Jean Albrengues,Mario A. Shields,David Ng,Chun Gwon Park,Alexandra Ambrico,Morgan E. Poindexter,Priya Upadhyay,Dale Uyeminami,Arnaud Pommier,Victoria Küttner,Emilis Bružas,Laura Maiorino,Carmelita Bautista,Ellese M. Carmona,Phyllis A. Gimotty,Douglas T. Fearon,Kenneth Chang,Scott K. Lyons,Kent E. Pinkerton,Lloyd C. Trotman,Michael S. Goldberg,Johannes T.‐H. Yeh,Mikala Egeblad
出处
期刊:Science [American Association for the Advancement of Science (AAAS)] 日期:2018-09-28卷期号:361 (6409)被引量:1077
Waking up in a trap Cancer patients who have undergone successful treatment can experience relapse of their disease years or even decades later. This is because cancer cells that have disseminated beyond the primary tumor site enter a state of dormancy, where they remain viable but not proliferating. Eventually, by mechanisms that are poorly understood, these clinically undetectable cells “wake up” and form actively growing metastases. Studying mouse models, Albrengues et al. found that sustained lung inflammation and the accompanying formation of neutrophil extracellular traps (NETs) could convert dormant cancer cells to aggressive lung metastases (see the Perspective by Aguirre-Ghiso). Awakening of these cells was associated with NET-mediated remodeling of the extracellular matrix and could be prevented by an antibody against the remodeled version of a matrix protein called laminin-111. Science , this issue p. eaao4227 ; see also p. 1314