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XB-ART-56459
Cell Rep 2018 May 29;239:2758-2769. doi: 10.1016/j.celrep.2018.04.102.
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Identification of Drivers of Aneuploidy in Breast Tumors.

Pfister K , Pipka JL , Chiang C , Liu Y , Clark RA , Keller R , Skoglund P , Guertin MJ , Hall IM , Stukenberg PT .


Abstract
Although aneuploidy is found in the majority of tumors, the degree of aneuploidy varies widely. It is unclear how cancer cells become aneuploid or how highly aneuploid tumors are different from those of more normal ploidy. We developed a simple computational method that measures the degree of aneuploidy or structural rearrangements of large chromosome regions of 522 human breast tumors from The Cancer Genome Atlas (TCGA). Highly aneuploid tumors overexpress activators of mitotic transcription and the genes encoding proteins that segregate chromosomes. Overexpression of three mitotic transcriptional regulators, E2F1, MYBL2, and FOXM1, is sufficient to increase the rate of lagging anaphase chromosomes in a non-transformed vertebrate tissue, demonstrating that this event can initiate aneuploidy. Highly aneuploid human breast tumors are also enriched in TP53 mutations. TP53 mutations co-associate with the overexpression of mitotic transcriptional activators, suggesting that these events work together to provide fitness to breast tumors.

PubMed ID: 29847804
PMC ID: PMC5997284
Article link: Cell Rep
Grant support: [+]

Species referenced: Xenopus
Genes referenced: e2f1 foxm1 h2bc21 kcnip3 mybl2 tp53

Disease Ontology terms: breast cancer

Article Images: [+] show captions
References [+] :
Bakhoum, Deviant kinetochore microtubule dynamics underlie chromosomal instability. 2009, Pubmed