RESUMEN
Background: Large-scale retrospective studies have identified implicit gender bias in citation behaviors across multiple medical fields. There are minimal resources to directly assess one's own citation behavior before publication at a laboratory level. In this study, we performed an internal audit of our own citation practices and behavior, looking at the representation of authors by gender in our own bibliographies. Methods: Bibliographies were collated from our laboratory's publications between 2015 and 2022 with a single senior author, who was excluded from participating in this study. Bibliographies were run through a simulation originally constructed and used by authors from the University of Pennsylvania that categorized authors of each article by gender: man or woman, according to external database records. Results: Of the 1697 citations, the first and last authorship sequences displayed to be 60.8% male/male, 10.1% male/female, 16.3% female/male and 12.8% female/female. Men-led articles within our laboratory cited 67.4% male/male articles in their bibliographies compared with women-led articles citing 53.9%. All laboratory bibliographies consisted of 77.1% male senior authors compared with 22.9% female senior authors. Conclusions: Our data confirm that a gender bias in citation practices exists at the laboratory level. Promisingly, these data also indicate that diversity within an individual laboratory group leads to diversity in representation; therefore, diversifying a team of researchers is prone to improve the overall work and success of the laboratory. We encourage laboratory groups to challenge their own biases by replicating their own results and discovering how these biases might be impacting their publications.
RESUMEN
Glioblastomas (GBMs) are highly aggressive, infiltrative, and heterogeneous brain tumors driven by complex driver mutations and glioma stem cells (GSCs). The neurodevelopmental transcription factors ASCL1 and OLIG2 are co-expressed in GBMs, but their role in regulating the heterogeneity and hierarchy of GBM tumor cells is unclear. Here, we show that oncogenic driver mutations lead to dysregulation of ASCL1 and OLIG2, which function redundantly to initiate brain tumor formation in a mouse model of GBM. Subsequently, the dynamic levels and reciprocal binding of ASCL1 and OLIG2 to each other and to downstream target genes then determine the cell types and degree of migration of tumor cells. Single-cell RNA sequencing (scRNA-seq) reveals that a high level of ASCL1 is key in defining GSCs by upregulating a collection of ribosomal protein, mitochondrial, neural stem cell (NSC), and cancer metastasis genes - all essential for sustaining the high proliferation, migration, and therapeutic resistance of GSCs.
