title: Living in CIN: Mitotic Infidelity and Its Consequences for Tumor Promotion and Suppression.
abstract: Errors in chromosome segregation during mitosis have been recognized as a hallmark of tumor cells since the late 1800s, resulting in the long-standing hypothesis that mitotic abnormalities drive tumorigenesis. Recent work has shown that mitotic defects can promote tumors, suppress them, or do neither, depending on the rate of chromosome missegregation. Here we discuss the causes of chromosome missegregation, their effects on tumor initiation and progression, and the evidence that increasing the rate of chromosome missegregation may be an effective chemotherapeutic strategy.
authors.affiliation: Molecular and Cellular Pharmacology Training Program, University of Wisconsin-Madison, Madison, WI 53705, USA.
authors.forename: Laura C
authors.initials: LC
authors.lastname: Funk
authors.affiliation: Molecular and Cellular Pharmacology Training Program, University of Wisconsin-Madison, Madison, WI 53705, USA.
authors.forename: Lauren M
authors.initials: LM
authors.lastname: Zasadil
authors.affiliation: Department of Cell and Regenerative Biology, Carbone Cancer Center, University of Wisconsin-Madison, 1111 Highland Avenue, 6109 WIMR I, Madison, WI 53705-2275, USA. Electronic address: baweaver@wisc.edu.
authors.forename: Beth A
authors.initials: BA
authors.lastname: Weaver
mesh_terms: D000782:Aneuploidy; D000818:Animals; D063646:Carcinogenesis / Q000473:pathology; D043171:Chromosomal Instability; D006801:Humans; D008938:Mitosis; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D016159:Tumor Suppressor Protein p53
keywords: CIN; aneuploidy; chromosomal instability; mitosis; mitotic checkpoint; spindle assembly checkpoint