Characterisation_of_checkpoint_deficient_tumours_to_identify_alterations_that_allow_survival_of_chromosomal_instable_cells. Characterisation_of_checkpoint_deficient_tumours_to_identify_alterations_that_allow_survival_of_chromosomal_instable_cells

Aneuploidy and chromsomal nistability are hallmarks of tumors. We have generated mouse models in which we can induce chromosomal instability by abrogating the sopindle checkpoint in a tissue of choice. In the T-cell compartment chromosomal instability dramatically accelerates p53-driven lymphomagenesis. We have generated a large cohort of chromosomal instable tumors. Whereas thse tumors are highly aneuploid and show whole chromosome abnormalities as expected as evidenced by aCGH, we also find focal amplifications and deletions, suggesting that whole chromosome instability coincided with structural chromosomal instability. As whole chromosomal instability is highly lethal to cells in tissue culture, we want top indentify genomic alterations that can explain the surcvival of these tumor cells in vivo.