Publications by authors named "Megan Siemann"
Article Synopsis
- Oncogenic mutations in and are key drivers of intraductal papillary mucinous neoplasms (IPMNs), which can lead to pancreatic cancer, and prior research showed that these mutations lead to cystic lesions in a specific mouse model.
- The study investigated how these mutations affect cell characteristics and gene expression using advanced transcriptional profiling techniques and CRISPR screens to find potential weaknesses in cells with these mutations.
- The findings revealed that co-expression of and led to a distinct gene signature and increased reliance on glycolysis, suggesting that targeting metabolic changes could be a promising strategy for treating or preventing IPMNs.
Tumors display rich cellular heterogeneity and typically consist of multiple co-existing clones with distinct genotypic and phenotypic characteristics. The acquisition of resistance to chemotherapy has been shown to contribute to the development of aggressive cancer traits, such as increased migration, invasion and stemness. It has been hypothesized that collective cellular behavior and cooperation of cancer cell populations may directly contribute to disease progression and lack of response to treatment.
View Article and Find Full Text PDFBackground & Aims: RNF43 is an E3 ubiquitin ligase that is recurrently mutated in pancreatic ductal adenocarcinoma (PDAC) and precursor cystic neoplasms of the pancreas. The impact of RNF43 mutations on PDAC is poorly understood and autochthonous models have not been characterized sufficiently. In this study, we describe a genetically engineered mouse model (GEMM) of PDAC with conditional expression of oncogenic Kras and deletion of the catalytic domain of Rnf43 in exocrine cells.
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