MicroRNA expression of pancreatic tumors
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE43796 | GEO | 2013/12/31
SECONDARY ACCESSION(S): PRJNA187453
REPOSITORIES: GEO
Similar Datasets
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. 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. 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.
2013-12-31 | GSE43795 | 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-cell lung carcinoma (SCLC) and large-cell neuroendocrine lung carcinoma (LCNEC) are high-grade lung neuroendocrine tumors (NET). However, comparative protein expression within SCLC and LCNEC remains unclear. Here, protein expression profiles were obtained via mass spectrometry-based proteomic analysis.
2019-05-14 | PXD013583 | JPOST Repository
Project description:MYCN overexpression is a hallmark of many tumors originating from neural cell precursors. We generated a transgenic mouse with Cre-conditional induction of MYCN in glial fibre acidic protein (GFAP) expressing cells resulting in the development of neuroendocrine tumors of the pancreas and the brain. The expression profiles of nine tumors from pancreas and three brain tumors were compared to non-malignant pancreas controls (GSM771025.CEL-GSM771027.CEL) from wildtype mice Expression profiles of tumors and controls were analysed using GSEA and ANOVA.
2016-03-01 | E-GEOD-73466 | biostudies-arrayexpress
Project description:Background: Treatment-related neuroendocrine prostate cancer (t-NEPC) is a highly aggressive form of prostate cancer (PCa). Understanding the molecular mechanisms driving t-NEPC may provide valuable therapeutic strategies. Methods: we performed a pan-cancer differential mRNA abundance analysis of neuroendocrine tumors (NET) and non-NETs using integrated datasets to identify potential driver genes in NEPC. Gain- and loss-of-function studies were performed in PCa cell lines and subcutaneous xenografts in mouse to characterize the role of Kinesin-like protein (KIF1A) in neuroendocrine (NE) differentiation. Western blot, qRT-PCR, immunoprecipitation (IP), nuclear and cytoplasmic protein extraction, CO-IP and immunofluorescence were performed to study the regulation of KIF1A to OGT. Results: We identified that KIF1A overexpression is highly correlated to NE differentiation. NE differentiation features in PCa, including NE marker gene expression, stemness and EMT, were impaired by KIF1A knockdown and promoted by KIF1A overexpression. Targeting KIF1A inhibited the growth of NE-differentiated PCa cells in vitro and in vivo. Mechanistically, KIF1A bound with OGT and regulated its protein expression and O-linked N-acetylglucosamine transferase activity. OGT nuclear translocation induced by elevated KIF1A inhibited OGT ubiquitin-proteasome pathway degradation in the cytoplasm and promoted intranuclear O-GlcNAcylation of β-catenin and OCT4. More importantly, our data revealed that OGT is critical for KIF1A induced NE differentiation and aggressive growth. Conclusion: KIF1A promotes NE differentiation through modeling OGT O-GlcNAcylation in PCa. Targeting KIF1A - OGT may impede the development of NEPC for a group of PCa patients with elevated KIF1A expression.
2024-10-23 | GSE266283 | GEO
Project description:Retinoblastoma (RB) is a malignant intraocular neoplasm occurs mostly in children. The malignancy caused due to altered miRNA expression in cancer tumors and circulating body fluids has been reported in several cancers. The aberrantly expressed microRNAs are useful for diagnosis and prognosticating the tumors. Circulating miRNAs have been identified as potential markers in neoplastic and non -neoplastic diseases. The aim of the study involves identifying microRNA signatures of serum of Retinoblastoma and possible use of differential miRNA as unique biomarker for RB. Agilent Single Color Whole miRNA microarray: 14 advanced stage Retinoblastoma Serum (pooled) Vs 14 Non-Retinoblastoma Serum (pooled) samples
2012-10-31 | E-GEOD-41321 | biostudies-arrayexpress
Project description:Serous (cystic) neoplasm (SCN) of the pancreas is usually benign cystic neoplasm and has unique biological characteristics that are different from those found in the normal pancreatic tissue or pancreatic ductal adenocarcinoma (PDAC) tissue. In order to investigate molecular mechanisms involved in the unique biological phenotypes of, we compared gene expression profiles of SCN tissues with those of normal pancreatic tissues or those of PDAC tissues.
2024-05-06 | GSE173969 | GEO