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| Name |
Campisi, Judith |
| Location
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Buck Institute for Research on Aging |
| Primary Field
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Medical Genetics, Hematology and Oncology |
| Secondary Field
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Cellular and Developmental Biology |
 Election Citation
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Campisi, more than any other scientist, pionered the concept of cellular senescence in aging and age-related pathologies. Her laboratory discovered the major senescence biomarkers, identified molecular pathways that regulate growth arrest and the secretory phenotype, and defined the role of senescent cells in inflammation, heralding the development of senolytic therapies. |
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Research Interests
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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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