Ontology highlight
ABSTRACT:
PROVIDER: PRJEB96895 | ENA |
REPOSITORIES: ENA
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Project description:We have shown that increased β-cell proliferation in functioning pancreatic neuroendocrine tumors (insulinomas) correlated with reduced expression of the long non-coding RNA Meg3 and increased expression of the oncogenic receptor c-Met. To investigate the target binding sites of Meg3 in and around the c-Met gene, we did ChIRP-Seq using biotinylated probes from the mouse Meg3 RNA sequence. This would help us better understand how Meg3 regulates ithe expression of c-Met to control β-cell proliferation in insulinoma cells.
2017-09-20 | GSE99798 | GEO
Project description:Methylome analysis in pituitary neuroendocrine tumors
| PRJEB50807 | ENA
Project description:This study investigates the molecular features of ACTH-secreting tumors to uncover gene expression patterns specific to this condition. By analyzing RNA-seq data from a diverse set of 36 samples, including pituitary adenomas with ACTH secretion, pituitary tissues, and other neuroendocrine tumors with ectopic ACTH secretion, we aim to identify distinct molecular signatures associated with ACTH production.
2025-02-17 | GSE275374 | GEO
Project description:MEG3 (Maternally Expressed Gene 3) is a non-coding RNA that is highly expressed in the normal human brain and pituitary. Expression of MEG3 is lost in gonadotroph-derived clinically non-functioning pituitary adenomas. Meg3 knock-out mice were generated to identify targets and potential functions of this gene in embryonic development and tumorigenesis. Gene expression profiles were compared in the brains of Meg3-null embryos and wild-type litter-mate controls using microarray analysis. Microarray data were analyzed with GeneSifter which uses Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and Gene Ontology (GO) classifications to identify signaling cascades and functional categories of interest within the data set. Differences were found in signaling pathways and ontologies related to angiogenesis between wild-type and knock-out embryos. Quantitative RT-PCR and histological staining showed increased expression of some VEGF pathway genes and increased cortical microvessel density in the knock-out embryos. These results are consistent with reported increases in VEGF signaling observed in human clinically non-functioning pituitary adenomas. In conclusion, Meg3 may play an important role in control of vascularization in the brain and may function as a tumor suppressor by preventing angiogenesis.
2010-12-17 | GSE18742 | GEO
Project description:MEG3 (Maternally Expressed Gene 3) is a non-coding RNA that is highly expressed in the normal human brain and pituitary. Expression of MEG3 is lost in gonadotroph-derived clinically non-functioning pituitary adenomas. Meg3 knock-out mice were generated to identify targets and potential functions of this gene in embryonic development and tumorigenesis. Gene expression profiles were compared in the brains of Meg3-null embryos and wild-type litter-mate controls using microarray analysis. Microarray data were analyzed with GeneSifter which uses Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and Gene Ontology (GO) classifications to identify signaling cascades and functional categories of interest within the data set. Differences were found in signaling pathways and ontologies related to angiogenesis between wild-type and knock-out embryos. Quantitative RT-PCR and histological staining showed increased expression of some VEGF pathway genes and increased cortical microvessel density in the knock-out embryos. These results are consistent with reported increases in VEGF signaling observed in human clinically non-functioning pituitary adenomas. In conclusion, Meg3 may play an important role in control of vascularization in the brain and may function as a tumor suppressor by preventing angiogenesis. Brains from 7 Meg3 knock-out and 6 wild-type E18.5 embryos from 5 litters. genotype: wild-type: 219_16 WT, 219_17 WT, 238_4 WT, 250_2 WT, 250_4 WT, 262_2 WT genotype: Meg3 knock-out: 148_15 KO, 219_12 KO, 238_1 KO, 238_5 KO, 250_1 KO, 250_3 KO, 262_1 KO biological replicate: 219_16 WT, 219_17 WT, 238_4 WT, 250_2 WT, 250_4 WT, 262_2 WT biological replicate: 148_15 KO, 219_12 KO, 238_1 KO, 238_5 KO, 250_1 KO, 250_3 KO, 262_1 KO
2010-12-17 | E-GEOD-18742 | biostudies-arrayexpress
Project description:DNA methylation pattern in somatotroph pituitary neuroendocrine tumors
| PRJNA941347 | ENA
Project description:Corticotropin (ACTH)-secreting pituitary adenomas give rise to a severe endocrinological disorder, i.e., Cushing’s disease, with multifaceted clinical presentation and treatment outcomes. Experimental studies suggested that disease variability is inherent to the pituitary tumor, thus pointing to the need for further studies into tumor biology. Aim of the present study was to evaluate transcriptome expression pattern in a large series of ACTH-secreting pituitary adenoma specimens, in order to identify molecular signatures of these tumors. Gene expression profiling of formalin-fixed paraffin-embedded specimens from 40 human ACTH-secreting pituitary adenomas revealed significant expression of genes involved in protein biosynthesis and ribosomal function, in keeping with neuroendocrine cell profile. Unsupervised cluster analysis identified three distinct gene profile clusters and several genes were uniquely overexpressed in a given cluster, accounting for different molecular signatures. Of note, gene expression profiles were associated with clinical features such as age and size of the tumor. Altogether, our study shows that corticotrope tumors are characterized by neuroendocrine gene expression profile and present subgroup-specific molecular features.
2018-06-18 | GSE93825 | GEO
Project description:Multilineage pituitary neuroendocrine tumors with PIT1/SF1 co-expression
| PRJNA1034042 | ENA
Project description:The MYC transcription factor requires MAX for DNA binding and widespread activation of gene expression in both normal and neoplastic cells. Surprisingly, inactivating mutations in MAX are associated with a subset of neuroendocrine cancers including pheochromocytoma, pituitary adenoma and small cell lung cancer. Neither the extent nor the mechanisms of MAX tumor suppression are well understood. Deleting Max across multiple mouse neuroendocrine tissues, we find Max inactivation alone produces pituitary adenomas while Max inactivation loss cooperates with Rb1/Trp53 loss to accelerate medullary thyroid C-cell and pituitary adenoma development. In the thyroid tumor cell lines, MAX loss triggers a striking shift in genomic occupancy by other members of the MYC network (MNT, MLX, MondoA) supporting metabolism, survival and proliferation of neoplastic neuroendocrine cells. Our work reveals MAX as a broad suppressor of neuroendocrine tumorigenesis through its ability to maintain a balance of genomic occupancies among the diverse transcription factors in the MYC network.
2025-03-15 | GSE286458 | GEO
Project description:Proteogenomic Landscape and Clinical Characterization of GH-producing pituitary adenomas/ somatotroph pituitary neuroendocrine tumors
| PRJNA881301 | ENA