Project description:We used Affymetrix GeneChipM-BM-. Human Exon 1.0 ST Arrays to identify alternative splicing events in 15 samples of PDAC compared to 6 non-tumor samples. Several commercial and open source software approaches for the analysis of differential splicing were tested and a subset of overlapping results was validated using RT-PCR and sequencing. Splicing variants could be validated in several genes closely related to cancer. Pathway analysis of genes predicted to be alternatively spliced revealed an enrichment of genes in categories closely related to cell-cell interactions and kinase activity. 15 samples of pancreatic ductal adenocarcinoma and 6 non tumor pancreatic samples were analyzed for alternative splicing events
Project description:To further development of our lncRNA and mRNA expression approach to pancreatic ductal adenocarcinoma(PDAC), we have employed lncRNA and mRNA microarray expression profiling as a discovery platform to identify lncRNA and mRNA expression in pancreatic ductal adenocarcinoma.Human pancreatic ductal adenocarcinoma tissues and normal pancreatic tissues from PDAC donors and other duodenum diseases donors. analyze mRNA and lncRNA expression in pancreatic ductal adenocarcinoma (PDAC) by microarray platform
Project description:To explore the potential involvement of circular RNAs (circRNAs) in pancreatic ductal adenocarcinoma (PDAC) oncogenesis, we conducted circRNA profiling in six pairs of human PDAC and adjacent normal tissue by microarray. Our results showed that clusters of circRNAs were aberrantly expressed in PDAC compared with normal samples, and provided potential targets for future treatment of PDAC and novel insights into PDAC biology. Analyze circular RNA expression in pancreatic ductal adenocarcinoma (PDAC) by microarray platform.
Project description:We studied the transcriptomics of pancreatic ductal adenocarcinoma (PDAC) and the role of a splicing factor called SF3B1 in this context. We generated mice that will develop PDAC via an inducible expression of KRASG12D; p53R172H specifically in the pancreas using a Ptf1a-Cre.
Project description:Pancreatic cancer (Pancreatic Ductal Adenocarcinoma; PDAC) is highly resistant to chemotherapy. Effective alternative therapies have yet to emerge, and therefore, chemotherapy remains the best available systematic treatment. The discovery of safe and available adjuncts that can improve chemotherapeutic efficacy could potentially improve survival outcomes. We show that a hyperglycemic state enhances the efficacy of conventional single- and multi-agent chemotherapies against PDAC. Molecular analyses of tumors exposed to relatively high glucose levels revealed that GCLC (catalytic subunit of glutamate-cysteine ligase), a key regulator of a metabolic pathway, glutathione biosynthesis, is diminished and underlies chemo-sensitization. Inhibition to GCLC phenocopied the effect of an induced hyperglycemic state in mouse models of PDAC, while rescuing the pathway abrogated the anti-tumor effects observed with chemotherapy treatment under high glucose conditions.
