Making young tumors old: a new weapon against cancer?
As the population of industrial nations ages, the incidence of cancer and cancer mortality is increasing. Intuitively, older organisms may be less able to cope with accumulated damage and thus be more prone to develop cancer. However, so far, the links between aging and cancer have been only partially explored. Strikingly, four recent studies now indicate that premature senescence accompanied by cell cycle arrest occurs in tumors initiated by an oncogenic mutation. Thus, senescence may act as a key tumor suppressor mechanism in young tumors in vivo.
Sage
Julien
J
Stanford University School of Medicine, CA 94305, USA. julsage@stanford.edu
D000818:Animals; D016922:Cellular Senescence / Q000235:genetics*; D018450:Disease Progression; D005819:Genetic Markers; D006801:Humans; D008223:Lymphoma / Q000235:genetics; D008297:Male; D051379:Mice; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy / Q000235:genetics*; D009506:Nevus / Q000235:genetics; D009857:Oncogenes / Q000502:physiology; D011230:Precancerous Conditions / Q000235:genetics; D011471:Prostatic Neoplasms / Q000378:metabolism / Q000473:pathology; D012878:Skin Neoplasms / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D005819:Genetic Markers; D016159:Tumor Suppressor Protein p53