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Judith Campisi, PhD

Judith Campisi, PhD

Lawrence Berkeley National Laboratory
Berkeley, California

Class of 2020

For groundbreaking contributions to the understanding of the links between aging and cancer and for her research related to identifying the molecular mechanisms associated with cellular senescence, aging, and tumorigenesis that has defined the role of DNA damage and repair in genomic instability and premature aging.

An internationally recognized leader, Dr. Campisi is celebrated for her contributions to the understanding of the link between aging and cancer and for her research focused on identifying the molecular mechanisms associated with cellular senescence. Her research has elucidated the dual roles of senescence, providing cells with a protective mechanism against cancer by ceasing proliferation, while also triggering a downstream cascade of tissue degeneration and inflammation harboring a pro-tumorigenic environment. Her key findings that demonstrated changes in expression of several genes, including downregulation of c-fos, began unraveling the molecular consequences of accumulated senescent cells. Her research group was the first to describe senescence associated secretory phenotype (SASP), a key characteristic of senescent cells which secrete inflammatory cytokines, immune modulators, growth factors and proteases. She definitively linked cellular aging and cancer in her groundbreaking work demonstrating that the accumulation of senescent cells leads to the proliferation of premalignant and malignant epithelial cells and tumorigenesis.  

Dr. Campisi has highlighted the immunological repercussions associated with senescence and how these immune system-related signals may affect an individual’s cancer risk. Her research team demonstrated that upon induction of genotoxic stress, SASP led to epithelial-mesenchymal transition of premalignant cells via paracrine signaling molecules interleukin-6 (IL-6) and IL-8. Furthermore, these studies demonstrated that overexpression of RAS and loss of function of P53 exacerbated SASP development. Her studies have also identified the mammalian target of rapamycin (mTOR) as a key regulator of SASP development, specifically by promoting translation of IL-1, and more recently, has elucidated the role that mitochondrial dysfunction plays in senescence. In addition to her investigations into the interplay between cellular senescence, aging, and tumorigenesis, her research has increased the understanding of the role of telomeres as well as DNA damage and repair in genomic stability and premature aging. 

Selected Awards and Honors 

2018 ~ Elected Member, National Academy of Sciences, Washington, DC 
2015 ~ ICCNS-Springer Award, International CCN Society, Paris, France 
2015 ~ International Prize in Natural Sciences and Medicine, Olav Thon Foundation, Oslo, Norway 
2013 ~ Schober Award, Martin-Luther University of Halle-Wittenberg, Saxony-Anhalt, Germany 
2011 ~ Elected Fellow, American Association for the Advancement of Science, Washington, DC 
2010 ~ Longevity Prize, Fondation IPSEN, Paris, France 
2003-2013 ~ Co-Chair, Task Force on Aging and Cancer, American Association for Cancer Research, Philadelphia, Pennsylvania 
2002 ~ Irving Wright Award of Distinction, American Federation for Aging Research, New York, NY 
1999 ~ Glenn Foundation Award, Gerontological Society of America, Washington, DC