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. 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. Selected Publications: 1: Wiley CD, Campisi J. From Ancient Pathways to Aging Cells-Connecting Metabolism and Cellular Senescence. Cell Metab. 2016 Jun 14;23(6):1013-21. 2: Wiley CD, Velarde MC, Lecot P, Liu S, Sarnoski EA, Freund A, Shirakawa K, Lim HW, Davis SS, Ramanathan A, Gerencser AA, Verdin E, Campisi J. Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype. Cell Metab. 2016 Feb 9;23(2):303-14. 3: Laberge RM, Sun Y, Orjalo AV, Patil CK, Freund A, Zhou L, Curran SC, Davalos AR, Wilson-Edell KA, Liu S, Limbad C, Demaria M, Li P, Hubbard GB, Ikeno Y, Javors M, Desprez PY, Benz CC, Kapahi P, Nelson PS, Campisi J. MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation. Nat Cell Biol. 2015 Aug;17(8):1049-61. 4: Demaria M, Ohtani N, Youssef SA, Rodier F, Toussaint W, Mitchell JR, Laberge RM, Vijg J, Van Steeg H, Dollé ME, Hoeijmakers JH, de Bruin A, Hara E, Campisi J. An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA. Dev Cell. 2014 Dec 22;31(6):722-33. 5: Campisi J. Cell biology: The beginning of the end. Nature. 2014 Jan 2;505(7481):35-6. 6: Campisi J. Aging, cellular senescence, and cancer. Annu Rev Physiol. 2013;75:685-705. 7: Campisi J. Parsing p53 Transactivation. Dev Cell. 2011 May 17;20(5):573-4. 8: Campisi J. Cellular senescence: putting the paradoxes in perspective. Curr Opin Genet Dev. 2011 Feb;21(1):107-12. 9: Rodier F, Coppé JP, Patil CK, Hoeijmakers WA, Muñoz DP, Raza SR, Freund A, Campeau E, Davalos AR, Campisi J. Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion. Nat Cell Biol. 2009 Aug;11(8):973-9. 10: Vijg J, Campisi J. Puzzles, promises and a cure for ageing. Nature. 2008 Aug 28;454(7208):1065-71. 11: Campisi J, d'Adda di Fagagna F. Cellular senescence: when bad things happen to good cells. Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40. Review. 12: Yaswen P, Campisi J. Oncogene-induced senescence pathways weave an intricate tapestry. Cell. 2007 Jan 26;128(2):233-4. Review. 13: Beausejour CM, Campisi J. Ageing: balancing regeneration and cancer. Nature. 2006 Sep 28;443(7110):404-5. 14: Campisi J. Suppressing cancer: the importance of being senescent. Science. 2005 Aug 5;309(5736):886-7. 15: Campisi J. Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell. 2005 Feb 25;120(4):513-22. Review. 16: Campisi J. Fragile fugue: p53 in aging, cancer and IGF signaling. Nat Med. 2004 Mar;10(3):231-2. 17: Parrinello S, Samper E, Krtolica A, Goldstein J, Melov S, Campisi J. Oxygen sensitivity severely limits the replicative lifespan of murine fibroblasts. Nat Cell Biol. 2003 Aug;5(8):741-7. 18: Campisi J. Cancer and ageing: rival demons? Nat Rev Cancer. 2003 May;3(5):339-49. Review.