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Thomas Kipps, MD, PhD, is Professor of Medicine, Evelyn and Edwin Tasch Chair in Cancer Research, and Deputy Director of Research Operations at the UC San Diego Moores Cancer Center. He received his Ph.D. in Immunology and M.D. from Harvard University and had his residency and fellowship training in Internal Medicine, Hematology, and Genetics at Stanford University.

Dr. Kipps has a national and international reputation for his work in cancer research, immunology, and gene therapy. He has been a leader in the field for many years, and has helped to develop standardized treatment protocols. He is the author of more than 300 publications and is the PI on several peer-reviewed grants, including an award from NCI/NIH to fund the Chronic Lymphocytic Leukemia Research Consortium (CRC). The CRC involves collaboration with eight other Cancer Centers around the United States and the UK. Dr. Kipps is also the Director of the Blood Cancer Research Fund at the UC San Diego Moores Cancer Center. The Blood Cancer Research Fund concentrates on developing cures for all types of blood related cancers, specifically Chronic Lymphocytic Leukemia (CLL).

Dr. Kipps has over 20 years’ experience in combining research and clinical care responsibilities. As deputy director of research operations, Dr. Kipps is working to further integrate basic and translational research investigators at the Moores Cancer Center with clinical investigators, epidemiologists, and physicians offering state-of-the art therapies for patients with various forms of cancer.

Research Interests
A major focus of Dr. Kipps’ research is the immunobiology and genetics of human B-cell malignancies, with emphasis on chronic lymphocytic leukemia (CLL). Dr. Kipps’ work has provided insight into the ontogeny of B cells that are subject to leukemia transformation and defined the highly restricted nature of the immunoglobulins expressed in this disease. In addition, he has defined genetic factors that contribute to the development and progression of this disease, identified biochemical pathways that enhance the growth or survival of leukemia B cells, identified means with which to elicit host anti-leukemia immune responses through vaccines generated via gene transfer, and identified promising new drugs and biologic agents that have activity in the treatment of this disease. He has made seminal observations on how the microenvironment can promote survival of CLL cells and defined strategies for mitigating the protective effects of the microenvironment on CLL cells survival in vivo. He has instigated and enabled work on selected leukemia cell samples of patients with sporadic or familial CLL that led to discovery of the role played by microRNA and ultraconserved, non-coding RNAs in the pathogenesis or progression of CLL in collaborations with the laboratory of Dr. Carlo Croce of the CLL Research Consortium (CRC). In other collaborations initiated through the CRC, Dr. Kipps also contributed to work on the epigenetic factors that contribute to pathogenesis in CLL.

The study on CLL cells serially collected from patients at time points before therapy, during therapy, or after relapse from therapy allows for investigation of the genetic and biologic features associated with tumor progression, therapeutic response, or resistance to therapy. Discovery of features that distinguish CLL from their normal cell counterparts has helped identify new targets for therapy and/or define surrogate markers associated with more rapid rates of cancer progression or resistance to standard therapy. These studies are integrated with a clinical investigative program that attracts patients seeking improved modalities of treatment for CLL. From this, Dr. Kipps has identified molecular markers that can segregate patients into subgroups that have different risks for disease-progression or different probabilities of response to conventional treatment. This also has allowed for testing the safety and relative efficacy of novel agents developed for treatment of all patients with CLL or subgroups of patients hypothesized to have the best potential response to novel forms of therapy.

Most recently, Dr. Kipps has discovered that the embryonic antigen ROR1 is expressed on CLL. ROR1 an embryonic type I membrane receptor tyrosine kinase-like surface protein. ROR1 was not expressed on normal, healthy adult tissues, but was found on the leukemia cells of virtually all cases of CLL and on the neoplastic cells of many patients with solid tumors. His work has demonstrated that patients immunized with autologous CLL cells transfected to express the CD40-ligand (CD154) can generate antibodies that are specific for this type I tyrosine kinase that apparently can block its capacity to function as a survival receptor for wnt5a. This work potentially could lead to development of novel vaccines for patients with this disease. Currently, Dr. Kipps is collaborating with other investigators at the UC San Diego Moores Cancer Center on developing monoclonal and recombinant antibodies specific for ROR1 and have identified one that can interfere with ROR1 signaling. The California Institute of Regenerative Medicine (CIRM) is funding this work.

Another project undertaken in the Kipps’ lab is to define the nature of immunoglobulin gene expression in normal and neoplastic B cells and to examine the relationship between B-cell receptor signaling events and mechanisms governing the pathogenesis and/or progression of CLL. In addition he is investigating the role of the microenvironment in support both normal and neoplastic B cell survival. In addition to his laboratory research, Dr. Kipps is actively involved in clinical research; having developed and/or conducted several phase I and phase II clinical trials.