Project description:RNA-sequencing was performed to determine the differences between cells that contain mutant p53 and a transactivation deficient mutant of p53 to determine why the TAD mutant cells don't form tumors.
Project description:To investigate the function of IL-23 and IL-22 on the intestinal epithelial cells, we analyzed the gene expression profiles in ileal and colonic epithelial cells of mice deficient in IL-23 and IL-22.
Project description:Transcriptional profiling was conducted on RNA from 23 breast cancer cell lines to identify genes whose expression level correlates with sensitivity of particular drug Keywords: comparison of sensitive group versus resistant group of cell lines to particular drug
Project description:Transcriptional profiling was conducted on RNA from 23 breast cancer cell lines to identify genes whose expression level correlates with sensitivity of particular drug Experiment Overall Design: Baseline gene expression profiling was performed using 23 breast cancer cell lines to identify genomic signatures highly correlated with in vitro sensitivity to a particular drug
Project description:We used microarrays to analyze the global expression patterns for 22 commercially available pancreatic cancer cell lines 22 pancreatic cancer cell lines were grown to 80% confluence in DMEM/FBS/PenStrep media and then harvested for total RNA
Project description:Analysis of mRNA profiles after MEK1/2 inhibition in human pancreatic cancer cell lines reveals pathways involved in drug sensitivity. We used microarrays to find gene expression patterns associated with drug response and also identified genes regulated by the MAP kinase pathway 22 pancreatic cell lines were grown in culture media containing serum and either treated with vehicle control or CI-1040 for 24 hours
Project description:We measured gene expression using RNA-sequencing for two cell lines (H-23 and H-358) parental and their sotorasib-resistant equivalent without treatment or treated with with G12C KRAS inhibitor sotorasib (AMG510)
Project description:Half of all human cancers lose p53 function by missense mutations, with an unknown fraction of these containing p53 in a self-aggregated, amyloid-like state. Here we show that a cell-penetrating peptide, ReACp53, designed to inhibit p53 amyloid formation, rescues p53 function in cancer cell lines and in organoids derived from high-grade serous ovarian carcinomas (HGSOC), an aggressive cancer characterized by ubiquitous p53 mutations. Rescued p53 behaves similarly to its wild-type counterpart in regulating target genes, reducing cell proliferation and increasing cell death. Intraperitoneal administration decreases tumor proliferation and shrinks xenografts in vivo. Our data show the effectiveness of targeting a specific aggregation defect of p53 and its potential applicability to HGSOCs.