Project description:Interventions: experimental group :PD-1 Knockout Engineered T Cells
Primary outcome(s): Number of participants with Adverse Events and/or Dose Limiting Toxicities as a Measure of Safety and tolerability of dose of PD-1 Knockout T cells using Common Terminology Criteria for Adverse Events (CTCAE v4.0) in patients
Study Design: historical control
Project description:To identify ARID1A-regulated genes in stomach cancer, we performed microarray profiling of RNA isolated from N87 stomach cancer cells, in which ARID1A expression was knocked down by two different siRNAs against ARID1A.
Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. Next-generation sequencing analysis was performed in control and ARID1A knockout MDA-MB-231 cells to investigate global gene expression changes.
Project description:mRNA-seq for HCT116 Parental and ARID1A knockdown cells, mRNA-seq for DLD1 Parental, ARID1A knockdown and ARID1A knockout cells, mRNA-seq for COLO320DM Parental and ARID1A knockdown and ARID1A knockout cells
Project description:A nonsense mutation in ARID1A was identified by next generation sequencing in non-dysplastic Barrett's esophagus [BE] tissue and esophageal adenocarcinoma [EAC] tissue of a patient diagnosed with EAC. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50), and 12.2% (12/98) of normal squamous epithelium, BE, low-, high-grade dysplasia, and EAC tissues, respectively. Enhanced cell growth, proliferation and invasion were observed upon ARID1A knockdown in EAC cells. ARID1A was knocked down in OE33 cells (Sample MS_1 and MS_3) using on-TARGET smartpool ARID1A siRNA. At the same time, OE33 cells were transfected with a non-targeting siRNA, and these experiments (Samples MS_2 and MS_4) functioned as mock controls. Cells were harvested after 48 hours and total RNA was extracted using the Rneasy kit (Qiagen) Aim Affymetrix Human PrimeView Gene Expression Array : to determine the downstream effectors of ARID1A that are likely to contribute to the oncogenic phenotype caused by ARID1A down-regulation. Two biological replicates of each condition (2x ARID1A knockdown, and 2x Mock) were used for the microarray experiment.
Project description:The study identifies genes that are regulated by the loss of the chromatin remodeller subunit ARID1A in colorectal cancer cell lines. This gene is frequently mutated in colorectal cancer.
Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. To investigate global chromatin remodeling, we performed ATAC–seq in ARID1A knockout and control MDA-MB-231 cells.
Project description:To investigate that ARID1A regulates transcription of genes encoding components of the GSH synthesis pathway, a genome-wide expression analysis of a panel of ARID1A-proficient and ARID1A-deficient cancer cells was performed.
Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. To explore global transcriptional activity, we performed chromatin immunoprecipitation followed by high-throughput sequencing (ChIP–seq) to investigate H3K4me3 histone modification of ARID1A knockout and control MDA-MB-231 cells.