellular transformation, proliferation and metastasis and thus has a role in oncogenicity. Expression microarray analyses predict D52 over-expression in many other cancer types, including multiple myeloma, Burkitt’s lymphoma, pancreatic cancer, testicular germ cell tumors, and melanoma. We have reported that vaccines targeting D52 elicit tumor- specific T cells but only limited tumor protection in murine models of cancer. Data from these D52 vaccine studies suggest that a subset of CD8+ T cells plays a regulatory role in suppressing vaccine induced D52-specific immunity and may play a role suppressing immunity to self proteins in general. A deeper understanding of the regulation of immunity to self onco-proteins is critical for the development of successful cancer vaccines. Our goal is to develop D52 as a systemic therapy or vaccine against cancer. Since D52 is over-expressed in many malignancies the long-term clinical impact could be wide reaching.