ACGH of Pancreatic Ductal Adenocarcinoma (PDAC) Cell Line and Xenografts
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE19852 | GEO | 2011/01/11
SECONDARY ACCESSION(S): PRJNA122125
REPOSITORIES: GEO
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Project description:PDAC tumor DNA hybridized against pooled normal genomic DNA DNA was extracted from tumor samples and hybridized against normal DNA in order to query copy number aberrations.
2011-01-11 | E-GEOD-19852 | biostudies-arrayexpress
Project description:Pancreatic adenocarcinoma (PDAC) is one of the most lethal human malignancies and a major health problem. Patient-derived xenografts (PDX) are appearing as a prime approach for preclinical studies despite being insufficiently characterized as a model of the human disease and its diversity. We generated subcutaneous PDX from PDAC samples obtained either surgically or using diagnostic biopsies (endoscopic ultrasound guided fine needle aspirate). The extensive multiomics characterization of the xenografts demonstrated that PDX is a suitable model for preclinical studies, representing the diversity of the primary cancers. We generated subcutaneous PDX from PDAC samples obtained either surgically or using diagnostic biopsies (endoscopic ultrasound guided fine needle aspirate). The variable 'MultiOmicsClassification' indicates the resulting sample's group. 'CIMPclass' is the CpG island methylator phenotype as estimated from the methylation arrays analysis. In this dataset, Illumina Infinium HumanCode-24 BeadChips SNP arrays were used to analyze the DNA xenografts samples from pancreatic ductal adenocarcinoma.
2017-12-12 | E-MTAB-5006 | biostudies-arrayexpress
Project description:Pancreatic adenocarcinoma (PDAC) is one of the most lethal human malignancies and a major health problem. Patient-derived xenografts (PDX) are appearing as a prime approach for preclinical studies despite being insufficiently characterized as a model of the human disease and its diversity. We generated subcutaneous PDX from PDAC samples obtained either surgically or using diagnostic biopsies (endoscopic ultrasound guided fine needle aspirate). The extensive multiomics characterization of the xenografts demonstrated that PDX is a suitable model for preclinical studies, representing the diversity of the primary cancers. the variable MultiOmicsClassification indicates the resulting sample's group. Whole-genome DNA methylation was analyzed using the Illumina Infinium HumanMethylation450 Beadchips. Integragen SA (Evry, France) carried out microarray experiments and hybridized to the BeadChip arrays following the manufacturer’s instructions. Illumina GenomeStudio software was used to extract the beta value DNA methylation score for each locus. We removed data from probes that contained SNPs or overlapped with a repetitive element that was not uniquely aligned to the human genome or regions of insertions and deletions in the human genome. The CpG Island Methylator Phenotype (CIMP) index was determined using methylation Illumina Infinium HumanMethylation450 BeadChips based on previous low throughput work (Toyota, 1999). In brief, all island CpG found to be unmethylated (<20% Beta-value) in all 25 normal pancreatic samples from the ICGC consortium (Nones, 2014) were selected. The CIMP index was calculated independently for each sample as the proportion of methylated (>30% Beta-value) CpGs among the selected normally unmethylated island CpG.
2017-12-12 | E-MTAB-5008 | biostudies-arrayexpress
Project description:Background/Aims: Microarray-based comparative genomic hybridisation (CGH) has allowed high-resolution analysis of DNA copy number alterations across the entire cancer genome. Recent advances in bioinformatics tools enable us to perform a robust and highly sensitive analysis of array CGH data and facilitate the discovery of novel cancer-related genes. Methods: We analysed a total of 29 pancreatic ductal adenocarcinoma (PDAC) samples (six cell lines and 23 microdissected tissue specimens) using 1 Mb-spaced CGH arrays. The transcript levels of all genes within the identified regions of genetic alterations were then screened using our Pancreatic Expression Database. Results: In addition to 238 high-level amplifications and 35 homozygous deletions, we identified 315 minimal common regions of “non-random” genetic alterations (115 gains and 200 losses) which were consistently observed across our tumour samples. The small size of these aberrations (median size of 880 kb) contributed to the reduced number of candidate genes included (on average 12 Ensembl-annotated genes). The database has further specified the genes whose expression levels are consistent with their copy number status. Such genes were UQCRB, SQLE, DDEF1, SLA, ERICH1 and DLC1, indicating that these may be potential target candidates within regions of aberrations. Conclusion: This study has revealed multiple novel regions that may indicate the locations of oncogenes or tumour suppressor genes in PDAC. Using the database, we provide a list of novel target genes whose altered DNA copy numbers could lead to significant changes in transcript levels in PDAC. (Harada et al. Pancreatology) Keywords: pancreatic ductal adenocarcinima, tissue microdissection, array CGH, genetic alterations A panel of 23 microdissected PDAC tissues and 6 PDAC-derived cell lines were analysed using Sanger's CGH arrays with 1 Mb resolution. Clinical info of the samples used is provided as a supplementary file.
2008-12-16 | E-GEOD-9672 | biostudies-arrayexpress
Project description:The aim of the study was to characterize a common molecular mechanism for paclitaxel resistance in Patu-T and Suit-2.028 PDAC cell lines. Despite the ATP-binding cassette (ABC) trasnsporters were already shown to be involved in various chemo-resistant forms of cancers but not in PDAC, the most likely impact of ABCB1 overexpression in PDAC cell models was taken into account in this dataset.
2024-01-26 | PXD040930 | Pride
Project description:Determine methylation pattern in PDAC a genome-wide analysis was performed in a cohort of 167 PDAC and 29 adjacent pancreatic tissues samples using the Infinium 450k methylation arrays (Illumina). 167 pancreatic tumors (PDAC) x 29 adjacent -non tumor samples.
2014-07-08 | E-GEOD-49149 | biostudies-arrayexpress
Project description:Gene expression analysis was performed on tumor-derived RNA from human PDAC xenograft to study the metabolic differences in the different PDAC subtypes
2021-12-31 | E-MTAB-10784 | biostudies-arrayexpress
Project description:The presence of some malignancies, such as cancer, impacts on peripheral blood mononuclear cells (PBMCs) gene expression profiling, suggesting the potential suitability of these genes as diagnostic and prognostic markers. The objective of this study was to identify new markers in peripheral blood that differentiate between PDAC patients and healthy controls as a means of facilitating early detection of the disease. 18 patients with unresectable PDAC were recruited. The diagnosis of PDAC was based on a positive biopsy of the pancreatic mass during the surgery. 18 gender, age, and habits matched healthy controls were also included. Whole genome cDNA microarray hybridization of PBMC samples was performed to identify potential PDAC markers.
2013-08-12 | E-GEOD-49641 | biostudies-arrayexpress
Project description:Determine methylation pattern in PDAC a genome-wide analysis was performed in a cohort of 167 PDAC and 29 adjacent pancreatic tissues samples using the Infinium 450k methylation arrays (Illumina).
2014-07-08 | GSE49149 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) has one of the worst survival rates of all cancers. ANO1 (TMEM16A) is a recently identified Ca(2+)-activated Cl(-) channel (CaCC) that is upregulated in several tumors. Although ANO1 was subject to extensive studies in the recent years, its pathophysiological function has only been poorly understood. The aim of the present study is to establish the significance of ANO1 in PDAC behavior and demarcate its roles in PDAC from those of the volume-regulated anion channel (VRAC). We performed qPCR and Western blot measurements on different PDAC cell lines (Panc-1, Mia PaCa 2, Capan-1, AsPC-1, BxPC-3) and compared the results to those obtained in a human pancreatic ductal epithelium (HPDE) cell line. All cancer cell lines showed an upregulation of ANO1 on mRNA and protein levels. Whole-cell patch-clamp recordings identified large Ca(2+) and voltage-dependent Cl(-) currents in PDAC cells. Using siRNA knockdown of ANO1 and three ANO1 inhibitors (T16Ainh-A01, CaCCinh-A01, and NS3728), we found that ANO1 is the main constituent of CaCC current in PDAC cells. We further characterized these three inhibitors and found that they had unspecific effects on the free intracellular calcium concentration. Functional studies on PDAC behavior showed that surprisingly inhibition of ANO1 did not influence cellular proliferation. On the other hand, we found ANO1 channel to be pivotal in PDAC cell migration as assessed in wound healing experiments.
| S-EPMC4464647 | biostudies-literature