Background: Multiple myeloma (MM) is a cytogenetically and molecularly heterogeneous hematological malignancy that remains mostly incurable, despite recent therapeutic progress. Clonal evolution due to chromosomal instability (CIN) in MM is considered to be one of the major driving forces of disease progression and acquisition of treatment resistance; however, the mechanisms underlying CIN are unclear. Faithful chromosomal segregation is tightly regulated by the coordinated functions of a series of mitotic checkpoint proteins, while the failure of this process potentially causes acquisition of additional chromosomal abnormalities that

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