Project description:Using two independently derived murine BXH2 cell lines, Ara-C resistant derivatives were developed by exposure to increasing concentrations of Ara-C. Microarray analysis comparing the Ara-C resistant cells to their Ara-C sensitive parental cell lines identified potential genes involved in Ara-C resistance. Two highly Ara-C-resistant cell lines, B117H and B140H, were derived from Ara-C-sensitive parental cell lines, B117P and B140P. Variations in gene expression between these Ara-C-resistant and -sensitive sets were studied. Three replicates per cell line.
Project description:To elucidate the epithelial cell diversity within the nasal inferior turbinates, a comprehensive investigation was conducted comparing control subjects to individuals with house dust mite-induced allergic rhinitis. This study aimed to delineate the differential expression profiles and phenotypic variations of epithelial cells in response to allergic rhinitis. This research elucidated distinct subpopulations and rare cell types of epithelial cells within the nasal turbinates, discerning alterations induced by allergic rhinitis. Furthermore, by interrogating transcriptomic signatures, the investigation provided novel insights into the cellular dynamics and immune responses underlying allergic rhinitis pathogenesis
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
Project description:To further characerize the arsenic trioxide (ATO) resistance in acutepromyelocytic leukemia, we had made NB4 cell line (arsenic sensitive) to be resistant to arsenic by exposing them to increasing concentration till they are resistant to it and we named it NB4-EV-AsR1. We have also used another cell line (UF1) which is by default resistant to arsenic. Comparing the GEP will give us novel pathways that can contirbute to arseic trioxide.
Project description:Previous and our results show that cells with mutant p53 are more sensitive to arsenic trioxide (ATO) induced cell growth inhibition. To explore the underling mechanisms, we conduct a detailed analysis of the globe transcriptional profiles of ATO regulated genes in breast, colon and lung cancer cells with different p53 status. We find p53 wild type cells are resistant to ATO induced globe dynamic transcriptional changes, thus resistant to ATO induced cell growth inhibition. P53 inhibitor PFTα releases p53 mediated transcriptional resistance and increases the sensitivity of ATO in p53 wild type tumor cells.
