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Showing 1–6 of 6 results
Advanced filters: Author: Patrick G. Pilie Clear advanced filters

  • Genes encoding key epigenetic regulators, including Lysine Demethylase 6A (KDM6A), are frequently mutated in bladder cancer. Here, the authors show that loss of KDM6A promotes formation of extrachromosomal circular DNA (eccDNA), genomic instability, and metabolic reprogramming, driving resistance to cisplatin chemotherapy while simultaneously enhancing sensitivity to immune checkpoint inhibitors.

    • Pratishtha Singh
    • Ranit D’Rozario
    • Sangeeta Goswami
    ResearchOpen Access
    Nature Communications
    Volume: 17, P: 1-23

  • PBRM1, encoding for a subunit of the SWI/SNF complex, is the second most frequently mutated gene in clear cell renal cell carcinoma (ccRCC). Here, the authors show that PBRM1 loss reduces IFNγ-mediated signalling resulting in a less immunogenic tumor microenvironment and that PBRM1 mutations correlate with lack of response to checkpoint inhibitor therapy in ccRCC patients..

    • Xian-De Liu
    • Wen Kong
    • Eric Jonasch
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-14

  • Ataxia telangiectasia and Rad3-related protein serine/threonine kinase (ATR) is a mediator of the cellular replication stress response that, upon activation, initiates a cascade of coordinated reactions that ultimately enables DNA repair. This biological function makes ATR an attractive therapeutic target in cancers with elevated replication stress or DNA-repair deficiency. This Review discusses the currently available results from clinical trials testing ATR inhibitors as well as challenges and solutions in the development of this therapeutic class.

    • Natalie Y. L. Ngoi
    • Patrick G. Pilié
    • Timothy A. Yap
    Reviews
    Nature Reviews Clinical Oncology
    Volume: 21, P: 278-293

  • Inhibition of poly(ADP-ribose) polymerase (PARP) is the paradigmatic example of synthetic lethal therapy and is predicated on exploiting DNA repair deficiencies that are a hallmark of cancer. In this Review, the authors review the progress made to date with PARP inhibitors and describe the expanding landscape of novel anticancer therapies targeting the DNA damage response. Potential predictive biomarkers, mechanisms of resistance and combinatorial strategies are discussed.

    • Patrick G. Pilié
    • Chad Tang
    • Timothy A. Yap
    Reviews
    Nature Reviews Clinical Oncology
    Volume: 16, P: 81-104