@entity5 formation is blocked by two barriers: replicative senescence and crisis. Senescence is triggered by short telomeres and is bypassed by disruption of @entity5 -suppressive pathways. After senescence bypass, cells undergo crisis, during which almost all of the cells in the population die. Cells that escape crisis harbour unstable genomes and other parameters of transformation. The mechanism of cell @entity204 during crisis remains unexplained. Here we show that @entity1 cells in crisis undergo spontaneous @entity1167 , resulting in @entity204 during mitosis or in the following cell cycle. This phenotype is induced by loss of @entity876 function, and is suppressed by telomerase overexpression. Telomere fusions triggered @entity1167 in @entity876 -compromised non-crisis cells, indicating that such fusions are the underlying cause of cell @entity204 . Exacerbation of mitotic @entity10205 by partial @entity7072 (also known as @entity7072 ) knockdown increased the ratio of cells that died during @entity1167 and sensitized @entity5 cells to mitotic poisons. We propose a crisis pathway wherein chromosome fusions induce @entity1167 , resulting in mitotic @entity10205 and cell @entity204 , thereby eliminating precancerous cells from the population.

Cell XXXX during crisis is mediated by mitotic @entity10205 .

@entity1 :: ('9606', 'Species') :: ['human'] @entity10205 :: ('MESH:C536801', 'Disease') :: ['telomere deprotection'] @entity7072 :: ('7014', 'Gene') :: ['TRF2', 'TERF2'] @entity5 :: ('MESH:D009369', 'Disease') :: ['Tumour', 'cancer', 'tumour'] @entity876 :: ('7157', 'Gene') :: ['p53'] @entity1167 :: ('MESH:D006323', 'Disease') :: ['mitotic arrest'] @entity204 :: ('MESH:D003643', 'Disease') :: ['death']
@entity204 :: (MESH:D003643,Disease) :: ['death']
