Faculty Profile
Dr. Kipps
Thomas Kipps, M.D., Ph.D.
Professor of Medicine
Deputy Director for Research
Moores UCSD Cancer Center
Office Address:
Division of Hematology-Oncology
University of California
Moores UCSD Cancer Center
3855 Health Sciences Drive, MC-0820
La Jolla, CA 92093
tkipps@ucsd.edu
Office: (858) 822-5635
FAX: (858) 822-5660
Education and Training
| BA | Biochemistry, Columbia University | 1971-1974 |
| MD, PhD | Immunology, Harvard Medical School | 1974-1979 |
| Residency | Stanford University | 1979-1982 |
| Fellowship | Hematology & Genetics, Stanford University | 1982-1985 |
Biography
Dr. Kipps is a UCSD Professor of Medicine and Deputy Director of Research at the Moores UCSD 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 is the author of more than 200 publications and is the PI on several peer-reviewed grants, including an award from NCI/NIH to fund the Chronic Lymphocytic Leukemia Consortium (CRC). The CRC involves collaboration with eight other Cancer Centers around the nation. Kipps has 20 years’ experience in combining research and clinical care responsibilities.
Research Interests
A major focus of Dr. Kipps' research is chronic lymphocytic leukemia (CLL). His work has defined the role of the zeta-associated protein of 70 kD (ZAP-70) in B cell receptor signaling in CLL and established the association between expression of intracellular kinase in CLL cells and risk for disease progression. His work has provided insight into on 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, Kipps 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 also defined 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 instigated and enabled work on selected leukemia cell samples of patients with familial CLL that led to discovery of the role played by microRNA in the pathogenesis of CLL in collaborations with the laboratory of Dr. Carlo Croce of the CLL Research Consortium (CRC). In addition, this work led to discovery of potential contribution of highly conserved non-coding RNA in the pathogeneis and progression of CLL. This work was the first to define a role for microRNA or ultraconserved non-coding RNA in any malignancy and was only made possible through the research collaborations that developed within the CLL Research Consortium (CRC), which was established and directed by Dr. Kipps. In other collaborations initiated through the CRC, Kipps also contributed to work on the epigenetic factors that contribute to pathogenesis in CLL. Most recently, Dr. Kipps has discovered that the embryonic antigen ROR1 is expressed on CLL. 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.
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.
Publications
Ranheim EA, Kipps TJ: Activated T cells induce expression of B7/BB1 on normal or leukemic B cells through CD40-dependent signal. J Exp Med 177:925-935, 1993.
Johnson TA, Rassenti LZ, Kipps TJ: Ig VH1 genes expressed in B-cell chronic lymphocytic leukemia exhibit distinctive molecular features. J Immunol 158: 235-246, 1997.
Cantwell MJ, Hua T, Pappas J, Kipps TJ: Acquired CD40-ligand deficiency in chronic lymphocytic leukemia. Nature Med 3:984-989, 1997.
Kato K, Cantwell MJ, Sharma S, Kipps TJ: Gene transfer of CD40-Ligand autologous immune recognition of chronic lymphocytic leukemia B cells. J Clin Invest 101:1133-1141, 1998.
Burger JA, Tsukada N, Burger M, Zvaifler NJ, Dell’Aquila M, Kipps TJ: Blood-derived “nurse-like” cells protect chronic lymphocytic leukemia B cells from spontaneous apoptosis via stromal-cell-derived factor-1. Blood 96:2655-2663, 2000.
Wierda WG, Cantwell MJ, Woods SJ, Rassenti LZ, Prussak CE, Kipps TJ: CD40-ligand (CD154) gene therapy for chronic lymphocytic leukemia. Blood 96(9):2917-2924, 2000.
Calin GA, Dumitru CA, Shimizu, M, Bichi R, Zupo S, Noch E, Aldler H, Rattan S, Keating M, Rai K, Rassenti L, Kipps T, Negrini M, Bullrich F, Croce CM: Frequent deletions and down-regulation of micro-RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia. Proc Natl Acad Sci U S A 99(24):15524-15529, 2002.
Chen L, Widhopf G, Huynh L, Rassenti L, Rai KR, Weiss A, Kipps TJ: Expression of ZAP-70 is associated with increased B-cell receptor signaling in chronic Lymphocytic leukemia. Blood 100(13): 4609-4614, 2002.
Rassenti LZ, Huynh L, Toy TL, Chen L, Keating MJ, Gribben JG, Neuberg DS, Flinn IW, Rai KR, Byrd JC, Kay NE, Greaves A, Weiss A, Kipps TJ: ZAP-70 is a stronger predictor of early disease progression than immunoglobulin mutational status in chronic Lymphocytic leukemia. N Engl J Med 351(9):893-900, 2004.
Fukuda T, Chen L, Endo T, Tang L, Lu D, Castro J, Widhopf GF, Rassenti L, Cantwell M, Prussak C, Carsonb DA, Kipps TJ: Antisera induced by infusions of autologous Ad-CD154-leukemia B cells identify ROR1 as an oncofetal antigen and receptor for Wnt5a. Proc Natl Acad Sci USA 105(8):3047-52, 2008
Laboratory
[text here] |
||
Laboratory Personnel
|
||
| Name | Title | Laboratory Focus |
| Anne Mette Buhl | Visiting Scholar | CLL-specific gene CLLU1 |
Liguang Chen |
Project Scientist |
Protein expression and signal transduction in CLL |
| Bing Cui | Postdoctoral Fellow | Gene therapy and immunotherapy studies in CLL |
| Jessie Fecteau | Postdoctoral Fellow | CLL microenvironment & immunotherapy |
| Arnon Kater | Visiting Scholar, Postdoctoral Fellow | Apoptosis regulation and targeted therapy in CLL |
| Laura Rassenti | Lead Project Scientist | Molecular genetic analyses of immunglobulins expressed in chronic lymphocytic leukemia & normal B cells. Analyzes prognostic markers for CLL. Director of the Tissue Core for the CRC |
| Christoph Steininger | Visiting Scholar | Role of infectious pathogens in CLL |
| George Widhopf | Project Scientist | Molecular characterization of immunoglobulin expressed by normal and leukemic B lymphocytes |
| Jianqiang Yu | Postdoctoral Fellow | Retrovirus making: Lentivirus, Adenovirus |
| Suping Zhang | Postdoctoral Fellow | Targeted therapy in CLL and signal transduction in cancer |
