Project description:Immune checkpoint blockade (ICB)-based or natural cancer immune responses largely eliminate tumours but require additional mechanisms to arrest cancer cells that escape from cytotoxic immune responses. We show that cancer immune control needs, in addition to cytotoxicity, senescence-inducing cell cycle regulators.
Project description:Transcriptional profiling of mouse pancreatic cancer cells comparing Pdx-1Cre LSL-KrasG12D P53L/L cells with Pdx-1Cre LSL-KrasG12D KLF10L/L P53L/L cells, and to determine the effects of KLF10 deficiency on murine PDAC gene expression.
Project description:To identify differentially regulated genes between wild-type and Pak1 deficient human breast cancer cells, we performed a comparative gene profiling study by using human whole genome arrays.
Project description:To identify differentially regulated genes between wild-type and Pak1 deficient mouse breast cancer cells, we performed a comparative gene profiling study by using mouse whole genome arrays.
Project description:To identify differentially regulated genes between wild-type and Pak1 deficient mouse breast cancer cells, we performed a comparative gene profiling study by using mouse whole genome arrays. We compared the gene expression profiles of Her2 positive : Pak1 deficient cells vs Her2 positive : Pak1 wild type cells. All the experiments were performed in duplicate using tumor derived cells from two different tumors per group.
Project description:Chymotrypsin-like elastase 1 (CELA1) is a serine protease that is neutralized by alpha-1 antitrypsin (AAT) and prevents emphysema in a murine antisense oligonucleotide model of AAT-deficient emphysema. We tested the role of CELA1 in emphysema development in this genetic model of AAT-deficiency following tracheal lipopolysaccharide (LPS), 10 months of cigarette smoke (CS) exposure, aging, and a low-dose tracheal porcine pancreatic elastase (LD-PPE) model we developed. In this last model, we performed proteomic analysis to understand differences in lung protein composition. We were unable to show that AAT-deficient mice developed more emphysema than wild type with escalating doses of LPS.