• Publications
  • Influence
Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor
A cell-nonautonomous mechanism by which p53 can restrain, and oncogenic RAS can promote, the development of age-related cancer by altering the tissue microenvironment is suggested. Expand
The senescence-associated secretory phenotype: the dark side of tumor suppression.
A senescence-associated secretory phenotype (SASP) is acquired that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression. Expand
Cellular senescence: when bad things happen to good cells
Understanding the causes and consequences of cellular senescence has provided novel insights into how cells react to stress, especially genotoxic stress, and how this cellular response can affect complex organismal processes such as the development of cancer and ageing. Expand
Persistent DNA damage signaling triggers senescence-associated inflammatory cytokine secretion
In addition to orchestrating cell-cycle checkpoints and DNA repair, a new and important role of the DDR is to allow damaged cells to communicate their compromised state to the surrounding tissue. Expand
Aging, cellular senescence, and cancer.
  • J. Campisi
  • Biology, Medicine
  • Annual review of physiology
  • 11 February 2013
The idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence is discussed. Expand
Four faces of cellular senescence
The challenge now is to understand the senescence response well enough to harness its benefits while suppressing its drawbacks. Expand
Senescent Cells, Tumor Suppression, and Organismal Aging: Good Citizens, Bad Neighbors
The senescence response may be antagonistically pleiotropic, promoting early-life survival by curtailing the development of cancer but eventually limiting longevity as dysfunctional senescent cells accumulate. Expand
Inflammatory networks during cellular senescence: causes and consequences.
The secreted factors that make up the proinflammatory phenotype of senescent cells are listed and the impact of these factors on tissue homeostasis is described and the cellular pathways/processes known to regulate this phenotype are summarized. Expand
Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases.
The session on inflammation of the Advances in Gerosciences meeting held at the National Institutes of Health/National Institute on Aging in Bethesda on October 30 and 31, 2013 was aimed at defining these important unanswered questions about inflammaging. Expand
Cellular senescence and the senescent secretory phenotype: therapeutic opportunities.
This work reviews the mechanisms that induce senescence and the SASP, their associations with chronic disease and frailty, therapeutic opportunities based on targeting senescent cells and the ASP, and potential paths to developing clinical interventions. Expand