Intrinsic tumour suppression.
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.
Lowe
Scott W
SW
Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA. lowe@cshl.edu
Cepero
Enrique
E
Evan
Gerard
G
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
D015513:Oncogene Proteins; D016159:Tumor Suppressor Protein p53