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  • Title: Polyploid mitosis and depolyploidization promote chromosomal instability and tumor progression in a Notch-induced tumor model.
    Author: Wang XF, Yang SA, Gong S, Chang CH, Portilla JM, Chatterjee D, Irianto J, Bao H, Huang YC, Deng WM.
    Journal: Dev Cell; 2021 Jul 12; 56(13):1976-1988.e4. PubMed ID: 34146466.
    Abstract:
    Ploidy variation is a cancer hallmark and is frequently associated with poor prognosis in high-grade cancers. Using a Drosophila solid-tumor model where oncogenic Notch drives tumorigenesis in a transition-zone microenvironment in the salivary gland imaginal ring, we find that the tumor-initiating cells normally undergo endoreplication to become polyploid. Upregulation of Notch signaling, however, induces these polyploid transition-zone cells to re-enter mitosis and undergo tumorigenesis. Growth and progression of the transition-zone tumor are fueled by a combination of polyploid mitosis, endoreplication, and depolyploidization. Both polyploid mitosis and depolyploidization are error prone, resulting in chromosomal copy-number variation and polyaneuploidy. Comparative RNA-seq and epistasis analysis reveal that the DNA-damage response genes, also active during meiosis, are upregulated in these tumors and are required for the ploidy-reduction division. Together, these findings suggest that polyploidy and associated cell-cycle variants are critical for increased tumor-cell heterogeneity and genome instability during cancer progression.
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