Judith Campisi, Ph.D
Professor at the Buck Institute for Research on Aging, Director of the Campisi lab
Dr. Campisi received a PhD in biochemistry from the State University of New York at Stony Brook and completed her postdoctoral training in cell cycle regulation at the Dana-Farber Cancer Institute and Harvard Medical School. As an assistant and associate professor at the Boston University Medical School, she studied the role of cellular senescence in suppressing cancer and soon became convinced that senescent cells also contributed to aging. She joined the Lawrence Berkeley National Laboratory as a senior scientist in 1991. In 2002, she started a second laboratory at the Buck Institute. At both institutions, Dr. Campisi established a broad program to understand the relationship between aging and age-related disease, with an emphasis on the interface between cancer and aging.
Dr. Campisi is a member of the National Academy of Sciences and a fellow of the American Association for the Advancement of Science.
She has received numerous awards for her research, including two MERIT awards from the National Institute on Aging and awards from the AlliedSignal Corporation, Gerontological Society of America, and American Federation for Aging Research. She is a recipient of the Longevity prize from the IPSEN Foundation, the Bennett Cohen award from the University of Michigan, and the Schober award from Halle University, and she is the first recipient of the international Olav Thon Foundation prize in Natural Sciences and Medicine. Dr. Campisi currently serves on advisory committees for the Alliance for Aging Research, Progeria Research Foundation, and NIA’s Intervention Testing Program. She is also an editorial board member for more than a dozen peer-reviewed journals. Dr. Campisi is a scientific founder of Unity Biotechnology, a California-based company focused on developing therapies for age-related pathologies. She has served on the scientific advisory boards of the Geron Corporation, Sierra BioScience, and Sangamo Biosciences.
Cellular senescence. Why is aging the largest risk for developing so many apparently disparate diseases, ranging from neurodegeneration to cancer? One answer to this question lies in the evolutionarily selected, stress-responsive state termed cellular senescence. Senescent cells cease proliferation, which prevents early life cancer. They also secrete numerous molecules that promote tissue repair and regeneration. However, because senescent cells gradually accumulate with age, they eventually cause tissue degeneration, chronic inflammation, and many age-related diseases, including, ironically, late life cancer. The Campisi lab studies the regulation and characteristics of cell states, with an emphasis on cellular senescence. We use simple and complex human and mouse cell cultures, intact human and mouse tissues, and mouse models to understand the molecular pathways that drive cellular senescence and other cell states. We also use genetic and pharmacological manipulations to understand how cell states cause both the degenerative diseases of aging as well as cancer and to design strategies to modulate or ameliorate their effects.
aging critical publications
Dimri, G., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens ,M., Rubelj, I., Pereira-Smith, O., Peacocke, M., Campisi, J. (1195 Sep 26). A novel biomarker identifies senescent human cells in culture and aging skin in vivo. Proc Natl Acad Sci USA, 92(20), 9363–67.
Krtolica, A., Parrinello, S., Lockett, S., Desprez, P., Campisi, J. (2001 Oct 9). Senescent fibroblasts promote epithelial cell growth and tumorigenesis: A link between cancer and aging. Proc Natl Acad Sci USA, 98(21), 12072–77.
Coppe, J. P., Patil, C. K., Rodier, F., Sun, Y., Munoz, D. P., Goldstein, J., Nelson, P. S., Desprez, P. Y., Campisi, J. (2008). Senescence-associated secretory phenotypes reveal cell non-autonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol, 6(12), 2853–68.
Rodier, F., Coppe, J. P., Patil, C. K., Hoeijmakers, W. A. M., Munoz, D. P., Raza, S. R., Freund, A., Campeau, E., Davalos, A. R., Campisi, J. (2009 Aug). Persistent DNA damage signaling triggers senescence-associated inflammatory cytokine secretion. Nature Cell Biol, 11(8), 973–79.
Demaria, M., Ohtani, N., Youssef, S. A., Rodier, F., Toussaint, W., Mitchell, J. R., Laberge, R. M., Vijg, J., van Steeg, H., Dolle, M. E., Hoeijmakers, J. H., de Bruin, A., Hara, E., Campisi, J. (2014 Dec 22). An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA. Dev Cell, 31(6), 722–33.
Laberge, R. M., Sun, Y., Orjalo, A. V., Patil, P. K., Freund, A., Zhou L., Curran, S. C., Davalos, A. R., Wilson-Edell, K. A., Liu, S., Limbad, C., Demaria, M., Li P., Hubbard, G. B., Ikeno, Y., Javors, M., Desprez, P. Y., Benz, C. C., Kapahi, P., Nelson, P. S., Campisi, J. (2015 Aug). mTOR regulates the tumor-promoting senescence secretory phenotype by promoting IL-1 translation. Nature Cell Biol, 17(8), 1049–61.
Velarde, M. C., Demaria, M., Melov, S., Campisi, J. (2015 Aug 18). Pleiotropic age-dependent effects of mitochondrial dysfunction on epidermal stem cells. Proc Natl Acad Sci USA, 112(33), 10407–12.
Wiley, C. D., Velarde, M. C., Lecot, P., Liu, S., Sarnoski, E. A., Shirakawa, K., Lim, H., Davis, S., Ramanathan, A., Gerencser, A. A., Verdin, E., Campisi, J. (2015 Dec 10). Mitochondrial dysfunction induces senescence with a distinct secretory phenotype. Cell Metab, 23(2), 303–14.
Demaria, M., O’Leary,, M. N., Chang J., Shao, L., Liu, S., Alimirah, F., Koenig, K., Le, C., Mitin, N., Deal, A. M., Alston, S., Academia, E. C., Kilmarx, S., Valdovinos, A., Wang, B., de Bruin, A., Kennedy, B. K., Melov, S., Zhou, D., Sharpless, N. E., Muss, H., Campisi, J. (2017 Feb). Cellular senescence promotes adverse effects of chemotherapy and cancer relapse. Cancer Discov, 7(2), 165–176.