Gene expression of pancreatic tumors
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE43795 | GEO | 2013/12/31
SECONDARY ACCESSION(S): PRJNA187452
REPOSITORIES: GEO
Similar Datasets
Project description:Solid-pseudopapillary neoplasm of pancreas(SPN), ductal adenocarcinoma(PCA), neuroendocrine tumor(NET) and non-neoplastic pancreas. To investigate the specific gene expression of SPN compared to other types of pancreatic tumor, we analyzed large-scale gene expressioin analysis to identify the molecular signature that may affect SPN tumorigenesis. Differentially expressed genes were analyzed on SPNs, PCAs, NETs and Non-neoplastic tissues. Solid-pseudopapillary neoplasm (SPN) is an uncommon pancreatic tumor with distinct clinicopathologic features. SPNs are characterized by mutations in exon 3 of CTNNB1. However, little is known about the gene and microRNA expression profiles of SPNs. Thus, we sought to characterize SPN-specific gene expression and identify the signaling pathways activated in these tumors. The mRNA expression profile of 14 SPNs, 6 pancreatic adenocarcinomas (PCAs), 6 pancreatic neuroendocrine tumors (NETs), and five non-neoplastic pancreatic tissues were analyzed.
2013-12-31 | E-GEOD-43795 | biostudies-arrayexpress
Project description:Solid-pseudopapillary neoplasm of pancreas (SPN), ductal adenocarcinoma (PCA), neuroendocrine tumor (NET) and non-neoplastic pancreas. comparison with gene expression of tumors and non-tumors To investigate the specific microRNA expression of SPN compared to other types of pancreatic tumor, we analyzed large-scale microRNA expressioin analysis to identify the molecular signature that may affect SPN tumorigenesis with mRNA expression profiles. Differentially expressed microRNAs were analyzed on SPNs, PCAs, NETs and Non-neoplastic tissues.
2013-12-31 | E-GEOD-43796 | biostudies-arrayexpress
Project description:Solid-pseudopapillary neoplasm of pancreas (SPN), ductal adenocarcinoma (PCA), neuroendocrine tumor (NET) and non-neoplastic pancreas. comparison with gene expression of tumors and non-tumors
2013-12-31 | GSE43796 | GEO
Project description:Solid pseudopapillary neoplasm (SPN) of pancreas is a rare pancreatic neoplasm with a low metastatic potential. Up to 10% of patients with localized disease at presentation will develop systemic metastases, usually in the peritoneum or the liver. Due to the rarity of SPNs and the overall excellent prognosis, reliable prognostic factors to predict malignant biological behavior remain undetermined. Therefore, we aimed to define clinical, histological, and microRNA patterns that are associated with metastatic disease. We conducted a retrospective single center study on all patients operated for SPN of pancreas between 1995 and 2018. Clinical and pathological data were collected, and expression patterns of 2578 human microRNAs were analyzed using microRNA array (Affimetrix 4.1) in normal pancreases (NPs), localized tumors (LTs), and metastatic tumors (MTs). The diagnosis of SPN was confirmed in 35 patients who included 28 females and 3 males, with a mean age of 33.8 ± 13.9 years. The only clinical factor associated with metastases was tumor size (mean tumor size 5.20 ± 3.78 in LT versus 8.13± 1.03 in MT, p < 0.012). Microscopic features of malignancy were not associated with metastases, nor were immunohistochemical stains, including the proliferative index KI67. Higher expressions of miR-184, miR-10a, and miR-887, and lower expressions of miR-375, miR-217, and miR-200c were observed in metastatic tissues on microarray, and validated by real-time polymerase chain reaction. Hierarchal clustering demonstrated that the microRNA expression pattern of MTs was significantly different from that of LTs. The only clinical factor associated with metastases of SPN of pancreas was tumor size. Histological features and immunohistological staining were not predictive of metastases. A panel of six microRNAs was differentially expressed in MTs, and these findings could potentially be used to predict tumor behavior. Validation of these results is needed in larger series.
2020-02-24 | GSE140719 | GEO
Project description:Small intestinal neuroendocrine tumors (SI-NETs) arise from serotonin-producing enterochromaffin cells. SI-NETs are often well-differentiated tumors and most patients have regional or distant metastases at initial presentation. MicroRNAs (miRs) are post-transcriptional regulators which are important in diverse biological processes and can function as tumor suppressor genes or oncogenes. This study aims to identify an exclusive SI-NETs miR profile that may have a critical role in development, diagnosis, prognosis and progression of these malignancies. Five human NET cell lines, one octreotide-treated CNDT2.5 cells, one microdissected normal enterochromaffin cells, three snap-frozen normal ileum specimens and 15 SI-NET specimens at different stage of malignancy, five primary tumors, five mesentery metastases and five liver metastases, were included in this study. Total RNA was hybridized onto Affymetrix GeneChipM-BM-. miR arrays for genome-wide profiling. Array data summarization, normalization, and quality control were performed using miRNA QC Tool software.
2013-03-01 | E-GEOD-33568 | biostudies-arrayexpress
Project description:Gene expression profiles of primary neuroendocrine tumors treated or not with 1µM Octreotide.We investigated 5 human neuroendocrine cell lines, CNDT2.5 and KRJ1, established from ileum NETs, QGP1 by a pancreatic NET, NCI H720 and NCI H727 from bronchopulmonary NETs. CNDT2.5 cell wereconstantly treated with 1µM octreotide for 10 and 16 months. We isolated total RNA (Ambion, PARIS Kit) from 5 WT cell lines and CNDT2.5 treated with octreotide (Santostatin, Novartis). Total RNA was hybridized onto the Affymetrix Human Gene 1.0 ST Array by Affymetrix Uppsala Platform, UU. SE (Uppsala, Sweden). We first wanted to verify whether the different cell lines may become reliable models to study neuroendocrine signaling pathways. The main objective of this project aimed at understanding the mechanisms by which octreotide (Sandostatin, Novartis) alter cellular growth and differentiation of CNDT2.5 cells. We therefore focused on intermediate (10 months) and long stimulation (16 months) events triggered by sandostatin, which lead variation of CNDT.2.5 cells gene expression to identify potential pivotal genes involved in the development of drug resistance in neuroendocrine cells.
2013-01-08 | E-MTAB-388 | biostudies-arrayexpress
Project description:The management of neuroendocrine tumors (NETs) is very variable, depending on many specific aspects, such as the type of tumor, spread and patient general health. Several advances have been made with the newly developed somatostatin analogues to cure this type of malignancies. Somatostain analogues such as octreotide have been used in clinic to treat patients with neuroendocrine tumors (NETs). However, the molecular mechanism leading either to successful therapy or acquired resistance to the analogues is still to large extent unclear. Patients develop drugs resistance during a long term treatment. Therefore, to identify the pivotal regulatory genes involved in the development of drug resistance is an actual challenge. We studied five human neuroendocrine tumor cell lines, CNDT2.5, KRJ1, QGP-1, NCI H720 and NCI H727. We also investigated a long-term treated CNDT2.5 by using octreotide. We performed gene expression profiling in all the human neuroendocrine cell lines. Keywords: Gene Expression profiling, treatment comparison We investigated 5 human neuroendocrine cell lines, CNDT2.5 and KRJ1, established from ileum NETs, QGP1 by a pancreatic NET, NCI H720 and NCI H727 from bronchopulmonary NETs. CNDT2.5 cell were constantly treated with 1M-BM-5M octreotide for 10 and 16 months. We isolated total RNA (Ambion, PARISM-bM-^DM-" Kit) from 5 WT cell lines and CNDT2.5 treated with octreotide (Santostatin, Novartis). Total RNA was hybridized onto the Affymetrix Human Gene 1.0 ST Array by Affymetrix Uppsala Platform, UU. SE (Uppsala, Sweden). We first wanted to verify whether the different cell lines may become reliable models to study neuroendocrine signaling pathways. The main objective of this project aimed at understanding the mechanisms by which octrotide (Sandostatin, Novartis) alter cellular growth and differentiation of CNDT2.5 cells. We therefore focused on intermediate (10 months) and long stimulation (16 months) events triggered by sandostatin, which lead variation of CNDT.2.5 cells gene expression to identify potential pivotal genes involved in the development of drug resistance in neuroendocrine cells.
2012-12-12 | E-GEOD-24358 | biostudies-arrayexpress
Project description:The striatum is organized into two major outputs formed by striatal projection neuron (SPN) subtypes with distinct molecular identities. In addition, the histochemical division into patch and matrix compartments represents an additional spatial organization, proposed to mirror a functional specialization in a motor-motivation dimension. To map the molecular diversity of SPNs in the context of the patch and matrix division, we genetically labeled mu-opioid receptor (Oprm1) expressing striatal neurons and performed single-nucleus RNA sequencing (snRNA-seq). This allowed us to establish new molecular definitions of the patch-matrix compartments, resulting in a molecular code for mapping patch SPNs at the cellular level. In addition, Oprm1 expression labeled exopatch SPNs, which we found to be molecularly distinct from both patch as well as neighboring matrix SPNs, thereby forming a separate molecular entity. At the cell-type level, we found an unexpected SPN diversity, leading to the identification of a new Col11a1+ striatonigral SPN type. At the tissue level, we found that mapping the spatial expression of a number of markers revealed new definitions of spatial domains in the striatum, which were conserved in the non-human primate brain. Interestingly, the spatial markers were cell-type independent and instead represented a spatial code that was found across all SPNs within a spatially restricted domain. This spatiomolecular map establishes a formal system for targeting and studying the striatal subregions and SPNs subtypes, beyond the classical striatonigral and striatopallidal division.
2019-11-01 | GSE139265 | GEO
Project description:Gastroentero-pancreatic neuroendocrine tumors (GEP-NETs) are a heterogenous group of neoplasms that arise from enterochromaffin cells of the gastrointestinal (GI) tract and pancreas. They account for 50-70% of all incident NETs. Due to the lack of symptoms in the early stage of disease and the frequency of nonspecific GI symptoms, GEP-NETs are difficult to diagnose.
Identification of effective biomarkers (such as Chromogranin A) to improve GEP-NET diagnosis, as well as to assess treatment efficacy, relapse and prognosis, is important for improving outcomes for patients with GEP-NETs.
The purpose of this study is to validate the performance of Brahms (BRAHMS) Chromogranin A II Kryptor (KRYPTOR) assay to monitor the course of disease in patients with well-defined GEP-NETs.
| 2295412 | ecrin-mdr-crc