Judith Campisi


United States
Also Known As

Judith Campisi is a cell and molecular biologist, recognized for her work on the relationship between aging and disease, especially the relationship between aging and cancer. Born in New York City, she received a PhD in biochemistry from the State University of New York Stony Brook and postdoctoral training at the Dana-Farber Cancer Institute and Harvard Medical School. She joined the faculty of the Boston University Medical School in the mid-1980s, before moving to the Lawrence Berkeley National Laboratory as a Senior Scientist in 1991. In 2002, she started a second laboratory at the Buck Institute for Research on Aging, where she is Professor. Her laboratory has made several pioneering discoveries regarding the cell autonomous and cell non-autonomous effects of cell fate decisions, with an emphasis on cellular senescence. Throughout her career, her research has challenged and altered existing paradigms in the fields of aging and cancer, and her laboratory continues to contribute new insights and ideas in these fields. Campisi has received numerous awards for her research, and is a member of the National Academy of Sciences. She serves on numerous national and international editorial and scientific advisory boards. Research Interests Judith Campisi’s laboratory studies the evolutionary trade-offs between protection from cancer and age-related phenotypes and pathologies. The research focuses on cellular senescence, a complex cell fate consisting of three linked phenotypic changes: an essentially permanent arrest of cell proliferation, resistance to cell death, and a multi-component senescence-associated secretory phenotype (SASP). Mammalian cells can enter a senescent state in response to a variety of stresses and physiological signals. In either case, the effects can be beneficial or deleterious, depending on the context. The proliferative arrest acts as a cell autonomous barrier to the development of cancer, but can eventually deplete tissues of stem or progenitor cells. Likewise, the SASP can, ironically, cell non-autonomously fuel cancer progression and/or disrupt normal tissue structures and functions, but can also promote tissue repair. Resistance to cell death ensures the persistence of senescent cells during tissue repair, but likely contributes to their accumulation during aging. A causal role for senescent cells in these diverse processes has now been established through the use of mouse models and pharmacological interventions. A major challenge for future research will be to determine how to mitigate the deleterious effects -- while preserving the beneficial effects -- of senescent cells.

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