Judith Campisi

Judith Campisi PhD

Judith Campisi received a PhD in biochemistry from the State University of New York at Stony Brook and completed her postdoctoral training in cell cycle regulation at the Dana-Farber Cancer Institute and Harvard Medical School. As an assistant and associate professor at the Boston University Medical School, she studied the role of cellular senescence in suppressing cancer and soon became convinced that senescent cells also contributed to aging. She joined 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, Dr Campisi established a broad program to understand the relationship between aging and age-related disease, with an emphasis on the interface between cancer and aging.

Dr Campisi has received numerous awards for her research, including two MERIT awards from the National Institute on Aging and awards from the AlliedSignal Corporation, Gerontological Society of America, and American Federation for Aging Research. She is a recipient of the Longevity prize from the IPSEN Foundation, the Bennett Cohen award from the University of Michigan, and the Schober award from Halle University, and she is the first recipient of the international Olav Thon Foundation prize in Natural Sciences and Medicine.

Dr Campisi currently serves on advisory committees for the Alliance for Aging Research, Progeria Research Foundation, and NIA’s Intervention Testing Program.


Curing the Incurable

Jack Kreindler & Parker Moss

The current status quo for the treatment of cancer is based on old data … which is not even captured from the vast majority of patients.  Cancers are also heterogeneous and rapidly evolving diseases. How can we shift cancer research and treatment to one of real world, continuous learning, enabled through layers of human and artificial intelligence, not buried deep in journals but available in real-time within the next generation of clinical user interfaces? 

At Exponential Medicine 2018, Dr. Jack Kreindler led an exploration of the topic with Parker Moss. Kreindler and Parker are helping build the United Kingdom’s SMART Grid for Cancer (S.ystems M.edicine and A.I with next gen R.andomized T.rials) to not only treat but truly study patients with currently incurable disease, to accelerate learning and democratize cures.

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The hallmarks of aging

Excerpt

Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution.

This review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects.

At first sight, cancer and aging may seem to be opposite processes: cancer is the consequence of an aberrant gain of cellular fitness, whereas aging is characterized by a loss of fitness. At a deeper level, however, cancer and aging share common origins. The time-dependent accumulation of cellular damage is widely considered to be the general cause of aging. Concomitantly, cellular damage may occasionally provide aberrant advantages to certain cells, which can eventually produce cancer. Therefore, cancer and aging can be regarded as two different manifestations of the same underlying process — namely, the accumulation of cellular damage. In addition, several of the pathologies associated with aging, such as atherosclerosis and inflammation, involve uncontrolled cellular overgrowth or hyperactivity.

Based on this conceptual framework, several critical questions have arisen in the field of aging regarding the physiological sources of aging-causing damage, the compensatory responses that try to re-establish homeostasis, the interconnection between the different types of damage and compensatory responses, and the possibilities to intervene exogenously to delay aging. We propose nine candidate hallmarks that are generally considered to contribute to the aging process and together determine the aging phenotype. Each hallmark should ideally fulfill the following criteria: (1) it should manifest during normal aging; (2) its experimental aggravation should accelerate aging; and (3) its experimental amelioration should retard the normal aging process and hence increase healthy lifespan.

FULL TEXT: Cell