Deletion of the MAD2L1 Spindle Assembly Checkpoint Gene Is Tolerated in Mouse Models of Acute T-Cell Lymphoma and Hepatocellular Carcinoma

    February 2017
    Floris Foijer, Lee A. Albacker, Björn Bakker, Diana C. J. Spierings, Ying Yue, Stephanie Z. Xie, Stephanie H. Davis, Annegret Lutum-Jehle, Darin Takemoto, Brian Hare, Brinley F. Furey, Roderick T. Bronson, Peter M. Lansdorp, Allan Bradley, Peter K. Sorger
    TLDR Deleting the MAD2L1 gene is tolerated in certain mouse cancer models.
    The study investigated the effects of deleting the MAD2L1 spindle assembly checkpoint gene in mouse models of acute T-cell lymphoma (T-ALL) and hepatocellular carcinoma (HCC). The researchers found that the deletion of MAD2L1 was tolerated in these models, leading to tissue-specific karyotypic changes and suggesting that the gene is not essential for the survival of these cancer cells. The findings highlighted the complexity of chromosomal instability (CIN) in cancer development and the importance of tissue-specific contexts, providing insights into the potential for targeting the spindle assembly checkpoint in cancer therapy. However, reviewers criticized the lack of novelty and overstated conclusions, recommending further exploration of the mechanisms driving tumorigenesis and the reasons for different tissue responses to MAD2 loss.
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