Publications by authors named "Christopher D Delaney"
Understanding how cellular pathways interact is crucial for treating complex diseases like cancer, yet our ability to map these connections systematically remains limited. Individual gene-gene interaction studies have provided insights , but they miss the emergent properties of pathways working together. To address this challenge, we developed a multi-gene approach to pathway mapping and applied it to CRISPR data from the Cancer Dependency Map .
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- Epigenetic dysregulation is linked to various cancers, particularly leukemias, and the study explores the role of Tudor domains in leukemia progression and treatment.
- Researchers used a CRISPR screen to find SGF29, a vital part of acetyltransferase complexes, which is important for gene expression and the development of leukemia.
- The study introduced a new strategy called CRISPR-SADD for drug discovery, helping to identify a promising inhibitor that targets SGF29's Tudor domain and shows effectiveness against leukemia, suggesting broad applicability for future drug development.
Identification of novel functional domains and characterization of detailed regulatory mechanisms in cancer-driving genes is critical for advanced cancer therapy. To date, CRISPR gene editing has primarily been applied to defining the role of individual genes. Recently, high-density mutagenesis via CRISPR tiling of gene-coding exons has been demonstrated to identify functional regions in genes.
View Article and Find Full Text PDFThere is a growing realization that endodontic infections are often polymicrobial, and may contain spp. Despite this understanding, the development of new endodontic irrigants and models of pathogenesis remains limited to mono-species biofilm models and is bacterially focused. The purpose of this study was to develop and optimize an interkingdom biofilm model of endodontic infection and use this to test suitable anti-biofilm actives.
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- MLL/SET methyltransferases, crucial for development and cancer, particularly influence histone 3 lysine 4 methylation; SETD1A is essential for the survival of acute myeloid leukemia (AML) cells.
- Research indicates that the enzymatic function of the SET domain isn't needed for AML cell survival; instead, a newly identified "FLOS" domain is vital.
- Disrupting the FLOS domain impairs DNA damage response genes and triggers p53-dependent apoptosis, suggesting that targeting SETD1A and cyclin K complexes could be a potential treatment for AML and other cancers.