Judith Campisi

Buck Institute for Research on Aging

Primary Section: 41, Medical Genetics, Hematology, and Oncology
Secondary Section: 22, Cellular and Developmental Biology
Membership Type:
Member (elected 2018)


Judith Campisi received a PhD in biochemistry from the State University of New York, postdoctoral training at the Dana Farber Cancer Institute and Harvard Medical School, and was an Assistant and Associate Professor at the Boston University Medical School faculty before joining 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. At both institutions, she established a broad program to understand the relationships between aging and disease, with an emphasis on cellular senescence, aging and cancer. Her laboratory has made several pioneering discoveries in these areas, and continues to explore the boundaries of knowledge about the relationships between cell fate decisions and disease. She has received numerous awards for her research, is an elected member of the National Academy of Sciences and American Academy for Cancer Research, and serves on numerous 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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