Gene expression profiling study by RNA-seq in PDX model based diffuse type gastric cancers.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA416330 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We established PDX lines from diffuse type gastric cancers (DGCs). Using these cells, we carried out RNA-seq based transcriptome profiling using 15 stomach samples including three PDX lines (HGC-3, HGC-8, and HGC-20) and normal-looking surrounding tissues. Via comparative analysis between cells and tissues, we identified significant gene set associated with each cell and observed that genes involved in AKT signalling pathway were commonly associated with all PDX lines.
2018-11-01 | GSE106338 | GEO
Project description:To identify the specific genes for intestinal-type and diffuse-type gastric cancers. We selected 18 intestinal-type gastric cancers and 12 diffuse-type gastric cancers showing typical characteristics on the form of cell growth (clustered or scattered) and the degree of differentiation (well/moderate or poor), and performed microarray analysis for obtaining genome-wide mRNA expression profiles.
2014-12-25 | E-GEOD-47007 | biostudies-arrayexpress
Project description:To identify the specific genes for intestinal-type and diffuse-type gastric cancers.
2014-12-25 | GSE47007 | GEO
Project description:The invasive potential of gastric cancers (GCs) defines the hallmarks of malignancies; however, the cellular components and their molecular features associated with tumor invasiveness in GC microenvironments (TME) are poorly understood. In this study, we constructed a comprehensive atlas of 23,060 single cells obtained from surgically dissected superficial and deep layers of five diffuse-type GC along with matched normal. As a result, seven major cell types were identified. Fibroblasts, endothelial cells, and myeloid cells were categorized as being enriched in the deep layers. Cell type-specific clustering further revealed that the superficial-to-deep layer transition is associated with enrichment in inflammatory endothelial cells and fibroblasts with upregulated CCL2 transcripts. This study reveals the spatial reprogramming of the TME that may underlie invasive tumor potential in diffuse-type GC. This TME profiling across tumor layers suggests new targets, such as CCL2, that can modify the TME to inhibit tumor progression in diffuse-type GC.
2021-08-09 | GSE167297 | GEO
Project description:Gastric cancer is a leading cause of death from cancer globally. Gastric cancer is classified into intestinal, diffuse and indeterminate subtypes based on histology according to the Laurén classification. The intestinal and diffuse subtypes, although different in histology, demographics and outcomes, are still treated in the same fashion. This study was designed to discover proteomic signatures of diffuse and intestinal subtypes. Mass spectrometry-based proteomics using tandem mass tags (TMT)-based multiplexed analysis was used to identify proteins in tumor tissues from patients with diffuse or intestinal gastric cancer with adjacent normal tissue control. A total of 7,804 or 5,166 proteins were identified from intestinal or diffuse subtype, respectively. This quantitative mass spectrometric analysis defined a proteomic signature of differential expression across the two subtypes, which included gremlin1 (GREM1), bcl-2-associated athanogene 2 (BAG2), olfactomedin 4 (OLFM4), thyroid hormone receptor interacting protein 6 (TRIP6) and melanoma-associated antigen 9 (MAGE-A9) proteins. Although GREM1, BAG2, OLFM4, TRIP6 and MAGE-A9 have all been previously implicated in tumor progression and metastasis, they have not been linked to intestinal or diffuse subtypes of gastric cancer. Using immunohistochemical labelling of a tissue microarray comprising of 132 cases of gastric cancer, we validated the proteomic signature obtained by mass spectrometry in the discovery cohort. Our findings should help investigate the pathogenesis of these gastric cancer subtypes and potentially lead to strategies for early diagnosis and treatment.
2022-02-17 | PXD026279 | Pride
Project description:Gastric cancers in young patients are aggressive and predominantly of diffuse histology. Also, they are more frequent in female. To identify transcriptome profile in this unique subset of gastric cancers, RNA-seq analyses were performed using frozen cancer tissue. Adjacent normal tissue of the same patients were used in differently expressed gene selection and fusion gene prediction.
| EGAS00001001859 | EGA
Project description:The incidence of diffuse gastric cancers (DGC) remains steadily high, but relatively small numbers of DGCs have been evaluated with whole exome sequencing (WES). Clinicopathological features of DGC vary according to age, but the molecular basis for these variations is unclear. To identify genomic alteration in this unique subset of gastric cancers, whole exome and SNP6 analyses were performed using frozen cancer tissue. The same analyses were also performed using blood of the same patients.
| EGAS00001001711 | EGA
Project description:BACKGROUND & AIMS: Gastric cancer is the second most frequent cause of death from cancer in the world, diffuse-type gastric cancer (DGC) exhibiting a poor prognosis. Germline mutations of CDH1, encoding E-cadherin, have been reported in hereditary DGCs, and genetic and/or epigenetic alterations of CDH1 are frequently detected in sporadic DGCs. Genetic alterations of TP53 are also frequently found in DGCs. To examine the synergistic effect of loss of E-cadherin and p53 on gastric carcinogenesis, we established a mouse line in which E-cadherin and p53 are specifically inactivated in the stomach parietal cell lineage. METHODS: We crossed Atp4b-Cre mice with Cdh1loxP/loxP and Trp53loxP/loxP mice, and examined the gastric phenotype of Atp4b-Cre+;Cdh1loxP/loxP;Trp53loxP/loxP mice. RESULTS: Non-polarization of E-cadherin-negative parietal cells and proton pump-negative atypical foci were observed in the transgenic mice. Intramucosal cancers and invasive cancers composed of poorly differentiated carcinoma cells and signet ring cells, which were histologically very similar to those in humans, were found from 6 and 9 months, respectively. Fatal DGCs developed at 100% penetrance within a year, frequently metastasized to lymph nodes, and had tumorigenic activity in immunodeficient mice. Gene expression profiling analyses also revealed that DGCs in the E-cadherin/p53-deficient mice resembled human DGCs. CONCLUSIONS: Our mouse line is the first genetically modified mouse model of DGC and very useful for clarifying the mechanism underlying gastric carcinogenesis, and provides a new approach to the treatment and prevention of DGC because of morphological and biochemical similarities with human DGC. Two-condition experiment, Gastric cancer vs. normal gastric mucosal tissues. Biological replicates: pooled control sample from five normal gastric mucosal tissues, three replicates from diffuse-type gastric cancer.
2011-12-04 | E-GEOD-25302 | biostudies-arrayexpress
Project description:Examine methylation changes in gene promoters in gastric cancers and matched normal control gastric epithelium, using Nimblegen arrays. Direct comparison of gastric cancers and matched normal control gastric epithelium
2013-06-14 | E-GEOD-40919 | biostudies-arrayexpress
Project description:Spatially distinct reprogramming of the tumor microenvironment based on tumor invasion in diffuse-type gastric cancers
| PRJNA704101 | ENA