Homo sapiens
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR182529.fastq.gz | Fastqsanger.gz | |||
| DRR182530.fastq.gz | Fastqsanger.gz | |||
| DRR182531.fastq.gz | Fastqsanger.gz | |||
| DRR182532_1.fastq.gz | Fastqsanger.gz | |||
| DRR182532_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 31 |
Similar Datasets
Project description:Pancreatic cancer is the fourth leading cancer-related death in United States. The clinical relevance of genomic imbalances in pancreatic cancer is uncertain. We performed array-comparative genomic hybridization (aCGH) in 44 resected pancreatic cancer specimens from a Korean cohort. We observed recurrent copy number gains were observed in chromosome 1q, 11q, 18q11.1-11.2, and 20q13.13; and losses in chromosome 2p, 9p, 10q, 14q, 15q, 18q12.2-23, 19q, 20q11.1, 21p, and 22q. High copy number gains, with log2 ratio >2.0, were observed in 4 cytobands, encoding genes such as G protein-coupled receptor 48, c-myc and gamma-catenin. By comparing the aCGH results of long survivors and short survivors, determined according to the median survival, we observed that loss of cytoband 18q22.3, encoding 5 genes, was the only alteration with significantly different frequencies. The copy number of the CPGL (Carboxypeptidase of glutamate-like) gene in cytoband 18q22.3 was found to be significantly associated with overall survival in univariate analyses (p=0.019 by log-rank test). This was subsequently assessed in the Italian cohort: 41 out of the 61 specimens carried deletion of the CPGL gene. Patients with deletion of the CPGL gene also had shorter overall survival (p=0.003 by log-rank test). Multivariate analysis of the two cohorts combined showed that loss of 18q22.3 / deletion of the CPGL gene was an independent poor prognostic factor for overall survival after adjusting for other factors which were found to impact the outcome (hazard ratio 2.72, p=0.0007). overexpression of the CPGL or its alternating splicing isoform CPGL-B in a pancreatic cancer cell lines resulted in slower proliferation of cells, G1 cell cycle arrest, and reduced migration activity. In conclusion, through aCGH analysis, we identified loss of 18q22.3 / deletion of the CPGL gene as potentially being an independent poor prognostic factor in resected pancreatic cancer. We further identified the CPGL gene as a potential tumor suppressor for pancreatic cancer cell lines. Array-comparative genomic hybridization was performed in 44 resected pancreatic cancer specimen from a Korean cohort. Genomic alteration relating to prognosis of the Korean cohort was further validated in a Italian cohort containing 61 resected pancreatic cancer specimens.
2011-04-21 | E-GEOD-28732 | biostudies-arrayexpress
Project description:In order to identify biologically relevant tumor markers with prognostic significance, we set out to analyze gene expression profiling of tumor and adjacent non-tumor tissues from PDAC cases. We compared the microarray gene-expression profiles of 45 matching pairs of pancreatic tumor and adjacent non-tumor tissues. This data set were used to obtained genes that were differentially expressed and associated with survival. 51 genes were selected for further validation. 90 total samples were analyzed. We compared gene expression profile of 45 pairs of pancreatic tumor and adjacent non-tumor tissues using Affymetrix GeneChip Human Gene 1.0 ST arrays. Tumor gene expression profiles were distinctly different from non-tumor profiles. Using ANOVA in Partek®, 7352 independent genes were found to be differentially expressed in tumors (P<0.01). We next performed Cox-regression analysis and identified 928 of the differentially expressed genes that were associated with survival (P<0.1). The list of genes was then subjected to pathway and biomarker analyses using Ingenuity Pathways Analysis (IPA). Based on literatures supporting their roles in cancer, 51 genes were selected for further analyses
2012-07-08 | E-GEOD-28735 | biostudies-arrayexpress
Project description:To evaluate the prognostic relevance of molecular subtypes and key transcription factors in pancreatic ductal adenocarcinoma (PDAC), we performed gene expression analysis of whole-tumor tissue obtained from 118 surgically resected PDAC and 13 control samples.
2016-08-17 | GSE62165 | GEO
Project description:Expression analysis of 36 pancreatic ductal adenocarcinoma tumors and matching normal pancreatic tissue samples from pancreatic cancer patients of the Clinical Institute Fundeni (ICF) using Affymetrix U133 Plus 2.0 whole-genome chips. Pairs of normal and tumor tissue samples were obtained at the time of surgery from resected pancreas of 36 pancreatic cancer patients. Gene expression was analyzed on Affymetrix U133 plus 2.0 whole genome microarrays. For three of the 36 normal-tumor sample pairs we carried out replicate microarray hybridizations in order to gauge the technical measurement errors. We thus performed 78 genechip hybridizations in total. A patient sample pair was excluded from further analysis since one of the samples did not meet the quality controls. The microarray data was subsequently normalized using the RMA algorithm.
2009-06-13 | E-GEOD-15471 | biostudies-arrayexpress
Project description:Despite extensive biological and clinical studies, including comprehensive genomics and transcriptomics analysis, pancreatic ductal adenocarcinoma (PDAC) remains a devastating disease, with poor survival and no effective therapies to date. Correlation networks are emerging as a powerful approach to infer tumor biology and to prioritize candidate genes as biomarkers or drug targets. In this study we applied a weighted co-expression analysis to the functionally relevant proteome of 20 surgically resected patients with PDAC. We obtained twelve modules with overlapping yet distinct biology, which implicated metabolism and ECM complexes in several modules. Notably, one module enriched for metabolic processes and epithelial-mesenchymal-transition (EMT) was significantly associated with overall survival (p=0.01) and was validated in public RNA data (p=0.02). The prognostic value of three proteins (SPTBN1, KHSRP and PYGL) belonging to this module was confirmed using immunohistochemistry in a cohort of 82 radically resected patients.
2020-09-01 | PXD015744 | Pride
Project description:Carboxypeptidase of glutamate-like gene as a tumor suppressor in pancreatic cancer cells and a prognostic marker for resected pancreatic cancer patients
| PRJNA140543 | ENA
Project description:Perineural invasion (PNI) is a pivotal prognostic factor in pancreatic cancer, associated with aggressive tumor behavior and adverse patient outcomes. Despite its recognized clinical impact, the molecular mechanisms underlying PNI are not well understood. In this study, we isolated perineural invasion-associated cancer-associated fibroblasts (pCAFs), which demonstrated a markedly enhanced capacity to promote neural invasion in pancreatic cancer compared to non-perineural invasion-associated CAFs (npCAFs). Utilizing single-cell, high-throughput sequencing, and metabolomics, we identified a significant upregulation of glycolysis in pCAFs, fostering a high-lactate tumor microenvironment conducive to cancer progression. pCAFs-derived lactate is absorbed by tumor cells, facilitating histone H3K18 lactylation. This epigenetic modification activates the transcription of neural invasion-associated genes such as L1CAM and SLIT1, thereby driving PNI in pancreatic cancer. Further exploration of metabolic reprogramming in pCAFs revealed enhanced acetylation of the glycolytic enzyme GAPDH, correlated with increased enzymatic activity and glycolytic flux. Targeting of GAPDH and lactylation modifications significantly inhibits neural invasion in a KPC mouse model. Clinical data suggested that high levels of H3K18 lactylation correlate with severe PNI and poorer patient prognosis. Our findings provide critical insights into the role of pCAFs in the PNI of pancreatic cancer, highlighting glycolytic reprogramming and lactate-driven histone modifications as potential therapeutic targets for PDAC.
2025-03-19 | GSE290654 | GEO
Project description:Perineural invasion (PNI) is a pivotal prognostic factor in pancreatic cancer, associated with aggressive tumor behavior and adverse patient outcomes. Despite its recognized clinical impact, the molecular mechanisms underlying PNI are not well understood. In this study, we isolated perineural invasion-associated cancer-associated fibroblasts (pCAFs), which demonstrated a markedly enhanced capacity to promote neural invasion in pancreatic cancer compared to non-perineural invasion-associated CAFs (npCAFs). Utilizing single-cell, high-throughput sequencing, and metabolomics, we identified a significant upregulation of glycolysis in pCAFs, fostering a high-lactate tumor microenvironment conducive to cancer progression. pCAFs-derived lactate is absorbed by tumor cells, facilitating histone H3K18 lactylation. This epigenetic modification activates the transcription of neural invasion-associated genes such as L1CAM and SLIT1, thereby driving PNI in pancreatic cancer. Further exploration of metabolic reprogramming in pCAFs revealed enhanced acetylation of the glycolytic enzyme GAPDH, correlated with increased enzymatic activity and glycolytic flux. Targeting of GAPDH and lactylation modifications significantly inhibits neural invasion in a KPC mouse model. Clinical data suggested that high levels of H3K18 lactylation correlate with severe PNI and poorer patient prognosis. Our findings provide critical insights into the role of pCAFs in the PNI of pancreatic cancer, highlighting glycolytic reprogramming and lactate-driven histone modifications as potential therapeutic targets for PDAC.
2025-03-05 | GSE290845 | GEO
Project description:Despite extensive biological and clinical studies, including comprehensive genomics and transcriptomics analysis, pancreatic ductal adenocarcinoma (PDAC) remains a devastating disease, with poor survival and no effective therapies to date. Correlation networks are emerging as a powerful approach to infer tumor biology and to prioritize candidate genes as biomarkers or drug targets. In this study we applied a weighted co-expression analysis to the functionally relevant proteome of 20 surgically resected patients with PDAC. We obtained twelve modules with overlapping yet distinct biology, which implicated metabolism and ECM complexes in several modules. Notably, one module enriched for metabolic processes and epithelial-mesenchymal-transition (EMT) was significantly associated with overall survival (p=0.01) and was validated in public RNA data (p=0.02). The prognostic value of three proteins (SPTBN1, KHSRP and PYGL) belonging to this module was confirmed using immunohistochemistry in a cohort of 82 radically resected patients.
2024-11-15 | MSV000096427 | MassIVE