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Gene expression-subcuteneous right CFPAC-1 tumor (human pancreatic ductal adenocarcinoma (PDAC) line) in humanized mice

ABSTRACT: Immunotherapy outcome prediction classifiers were successfully constructed through expression profiling of a total of 594 genes in PDAC right tumors from humanized mice treated with immunotherapy

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE167113 | GEO | 2021/02/20

REPOSITORIES: GEO

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Gene expression-subcuteneous right CFPAC-1 tumor (human pancreatic ductal adenocarcinoma (PDAC) line) in humanized mice

Project description:Gene expression-subcuteneous right CFPAC-1 tumor (human pancreatic ductal adenocarcinoma (PDAC) line) in humanized mice

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A Study of ELI-002 in Subjects With KRAS Mutated Pancreatic Ductal Adenocarcinoma (PDAC) and Other Solid Tumors

Project description:This is a Phase 1 study to assess the safety and efficacy of ELI-002 immunotherapy (a lipid-conjugated immune-stimulatory oligonucleotide [Amph-CpG-7909] plus a mixture of lipid-conjugated peptide-based antigens [Amph-Peptides]) as adjuvant treatment of minimal residual disease (MRD) in subjects with KRAS/neuroblastoma ras viral oncogene homolog (NRAS) mutated PDAC or other solid tumors.

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Genome-wide DNA methylation patterns in pancreatic ductal adenocarcinoma (PDAC)

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Human Pancreatic Ductal Adenocarcinoma (PDAC), LC-MS/MS

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Expression data from peripheral blood in pancreatic ductal adenocarcinoma (PDAC) patients

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

Expression profiling of pancreatic ductal adenocarcinoma

Project description:Pancreatic ductal adenocarcinoma (PDAC) has the worst prognosis of all common cancers, but divergent outcomes are apparent between patients. To delineate the intertumor heterogeneity that contributes to this, we aimed to identify clinically distinct gene expression-based subgroups. From a cohort of 345 resected pancreatic cancer cases, 90 samples with confirmed diagnosis of PDAC and sufficient tumor content were available for gene expression analysis by RNA sequencing. Unsupervised classification was applied, and a classifier was constructed. Species-specific transcript analysis on matching patient-derived xenografts (PDX, N=14) allowed construction of tumor- and stroma-specific classifiers for use on PDX models and cell lines.

2020-01-25 | E-MTAB-6830 | biostudies-arrayexpress

Array CGH analysis for 29 pancreatic ductal adenocarcinoma (PDAC) samples

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

Stromal evolution of cancer-associated fibroblasts in PDAC GEMMs

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aCGH of Pancreatic Ductal Adenocarcinoma (PDAC) Cell Line and Xenografts

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

First-in-class humanized antibody against alternatively spliced tissue factor augments anti-metastatic efficacy of chemotherapy in a preclinical model of pancreatic ductal adenocarcinoma

Project description:Alternatively spliced tissue factor (asTF) promotes progression of pancreatic ductal adenocarcinoma (PDAC) by activating beta1-integrins on PDAC cell surfaces. hRabMab1, a first-in-class, humanized, inhibitory, anti-asTF antibody we recently developed, can suppress PDAC primary tumor growth as a single agent. Whether hRabMab1 has the potential to suppress metastases in PDAC is unknown. Study results. When administered alone, hRabMab1 achieved only marginal penetration of experimental tumor tissue; however, hRabMab1 was abundant in tumor tissue when co-administered with gem/PTX which resulted in a significant decrease in tumor cell proliferation; leukocyte infiltration; and neovascularization. Gem/PTX alone reduced primary tumor volume, but not metastatic spread; only the combination of hRabMab1 and gem/PTX significantly reduced metastatic spread. RNAseq analysis of primary tumors showed that the addition of hRabMab1 to gem/paclitaxel enhanced the downregulation of tubulin binding and microtubule motor activity. In the liver, hRabMab1 reduced liver metastasis as a single agent. Only the combination of hRabMab1 and gem/PTX eliminated tumor cell-induced leukocytosis. Conclusions. This study demonstrates that hRabMab1 may help suppress metastasis in PDAC.

2024-12-31 | GSE252286 | GEO

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