title: Intrinsic tumour suppression.
abstract: Mutations that drive uncontrolled cell-cycle progression are requisite events in tumorigenesis. But evolution has installed in the proliferative programmes of mammalian cells a variety of innate tumour-suppressive mechanisms that trigger apoptosis or senescence, should proliferation become aberrant. These contingent processes rely on a series of sensors and transducers that act in a coordinated network to target the machinery responsible for apoptosis and cell-cycle arrest at different points. Although oncogenic mutations that disable such networks can have profound and varied effects on tumour evolution, they may leave intact latent tumour-suppressive potential that can be harnessed therapeutically.
authors.affiliation: Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA. lowe@cshl.edu
authors.forename: Scott W
authors.initials: SW
authors.lastname: Lowe
authors.forename: Enrique
authors.initials: E
authors.lastname: Cepero
authors.forename: Gerard
authors.initials: G
authors.lastname: Evan
mesh_terms: D000818:Animals; D017209:Apoptosis; D019008:Drug Resistance, Neoplasm; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000473:pathology*; D015513:Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D015513:Oncogene Proteins; D016159:Tumor Suppressor Protein p53