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Showing 1–6 of 6 results
Advanced filters: Author: Ariella B. Hanker Clear advanced filters

  • CDK4/6 inhibitors have improved outcomes for patients with ER+ breast cancer, however, those with loss of RB1 function often fail to respond. Here, the authors identify a vulnerability of ER + /RB1- breast cancer on PRMT5 and via dual blockade of ER and PRMT5 therapeutically target this in patient-derived xenograft models.

    • Chang-Ching Lin
    • Tsung-Cheng Chang
    • Carlos L. Arteaga
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-16

  • The 17q23 amplicon is associated with poor outcome in ER+ breast cancers, but the causal genes responsible endocrine resistance in this region are unclear. In this study, the authors demonstrate that PRR11 located at 17q23, is critical for conferring endocrine resistance through activation of PI3K signalling and therefore propose PI3K inhibition as a treatment for PRR11-amplified breast cancers.

    • Kyung-min Lee
    • Angel L. Guerrero-Zotano
    • Carlos L. Arteaga
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-15

  • Spacia is a multiple-instance learning model for cell–cell communication (CCC) interference in single-cell resolution spatially resolved transcriptomics data. Spacia can map complex CCCs by modeling cell proximity and CCC-driven gene perturbation.

    • James Zhu
    • Yunguan Wang
    • Tao Wang
    Research
    Nature Methods
    Volume: 21, P: 1830-1842

  • Kornelia Polyak, Franziska Michor and colleagues report a novel method, STAR-FISH, for combined in situ single-cell analysis of point mutations and copy number alterations in archived tissue samples. They apply STAR-FISH to clinically relevant PIK3CA mutations and HER2 amplifications and observe associations between intratumoral diversity and clinical outcome.

    • Michalina Janiszewska
    • Lin Liu
    • Kornelia Polyak
    Research
    Nature Genetics
    Volume: 47, P: 1212-1219

  • Era+ breast cancer patients often develop resistance to endocrine therapy. Here, the authors show that FGFR1 amplification is a resistance mechanism to CDK4/6 inhibitor and endocrine therapy and that combined treatment with FGFR, CDK4/6, and anti-estrogens is a potential therapeutic strategy in Era+ breast cancer tumors.

    • Luigi Formisano
    • Yao Lu
    • Carlos L. Arteaga
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-14