A mechanism linking extra centrosomes to chromosomal instability (CIN) is described. Extra centrosomes promote chromosome missegregation during bipolar cell division by causing a transient 'multipolar spindle intermediate' in which merotelic kinetochore-microtubule attachments accumulate before centrosome clustering and anaphase. This leads to an increased frequency of lagging chromosomes and chromosome missegregation, contributing to CIN. The study shows that extra centrosomes are sufficient to cause chromosome missegregation even after centrosomes cluster into two poles. The findings suggest that extra centrosomes are a common cause of CIN in human cancer. The study also demonstrates that multipolar cell divisions are rare and that the progeny of such divisions are typically inviable. The presence of extra centrosomes correlates with an increased frequency of lagging chromosomes during anaphase. The study provides a direct mechanistic link between extra centrosomes and CIN, two common characteristics of solid tumors. The results suggest that the mechanism described may be a common underlying cause of CIN in human cancer. The study also shows that extra centrosomes can lead to chromosome missegregation even after centrosomes cluster into two poles. The study highlights the importance of understanding the mechanisms underlying CIN in cancer. The study also shows that extra centrosomes can lead to chromosome missegregation even after centrosomes cluster into two poles. The study provides a direct mechanistic link between extra centrosomes and CIN, two common characteristics of solid tumors. The results suggest that the mechanism described may be a common underlying cause of CIN in human cancer.A mechanism linking extra centrosomes to chromosomal instability (CIN) is described. Extra centrosomes promote chromosome missegregation during bipolar cell division by causing a transient 'multipolar spindle intermediate' in which merotelic kinetochore-microtubule attachments accumulate before centrosome clustering and anaphase. This leads to an increased frequency of lagging chromosomes and chromosome missegregation, contributing to CIN. The study shows that extra centrosomes are sufficient to cause chromosome missegregation even after centrosomes cluster into two poles. The findings suggest that extra centrosomes are a common cause of CIN in human cancer. The study also demonstrates that multipolar cell divisions are rare and that the progeny of such divisions are typically inviable. The presence of extra centrosomes correlates with an increased frequency of lagging chromosomes during anaphase. The study provides a direct mechanistic link between extra centrosomes and CIN, two common characteristics of solid tumors. The results suggest that the mechanism described may be a common underlying cause of CIN in human cancer. The study also shows that extra centrosomes can lead to chromosome missegregation even after centrosomes cluster into two poles. The study highlights the importance of understanding the mechanisms underlying CIN in cancer. The study also shows that extra centrosomes can lead to chromosome missegregation even after centrosomes cluster into two poles. The study provides a direct mechanistic link between extra centrosomes and CIN, two common characteristics of solid tumors. The results suggest that the mechanism described may be a common underlying cause of CIN in human cancer.