Similar Datasets
Project description:Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are rare and heterogeneous tumors presenting a wide spectrum of different clinical and biological characteristics. In these tumors, the histological evaluation is a crucial element of clinical management. Currently, tumor grading, determined by Ki-67 staining and mitotic counts, is the most reliable predictor of prognosis. This scoring method is time-consuming and a high reproducibility cannot be achieved. Novel approaches are needed to support histological evaluation and prognosis. In this study, starting from a microarray analysis, we defined the miRNAs signature for poorly differentiated NETs (G3) compared to well differentiated NETs (G1 and G2) consisting of 56 deregulated miRNAs. Moreover, we identified 8 miRNAs that were expressed in all GEP-NETs grades but at different level. Among these miRNAs, we found miR-96-5p that raised its expression levels from grade 1 to grade 3; inversely, its target FOXO1 was decrease from grade 1 to grade 3. Our results reveal that the miRNAs expression profile of GEP-NET correlates their expression with grading showing a potential advantage of miRNA quantification to aid clinicians in the classification of common GEP-NETs subtypes.
2020-08-04 | GSE135034 | GEO
Project description:GEP of the murine cell line BAL17 (BALB/c)
2013-04-10 | GSE38675 | GEO
Project description:GEP signatures of primary breast cells radiation treated.
| PRJNA435496 | ENA
Project description:This study aims to elucidate the transcriptomic changes and metabolic reprogramming in gastroenteropancreatic neuroendocrine tumor (GEP-NET) cells following PIKfyve inhibition, using both genetic (CRISPR-mediated knockdown) and pharmacological (Apilimod treatment) approaches. The research focuses on the impact of PIKfyve inhibition on lipid metabolism, cholesterol homeostasis, and mTOR signaling in QGP-1, BON-1, and GOT-1 cell lines. By analyzing RNA sequencing data from these experimental conditions, we seek to identify differentially expressed genes and enriched pathways associated with PIKfyve inhibition. This investigation is part of a broader effort to develop novel combination therapies that could potentially overcome resistance to mTOR inhibitors, the current standard of care for advanced GEP-NETs. The study's findings may provide insights into the therapeutic potential of targeting PIKfyve-driven lipid metabolism in combination with mTOR inhibition, potentially offering new strategies to improve treatment efficacy and patient outcomes in GEP-NETs and other mTOR-driven cancers.
2026-01-26 | GSE293842 | GEO
Project description:The aggressive clinical behavior of mantle cell lymphoma (MCL) is attributed to specific genetic and molecular mechanisms involved in its pathogenesis, mainly the t(11;14)(q13;q32) traslocation and cyclin D1 (CCND1) overexpression. Nevertheless, evidence of a certain degree of heterogeneity has been disclosed by gene expression profile (GEP) and (immuno)genetic/immunohistochemistry studies. AIM: To use a GEP approach in MCL cell line models.
2017-12-31 | GSE89615 | GEO
Project description:This study aims to elucidate the transcriptomic changes and metabolic reprogramming in gastroenteropancreatic neuroendocrine tumor (GEP-NET) cells following PIKfyve inhibition, using both genetic (CRISPR-mediated knockdown) and pharmacological (Apilimod treatment) approaches. The research focuses on the impact of PIKfyve inhibition on lipid metabolism, cholesterol homeostasis, and mTOR signaling in QGP-1, BON-1, and GOT-1 cell lines. By analyzing RNA sequencing data from these experimental conditions, we seek to identify differentially expressed genes and enriched pathways associated with PIKfyve inhibition. This investigation is part of a broader effort to develop novel combination therapies that could potentially overcome resistance to mTOR inhibitors, the current standard of care for advanced GEP-NETs. The study's findings may provide insights into the therapeutic potential of targeting PIKfyve-driven lipid metabolism in combination with mTOR inhibition, potentially offering new strategies to improve treatment efficacy and patient outcomes in GEP-NETs and other mTOR-driven cancers.
2026-01-26 | GSE293843 | GEO
Project description:GEP of the murine cell line BAL17 (BALB/c) BAL17- / BAL17VII-induced primary CNS lymphoma analysis. 5x10^5 cells were implanted into the brain of BALB/c wt mice and analyzed 21 and 28 days post implantation. The cell lines were also analyzed.
2013-04-10 | E-GEOD-38675 | biostudies-arrayexpress
Project description:Expression profile of human GEP-NET tumors, including 113 fresh frozen biopsies of primary and metastatic tumours originating from pancreas (P-NET, 83 primary and 30 metastasis), 81 from small intestine (SI-NET, 44 primary and 37 metastasis), and 18 from rectum (RE-NET, 3 primary and 15 metastasis).
2018-02-25 | GSE98894 | GEO
Project description:Collagen, the most abundant organic compound of vertebrate organisms, is a supramolecular protein-made polymer. Details of its subtle post-translational maturation largely determine the mechanical properties of connective tissues. Its assembly requires massive, heterogeneous prolyl-4-hydroxylation (P4H), catalyzed by Prolyl-4-hydroxylases (P4HA1-3), providing thermostability to its elemental, triple helical building block. So far, there was no evidence of tissue-specific regulation of P4H, nor of a differential substrate repertoire of P4HAs. Here, the positional P4H profiles of collagen extracted from bone, skin, and tendon were compared, revealing lower hydroxylation of most GEP/GDP motifs in the tendon, across homeotherms. P4HA2 mRNA was found low in tendon. Invalidation of P4HA2, unlike decreased, generalized P4H activity, in the ATDC5 cellular model of collagen assembly, mimicked the tendon-related P4H profile. Therefore, P4HA2 has a better ability than other P4HAs to hydroxylate GEP/GDP motifs and the differential expression of P4HAs in tissues dictates the positional P4H profile of collagen, which participates in determining tissue specificities of its assembly.
2023-01-03 | MSV000091002 | MassIVE
Project description:In this work, we compared gene expression profile (GEP) of K562 cells transduced with the retroviral vector LCALRins5IDN or LCALRdel52IDN with K562 cells transduced with LwtCALRIDN In order to unravel MPL-independent mechanisms underlying the effect of CALR mutations on MPN pathogenesis, we analysed the transcriptional changes induced by the CALRins5 or CALRdel52 overexpression in K562 cells, which lack MPL expression
2019-08-04 | GSE114414 | GEO