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Velcrin molecular glues induce apoptosis in glioblastomas with high and expression.
Aquilanti E, Goldoni S, Baker A, et al. Velcrin molecular glues induce apoptosis in glioblastomas with high and expression. Neuro-oncology advances. 2024;6(1):vdae115. doi:10.1093/noajnl/vdae115DOIGoogle ScholarPubMed
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Multi-scale signaling and tumor evolution in high-grade gliomas.
Liu J, Cao S, Imbach KJ, et al. Multi-scale signaling and tumor evolution in high-grade gliomas. Cancer cell. 2024;42(7):1217-1238.e19. doi:10.1016/j.ccell.2024.06.004DOIGoogle ScholarPubMed
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Integrative spatial analysis reveals a multi-layered organization of glioblastoma.
Greenwald AC, Darnell NG, Hoefflin R, et al. Integrative spatial analysis reveals a multi-layered organization of glioblastoma. Cell. 2024. doi:10.1016/j.cell.2024.03.029DOIGoogle ScholarPubMed
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Layer-by-Layer Polymer Functionalization Improves Nanoparticle Penetration and Glioblastoma Targeting in the Brain.
Pickering AJ, Lamson NG, Marand MH, Hwang W, Straehla JP, Hammond PT. Layer-by-Layer Polymer Functionalization Improves Nanoparticle Penetration and Glioblastoma Targeting in the Brain. ACS nano. 2023;17(23):24154-24169. doi:10.1021/acsnano.3c09273DOIGoogle ScholarPubMed
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Antigen presentation deficiency, mesenchymal differentiation, and resistance to immunotherapy in the murine syngeneic CT2A tumor model.
Iorgulescu B, Ruthen N, Ahn R, et al. Antigen presentation deficiency, mesenchymal differentiation, and resistance to immunotherapy in the murine syngeneic CT2A tumor model. Frontiers in immunology. 2023;14:1297932. doi:10.3389/fimmu.2023.1297932DOIGoogle ScholarPubMed
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CTLA-4 blockade induces CD4 T cell IFNγ-driven microglial phagocytosis and anti-tumor function in glioblastoma.
Chen D, Varanasi SK, Hara T, et al. CTLA-4 blockade induces CD4 T cell IFNγ-driven microglial phagocytosis and anti-tumor function in glioblastoma. Immunity. 2023. doi:10.1016/j.immuni.2023.07.015DOIGoogle ScholarPubMed
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A comprehensive genomic study of 390 H3F3A-mutant pediatric and adult diffuse high-grade gliomas, CNS WHO grade 4.
Williams EA, Brastianos PK, Wakimoto H, et al. A comprehensive genomic study of 390 H3F3A-mutant pediatric and adult diffuse high-grade gliomas, CNS WHO grade 4. Acta neuropathologica. 2023. doi:10.1007/s00401-023-02609-6DOIGoogle ScholarPubMed
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CAR T cell killing requires the IFNγR pathway in solid but not liquid tumours.
Larson RC, Kann MC, Bailey SR, et al. CAR T cell killing requires the IFNγR pathway in solid but not liquid tumours. Nature. 2022;604(7906):563-570. doi:10.1038/s41586-022-04585-5DOIGoogle ScholarPubMed
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Analysis of chromatin accessibility uncovers TEAD1 as a regulator of migration in human glioblastoma.
Tome-Garcia J, Erfani P, Nudelman G, et al. Analysis of chromatin accessibility uncovers TEAD1 as a regulator of migration in human glioblastoma. Nat Commun. 2018;9(1):4020. doi:10.1038/s41467-018-06258-2DOIGoogle ScholarPubMed
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GABPβ1L Wakes Up TERT.
Rahme GJ, Gaskell E, Bernstein BE. GABPβ1L Wakes Up TERT. Cancer Cell. 2018;34(3):358-360. doi:10.1016/j.ccell.2018.08.011DOIGoogle ScholarPubMed
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In March of 2020, Broad Institute converted a clinical genetics processing lab into a large-scale COVID-19 testing facility in less than two weeks.

We've screened more than 1,275 cancer cell lines as part of the Cancer Dependency Map (DepMap).

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Through Broad's Scientists in the Classroom program, Broad researchers visit every 8th grade classroom in Cambridge each year to talk about genetics and evolution.

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In November 2022, Broad’s Genomics Platform sequenced its 500,000th whole human genome, a mere four years after sequencing its 100,000th.

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Working with Addgene, Broad Institute has shared CRISPR genome-editing reagents with researchers at more than 3,200 institutions in 76 countries.

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