6 research outputs found

    Improving Access and Discovery of LGBTQIA+ Materials Across Collection Services Workflows

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    Archival descriptive practices have traditionally obfuscated the existence of or excluded entirely the experiences of LGBTQIA+ people. The development of reparative archival description practices compels archivists to reassess how best to elevate the voices of queer creators and subjects within their collections. In addition, the development of LGBTQIA+ community-generated resources allow archivists to more easily understand and implement the perspectives of queer communities to make archival resources more accessible to and discoverable by those communities. This article will discuss how a special collections library is improving the accessibility of their holdings relating to LGBTQIA+ histories by: 1) auditing archival description to identify outdated description and archival silences; 2) reviewing and revising language which obscured LGBTQIA+ relationships; and 3) developing description at the point of accession that highlights queer histories, relationships, and individuals in order to make LGBTQIA materials more accessible to their communities

    Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma

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    Medulloblastoma is a highly malignant paediatric brain tumour currently treated with a combination of surgery, radiation and chemotherapy, posing a considerable burden of toxicity to the developing child. Genomics has illuminated the extensive intertumoral heterogeneity of medulloblastoma, identifying four distinct molecular subgroups. Group 3 and group 4 subgroup medulloblastomas account for most paediatric cases; yet, oncogenic drivers for these subtypes remain largely unidentified. Here we describe a series of prevalent, highly disparate genomic structural variants, restricted to groups 3 and 4, resulting in specific and mutually exclusive activation of the growth factor independent 1 family proto-oncogenes, GFI1 and GFI1B. Somatic structural variants juxtapose GFI1 or GFI1B coding sequences proximal to active enhancer elements, including super-enhancers, instigating oncogenic activity. Our results, supported by evidence from mouse models, identify GFI1 and GFI1B as prominent medulloblastoma oncogenes and implicate 'enhancer hijacking' as an efficient mechanism driving oncogene activation in a childhood cancer
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