Integrated transcriptome meta-analysis of pancreatic ductal adenocarcinoma and matched adjacent pancreatic tissues.

{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:33194391", "kind": "science-record", "revision": 7, "content_hash": "sha256:3189bb522e9bc8a04eb1463933c0d17c1260ef832bfe33c802c5c103d1eb62e8", "created_at": "2026-11-01T15:41:16Z", "updated_at": "2026-11-01T22:02:32Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Integrated transcriptome meta-analysis of pancreatic ductal adenocarcinoma and matched adjacent pancreatic tissues.", "doi": "10.7717/peerj.10141", "pmid": "33194391", "authors": ["Sevcan Atay"], "journal": "PeerJ", "year": 2020, "abstract": "A comprehensive meta-analysis of publicly available gene expression microarray data obtained from human-derived pancreatic ductal adenocarcinoma (PDAC) tissues and their histologically matched adjacent tissue samples was performed to provide diagnostic and prognostic biomarkers, and molecular targets for PDAC. An integrative meta-analysis of four submissions (GSE62452, GSE15471, GSE62165, and GSE56560) containing 105 eligible tumor-adjacent tissue pairs revealed 344 differentially over-expressed and 168 repressed genes in PDAC compared to the adjacent-to-tumor samples. The validation analysis using TCGA combined GTEx data confirmed 98.24% of the identified up-regulated and 73.88% of the down-regulated protein-coding genes in PDAC. Pathway enrichment analysis showed that \"ECM-receptor interaction\", \"PI3K-Akt signaling pathway\", and \"focal adhesion\" are the most enriched KEGG pathways in PDAC. Protein-protein interaction analysis identified FN1, TIMP1, and MSLN as the most highly ranked hub genes among the DEGs. Transcription factor enrichment analysis revealed that TCF7, CTNNB1, SMAD3, and JUN are significantly activated in PDAC, while SMAD7 is inhibited. The prognostic significance of the identified and validated differentially expressed genes in PDAC was evaluated via survival analysis of TCGA Pan-Cancer pancreatic ductal adenocarcinoma data. The identified candidate prognostic biomarkers were then validated in four external validation datasets (GSE21501, GSE50827, GSE57495, and GSE71729) to further improve reliability. A total of 28 up-regulated genes were found to be significantly correlated with worse overall survival in patients with PDAC. Twenty-one of the identified prognostic genes (ITGB6, LAMC2, KRT7, SERPINB5, IGF2BP3, IL1RN, MPZL2, SFTA2, MET, LAMA3, ARNTL2, SLC2A1, LAMB3, COL17A1, EPSTI1, IL1RAP, AK4, ANXA2, S100A16, KRT19, and GPRC5A) were also found to be significantly correlated with the pathological stages of the disease. The results of this study provided promising prognostic biomarkers that have the potential to differentiate PDAC from both healthy and adjacent-to-tumor pancreatic tissues. Several novel dysregulated genes merit further study as potentially promising candidates for the development of more effective treatment strategies for PDAC.", "claims": [{"id": "claim-method", "statement": "The random-effects method (DerSimonian & Laird, 1986), which takes into account the variance of heterogeneity between studies, was used to perform the meta-analysis.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:33194391", "locator": "sections[5] \"Standard meta-analysis\" paragraph 2", "quote": "The random-effects method (DerSimonian & Laird, 1986), which takes into account the variance of heterogeneity between studies, was used to perform the meta-analysis."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The following information was supplied regarding data availability:The data is available at NCBI GEO: GSE62452, GSE15471, GSE62165, GSE56560, GSE21501, GSE50827, GSE57495, GSE71729.The TCGA-PAAD and TCGA-Pan-cancer raw data is available at UCSC Zena (available at https://xenabrowser.net/datapages/).", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:33194391", "locator": "sections[22] \"Additional Information and Declarations\" paragraph 4", "quote": "The following information was supplied regarding data availability:The data is available at NCBI GEO: GSE62452, GSE15471, GSE62165, GSE56560, GSE21501, GSE50827, GSE57495, GSE71729.The TCGA-PAAD and TCGA-Pan-cancer raw data is available at UCSC Zena (available at https://xenabrowser.net/datapages/)."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": null, "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:33194391"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. 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The physical bench the paper used is not, so a physical validation cannot be run here."}, "data": {"tier": "R1", "reachable": true, "accessions": ["GSE62452", "GSE15471", "GSE62165", "GSE56560", "GSE21501", "GSE50827", "GSE57495", "GSE71729"], "resolved_accessions": ["GSE62452", "GSE15471", "GSE62165", "GSE56560", "GSE21501", "GSE50827", "GSE57495", "GSE71729"], "statements": ["The following information was supplied regarding data availability:The data is available at NCBI GEO: GSE62452, GSE15471, GSE62165, GSE56560, GSE21501, GSE50827, GSE57495, GSE71729.The TCGA-PAAD and TCGA-Pan-cancer raw data is available at UCSC Zena (available at https://xenabrowser.net/datapages/)."], "basis": "The paper names GSE62452, GSE15471, GSE62165, GSE56560, GSE21501, GSE50827, GSE57495, GSE71729 in NCBI Gene Expression Omnibus and the accession resolves in the repository. 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