Résumé
Many cancer treating compounds used in chemotherapies the so called antimitotics target the mitotic spindle Spindle defects in turn trigger activation of the SAC (spindle assembly checkpoint) a surveillance mechanism that transiently arrests cells in mitosis to provide the time for error correction When the SAC is satisfied it is silenced However after a variable amount of time cells escape from the mitotic arrest even if the SAC is not satisfied through a process called adaptation or mitotic slippage Adaptation weakens the killing properties of antimitotics ultimately giving rise to resistant cancer cells We summarize here the mechanisms underlying this process and propose a strategy to identify the factors involved using budding yeast as a model system Inhibition of factors involved in SAC adaptation could have important therapeutic applications by potentiating the ability of antimitotics to cause cell death