Judith Campisi, PhD, Professor

Mechanisms that link tumor suppression and the development of cancer to aging and the major diseases associated with aging

Judith Campisi has received international recognition for her contributions to understanding why age is the largest single risk factor for developing a panoply of diseases, ranging from neurodegeneration to cancer. Her highly acclaimed research integrates the genetic, environmental and evolutionary forces that result in aging and age-related diseases, and identifies pathways that can be modified to mitigate basic aging processes. See video interview.

Dr. Campisi also makes significant contributions to understanding why aging is the largest single risk factor for developing cancer. She is widely recognized for her work on senescent cells -- older cells that have stopped dividing -- and their influence on aging and cancer. Senescence occurs when cells experience certain types of stress, especially stress that can damage the genome. The senescence response helps prevent cancer by blocking damaged cells from multiplying. But there is a trade off - the lingering senescent cells may also cause harm to the body. The Campisi lab found evidence that senescent cells can disrupt normal tissue functions and, ironically, drive the progression of cancer over time. Senescent cells also promote inflammation, which is a common feature of all major age-related diseases. Dr. Campisi is collaborating with many other research groups at the Buck Institute to examine other suspected influences of senescent cells on other diseases of aging. Her research is shedding light on anti-cancer genes, DNA repair mechanisms that promote longevity, molecular pathways that protect cells against stress, and stem cells and their role in aging and age-related disease.

Dr. Campisi received a PhD in Biochemistry from the State University New York at Stony Brook and completed postdoctoral training at the Harvard Medical School. As an assistant professor at the Boston University Medical School, she became interested in the control of cellular senescence and its role in tumor suppression and aging. She joined the Lawrence Berkeley National Laboratory as a Senior Scientist in 1991. She established a second laboratory at the Buck Institute in 2002. At both institutions, she established a broad program to understand various aspects of aging, with an emphasis on the interface between cancer and aging. The Campisi laboratory has made several pioneering discoveries in these areas, and her research continues to challenge and alter existing paradigms. In recognition of the quality of her research and leadership in the field, she has received numerous awards, including two MERIT awards from the US National Institute on Aging, and awards from the AlliedSignal Corporation, Gerontological Society of America, American Federation for Aging Research, and, most recently, the Longevity prize from the IPSEN Foundation. She currently serves on numerous national and international editorial and advisory boards.

Media Expertise
Dr. Campisi welcomes media inquiries on the following subjects:
The aging process, cancer, cancer and aging, inflammation and aging, senescence.

jcampisi@buckinstitute.org
Phone: 415-209-2066
Administrative Lab Coordinator: Shelly Jennings
sjennings@buckinstitute.org
Phone: 415-209-2002

Aging is controlled by genes and the environment, and poses the largest single risk for developing a panoply of diseases, both degenerative (e.g., Alzheimer’s disease, osteoporosis, cardiovascular disease) and hyperproliferative (e.g., cancer). Why do organisms age, and why do these diseases rise exponentially with age? My laboratory aims to understand the molecular and cellular basis of aging in mammals.

- Judith Campisi, PhD

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Recent Publications

2014

Juan Carlos Sepúlveda, María Tomé... Manuel A González "Cell senescence abrogates the therapeutic potential of human mesenchymal stem cells in the lethal endotoxemia model." Stem Cells 32:7 1865-77
Claudio Franceschi, Judith Campisi... Judith Campisi "Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases." J. Gerontol. A Biol. Sci. Med. Sci. 69 Suppl 1 S4-9
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