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Rare gene deletions in genetic generalized and Rolandic epilepsies.
Jabbari K, Bobbili DR, Lal D, et al. Rare gene deletions in genetic generalized and Rolandic epilepsies. PLoS One. 2018;13(8):e0202022. doi:10.1371/journal.pone.0202022DOIGoogle ScholarPubMed
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Complex and Dynamic Chromosomal Rearrangements in a Family With Seemingly Non-Mendelian Inheritance of Dopa-Responsive Dystonia.
Lohmann K, Redin C, Tönnies H, et al. Complex and Dynamic Chromosomal Rearrangements in a Family With Seemingly Non-Mendelian Inheritance of Dopa-Responsive Dystonia. JAMA Neurol. 2017;74(7):806-812. doi:10.1001/jamaneurol.2017.0666DOIGoogle ScholarPubMed
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Genomic and Functional Approaches to Understanding Cancer Aneuploidy.
Taylor AM, Shih J, Ha G, et al. Genomic and Functional Approaches to Understanding Cancer Aneuploidy. Cancer Cell. 2018;33(4):676-689.e3. doi:10.1016/j.ccell.2018.03.007DOIGoogle ScholarPubMed
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Heterogeneous contribution of microdeletions in the development of common generalised and focal epilepsies.
Pérez-Palma E, Helbig I, Klein KM, et al. Heterogeneous contribution of microdeletions in the development of common generalised and focal epilepsies. J Med Genet. 2017;54(9):598-606. doi:10.1136/jmedgenet-2016-104495DOIGoogle ScholarPubMed
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Kctd13 deletion reduces synaptic transmission via increased RhoA.
Escamilla CO, Filonova I, Walker AK, et al. Kctd13 deletion reduces synaptic transmission via increased RhoA. Nature. 2017;551(7679):227-231. doi:10.1038/nature24470DOIGoogle ScholarPubMed
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KANSL1 variation is not a major contributing factor in self-limited focal epilepsy syndromes of childhood.
Myers KA, McGlade A, Neubauer BA, et al. KANSL1 variation is not a major contributing factor in self-limited focal epilepsy syndromes of childhood. PLoS One. 2018;13(1):e0191546. doi:10.1371/journal.pone.0191546DOIGoogle ScholarPubMed
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Proteogenomics connects somatic mutations to signalling in breast cancer.
Mertins P, Mani DR, Ruggles KV, et al. Proteogenomics connects somatic mutations to signalling in breast cancer. Nature. 2016;534(7605):55-62. doi:10.1038/nature18003DOIGoogle ScholarPubMed
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Multiple mechanisms disrupt the let-7 microRNA family in neuroblastoma.
Powers JT, Tsanov KM, Pearson DS, et al. Multiple mechanisms disrupt the let-7 microRNA family in neuroblastoma. Nature. 2016;535(7611):246-51. doi:10.1038/nature18632DOIGoogle ScholarPubMed
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An erythroid differentiation signature predicts response to lenalidomide in myelodysplastic syndrome.
Ebert BL, Galili N, Tamayo P, et al. An erythroid differentiation signature predicts response to lenalidomide in myelodysplastic syndrome. PLoS Med. 2008;5(2):e35. doi:10.1371/journal.pmed.0050035DOIGoogle ScholarPubMed
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Allelotype analysis of mouse lung carcinomas reveals frequent allelic losses on chromosome 4 and an association between allelic imbalances on chromosome 6 and K-ras activation.
Hegi ME, Devereux TR, Dietrich WF, et al. Allelotype analysis of mouse lung carcinomas reveals frequent allelic losses on chromosome 4 and an association between allelic imbalances on chromosome 6 and K-ras activation. Cancer Res. 1994;54(23):6257-64.Google 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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