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Showing 1–9 of 9 results
Advanced filters: Author: Benjamin Ellezam Clear advanced filters

  • Osteosarcomas (OS) are aggressive bone tumors which have no actionable recurrent driver mutations. Here the authors identify aberrant expression of EZHIP in a subset of OS patients as an oncogenic driver, which exhibits vulnerability to epigenetic therapies.

    • Wajih Jawhar
    • Geoffroy Danieau
    • Livia Garzia
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-17

  • Lysine27-to-methionine mutations in histone H3 genes (H3K27M) occur in a subgroup of gliomas and decrease genome-wide H3K27 trimethylation. Here the authors utilise primary H3K27M tumour lines and isogenic CRISPR-edited controls and show that H3K27M induces defective chromatin spread of PRC2-mediated repressive H3K27me2/me3.

    • Ashot S. Harutyunyan
    • Brian Krug
    • Jacek Majewski
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-13

  • Histone H3-mutant gliomas are deadly brain tumours and the tumour microenvironment is not fully understood. Here the authors profile the immune microenvironment from human samples and mouse models and implicate myeloid cells in immune suppression and show inhibition of myeloid cells and checkpoint blockade demonstrates therapeutic benefits in mice.

    • Augusto Faria Andrade
    • Alva Annett
    • Nada Jabado
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-17

  • A single-cell transcriptomic atlas from embryonal pons and forebrain provides insights into the developmental origins of pediatric brain tumors. The study identifies impaired differentiation of specific neural progenitors as a common mechanism underlying these cancers.

    • Selin Jessa
    • Alexis Blanchet-Cohen
    • Claudia L. Kleinman
    Research
    Nature Genetics
    Volume: 51, P: 1702-1713

  • Diffuse Intrinsic Pontine Gliomas are diagnosed by sampling a small portion of the tumour. Here, using multiple samples from tumours, the authors analyse the spatial and temporal distribution of driver mutations revealing that H3K27M mutations arise first in tumorigenesis followed by a specific invariable sequence of driver mutations, which are homogeneously distributed across the tumour mass.

    • Hamid Nikbakht
    • Eshini Panditharatna
    • Javad Nazarian
    ResearchOpen Access
    Nature Communications
    Volume: 7, P: 1-8