Roy A. Jensen, M.D.

Professor, Pathology and Laboratory Medicine
Professor, Cancer Biology
Director, The University of Kansas Cancer Center
William R. Jewell, M.D. Distinguished Kansas Masonic Professor of Cancer Research and Director, Kansas Masonic Cancer Research Institute, University of Kansas Medical Center
rjensen@kumc.eduMore:
Professional Background
Dr. Jensen was appointed the director of The University of Kansas Cancer Center (KU Cancer Center) in 2004. As a result of a broad-based university, community, and regional effort, The University of Kansas Cancer Center was designated as a cancer center by the National Cancer Institute (NCI) in July 2012. Dr. Jensen is currently Professor of Pathology and Laboratory Medicine, Professor of Anatomy and Cell Biology, Professor of Cancer Biology, and the William R. Jewell, M.D. Distinguished Kansas Masonic Professor at the University of Kansas Medical Center. Prior to his appointment at KU Cancer Center, Jensen was a member of the Vanderbilt-Ingram Cancer Center and a faculty member in Pathology, Cell Biology, and Cancer Biology for 13 years.
Dr. Jensen graduated from Vanderbilt University School of Medicine in 1984, and remained there to complete a residency in Anatomic Pathology and a Surgical Pathology fellowship with Dr. David Page. Following his clinical training he accepted a postdoctoral fellowship at the NCI in the laboratory of Dr. Stuart Aaronson. After he joined the faculty at Vanderbilt University, Dr. Jensen focused his research on understanding the function of BRCA1 and BRCA2 and their role in breast neoplasia, and in the characterization of premalignant breast disease at both the morphologic and molecular levels. He currently has over 150 scientific publications and has lectured widely on the clinical and molecular aspects of breast cancer pathology.
Dr. Jensen has served on numerous grant review panels, study sections, and site visit teams for the NIH, the Department of Defense-Breast Cancer Research Program, the Medical Research Council of Canada, the California Breast Cancer Research Program, and the Susan G. Komen Breast Cancer Foundation. Jensen serves on the Science Policy and Governmental Affairs Committees for the American Association for Cancer Research, and the Federation of American Societies for Experimental Biology. In addition, he is a member of the American Association of Cancer Researcher Publications Committee, and the Science Policy Working Group of the American Society for Investigative Pathology, and co-chairs the research committee for C-Change. In 2013, he chaired the program committee for AACI's annual meeting and was elected to the association's Board of Directors. Jensen also serves on Subcommittee A for the NCI; as Chair of the University of Oklahoma Stephenson Cancer Center External Advisory Board; and as a member of the Georgia Cancer Center, Augusta University External Advisory Board.
Education and Training
- MD, Vanderbilt Univ.
- BS, Pittsburg State Univ.
- AA, Neosho County Cmty. Col.
Research
Overview
Dr. Jensen's research has been with the breast cancer susceptibility gene 1 (BRCA1) and breast cancer for more than 20 years. He was part of the team to provide the first evidence that BRCA1 was a tumor suppressor. Currently, Jensen's lab has several projects aimed at understanding BRCA1 regulation and how we might enhance the ability of BRCA1 to act as a tumor suppressor.
BRCA1 has been intensely investigated and mutations in the BRCA1 gene have been found to account for half of the hereditary breast cancer cases and almost all hereditary breast and ovarian cancer cases. Although the role of BRCA1 in sporadic breast and ovarian cancer is still uncertain, decreased BRCA1 expression often accompanies sporadic breast cancer progression. However, data published from Jensen's lab demonstrates that the overexpression of BRCA1 in the murine mammary gland provides protection against mutagen-induced mammary neoplasia. This work supports the hypothesis that an increase in BRCA1 can provide protection against tumors. Therefore, one project in the laboratory developed a stable human breast cancer cell line containing integrated copies of a BRCA1 promoter-driven luciferase reporter plasmid and screened over 100,000 compounds for their ability to increase BRCA1 expression. The overall objective of this project is to identify a drug that will increase BRCA1 and restore its tumor suppressor activity. This project shows promise for the discovery of a new agent to prevent or treat breast cancer.
Another project in the lab aims to identify cellular components as regulators of BRCA1 expression and function. DNA damage repair is a critical BRCA1 function that has been extensively investigated and is the focus of our cell-based functional assay developed to identify potential regulatory kinases of BRCA1 expression and function. DNA damage leads to the localization of several proteins involved in the repair of DNA, including BRCA1 and these repair sites are visualized as nuclear foci using fluorescence-based microscopy. Additionally, kinases modulate a variety of cell-specific responses, including signal transduction and DNA damage repair. These kinases can be selectively targeted for knockdown using siRNA to investigate the effect of a kinase on BRCA1 foci formation. Changes in either BRCA1 expression or activity will be reflected in observable alterations in BRCA1 foci formation. We have established the experimental parameters of the functional assay and are currently screening an siRNA kinase library for regulators of BRCA1 expression.
Publications
- Jensen, R., A, Page, D., L, Dupont, W., D, Rogers, L., W. 1989. Invasive breast cancer risk in women with sclerosing adenosis.. Cancer, 64 (10), 1977-83
- Stecklein, S., R, Kumaraswamy, E, Behbod, F, Wang, W, Chaguturu, V, Harlan-Williams, L., M, Jensen, R., A. 2012. BRCA1 and HSP90 cooperate in homologous and non-homologous DNA double-strand-break repair and G2/M checkpoint activation.. Proceedings of the National Academy of Sciences of the United States of America, 109 (34), 13650-5
- Dandawate, P, Subramaniam, D, Panovich, P, Standing, D, Krishnamachary, B, Kaushik, G, Thomas, S., M, Dhar, A, Weir, S., J, Jensen, R., A, Anant, S. 2020. Cucurbitacin B and I inhibits colon cancer growth by targeting the Notch signaling pathway.. Scientific reports, 10 (1), 1290
- Dandawate, P, Kaushik, G, Ghosh, C, Standing, D, Ali Sayed, A., A, Choudhury, S, Subramaniam, D, Manzardo, A, Banerjee, T, Santra, S, Ramamoorthy, P, Butler, M, Padhye, S., B, Baranda, J, Kasi, A, Sun, W, Tawfik, O, Coppola, D, Malafa, M, Umar, S, Soares, M., J, Saha, S, Weir, S., J, Dhar, A, Jensen, R., A, Thomas, S., M, Anant, S. 2020. Diphenylbutylpiperidine Antipsychotic Drugs Inhibit Prolactin Receptor Signaling to Reduce Growth of Pancreatic Ductal Adenocarcinoma in Mice.. Gastroenterology, 158 (5), 1433-1449.e27
- Pollack, S, Igo, Jr, R., P, Jensen, R., A, Christiansen, M, Li , X, Cheng, C., Y, Ng MCY, Smith, A., V, Rossin, E., J, Segrè, A., V, Davoudi, S, Tan, G., S, Ida Chen, Y., D, Kuo, J., Z, Dimitrov, L., M, Stanwyck, L., K, Meng, W, Hosseini, S., M, Imamura, M, Nousome, D, Kim, J, Hai, Y, Jia, Y, Ahn, J, Leong, A, Shah, K, Park, K., H, Guo, X, Ipp, E, Taylor, K., D, Adler, S., G, Sedor, J., R, Freedman, B., I, Lee, I., T, Sheu, W., H, Kubo, M, Takahashi, A, Hadjadj, S, Marre, M, Tregouet, D., A, Mckean-Cowdin, R, Varma, R, McCarthy, M., I, Groop, L, Ahlqvist, E, Lyssenko, V, Agardh, E, Morris, A, Doney ASF, Colhoun, H., M, Toppila, I, Sandholm, N, Groop, P., H, Maeda, S, Hanis, C., L, Penman, A, Chen, C., J, Hancock, H, Mitchell, P, Craig, J., E, Chew, E., Y, Paterson, A., D, Grassi, M., A, Palmer, C, Bowden, D., W, Yaspan, B., L, Siscovick, D, Cotch, M., F, Wang, J., J, Burdon, K., P, Wong, T., Y, Klein BEK, Klein, R, Rotter, J., I, Iyengar, S., K, Price, A., L, Sobrin, L. 2020. Erratum. Multiethnic Genome-Wide Association Study of Diabetic Retinopathy Using Liability Threshold Modeling of Duration of Diabetes and Glycemic Control. Diabetes 2019;68:441-456.. Diabetes, 69 (6), 1306
- Jensen RAA, Thomsen, D., K, Bliksted, V., F, Ladegaard, N. 2020. Narrative Identity in Psychopathology: A Negative Past and a Bright but Foreshortened Future.. Psychiatry research, 290, 113103
- Mudaranthakam, D., P, Harlan-Williams, L., M, Jensen, R., A, Kuo, H, Garimella, V, Chen, R., C, Mayo, M., S, Krebill, H. 2020. OPTIK: a database for understanding catchment areas to guide mobilization of cancer center assets.. Database : the journal of biological databases and curation, 2020
- Li , D, Harlan-Williams, L., M, Kumaraswamy, E, Jensen, R., A. 2019. BRCA1-No Matter How You Splice It.. Cancer research, 79 (9), 2091-2098
- Pollack, S, Igo, Jr, R., P, Jensen, R., A, Christiansen, M, Li , X, Cheng, C., Y, Ng MCY, Smith, A., V, Rossin, E., J, Segrè, A., V, Davoudi, S, Tan, G., S, Ida Chen, Y., D, Kuo, J., Z, Dimitrov, L., M, Stanwyck, L., K, Meng, W, Hosseini, S., M, Imamura, M, Nousome, D, Kim, J, Hai, Y, Jia, Y, Ahn, J, Leong, A, Shah, K, Park, K., H, Guo, X, Ipp, E, Taylor, K., D, Adler, S., G, Sedor, J., R, Freedman, B., I, Lee, I., T, Sheu, W., H, Kubo, M, Takahashi, A, Hadjadj, S, Marre, M, Tregouet, D., A, Mckean-Cowdin, R, Varma, R, McCarthy, M., I, Groop, L, Ahlqvist, E, Lyssenko, V, Agardh, E, Morris, A, Doney ASF, Colhoun, H., M, Toppila, I, Sandholm, N, Groop, P., H, Maeda, S, Hanis, C., L, Penman, A, Chen, C., J, Hancock, H, Mitchell, P, Craig, J., E, Chew, E., Y, Paterson, A., D, Grassi, M., A, Palmer, C, Bowden, D., W, Yaspan, B., L, Siscovick, D, Cotch, M., F, Wang, J., J, Burdon, K., P, Wong, T., Y, Klein BEK, Klein, R, Rotter, J., I, Iyengar, S., K, Price, A., L, Sobrin, L. 2020. Erratum. Multiethnic Genome-Wide Association Study of Diabetic Retinopathy Using Liability Threshold Modeling of Duration of Diabetes and Glycemic Control. Diabetes 2019;68:441-456.. Diabetes, 69 (6), 1306
- Vekaria, P., H, Kumar, A, Subramaniam, D, Dunavin, N, Vallurupalli, A, Schoenen, F, Ganguly, S, Anant, S, McGuirk, J., P, Jensen, R., A, Rao, R. 2019. Functional cooperativity of p97 and histone deacetylase 6 in mediating DNA repair in mantle cell lymphoma cells.. Leukemia, 33 (7), 1675-1686