Publications by authors named "Courtney D Dill"

Article Synopsis
  • Identified noncoding driver mutations in pancreatic ductal adenocarcinoma (PDAC) by mapping accessible chromatin regions and histone modifications in pancreatic cell lines and tissues, integrating this data with whole-genome mutations from 506 PDAC cases.
  • *From 3,614 noncoding somatic mutations (NCSMs) found, 178 were shown to significantly affect gene activity, highlighting their potential role in cancer progression.
  • *Further experiments pinpointed specific genes impacted by these mutations, with a focus on one gene (KLF9) that showed reduced expression due to interference from NCSMs, establishing it as a possible PDAC driver gene.
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The molecular mechanisms underlying chemoresistance in some newly diagnosed multiple myeloma (MM) patients receiving standard therapies (lenalidomide, bortezomib, and dexamethasone) are poorly understood. Identifying clinically relevant gene networks associated with death due to MM may uncover novel mechanisms, drug targets, and prognostic biomarkers to improve the treatment of the disease. This study used data from the MMRF CoMMpass RNA-seq dataset (N = 270) for weighted gene co-expression network analysis (WGCNA), which identified 21 modules of co-expressed genes.

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Background: Chronic lymphocytic leukemia (CLL) is an indolent heme malignancy characterized by the accumulation of CD5 CD19 B cells and episodes of relapse. The biological signaling that influence episodes of relapse in CLL are not fully described. Here, we identify gene networks associated with CLL relapse and survival risk.

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We aimed to identify triple-negative breast cancer (TNBC) drivers that regulate survival time as predictive signatures that improve TNBC prognostication. Breast cancer (BrCa) transcriptomic tumor biopsies were analyzed, identifying network communities enriched with TNBC-specific differentially expressed genes (DEGs) and correlated strongly to TNBC status. Two anticorrelated modules correlated strongly to TNBC subtype and survival.

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The tumor immune microenvironment (TIME) consists of multiple cell types that contribute to the heterogeneity and complexity of prostate cancer (PCa). In this study, we sought to understand the gene-expression signature of patients with primary prostate tumors by investigating the co-expression profiles of patient samples and their corresponding clinical outcomes, in particular "disease-free months" and "disease reoccurrence". We tested the hypothesis that the CXCL13-CXCR5 axis is co-expressed with factors supporting TIME and PCa progression.

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