Gene expression profiling of Nodular fasciitis
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE78991 | GEO | 2016/06/30
SECONDARY ACCESSION(S): PRJNA314591
REPOSITORIES: GEO
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Project description:Nodular fasciitis (NF) is a rapidly growing cellular mass composed of fibroblasts/myofibroblasts, usually localized in subcutaneous tissues, that typically undergoes fibrosis and almost never recurs. Desmoid tumors (DT) are rare forms of fibroblastic/myofibroblastic growth that arise in deep soft tissues, display propensity for local infiltration and recurrence but fail to metastasize. Given that both entities are primarily fibroblastic/myofibroblastic lesions with overlapping histological features, we compared their gene expression profile to identify differentially expressed genes that may provide not only potential diagnostic markers but also clues as to the pathogenesis of each disorder. Differentially expressed transcripts (89 clones displaying increased expression in DT and 246 clones displaying increased expression in NF), included genes encoding several receptor and non-receptor tyrosine kinases (EPHB3, PTPRF, GNAZ, SYK, LYN, EPHA4, BIRC3), transcription factors (TWIST1, PITX2, EYA2, OAS1, MITF, TCF20), and members of the Wnt signaling pathway (AXIN2, WISP1, SFRP). Remarkably, almost one fourth of the differentially expressed genes encode proteins associated with inflammation and tissue remodeling, including members of the interferon (IFN), tumor necrosis factor (TNF) and transforming growth factor beta (TGF-beta) signaling pathways as well as metalloproteinases (MMP1, 9, 13, 23), urokinase plasminogen activator (PLAU) and cathepsins. Our observations provide the first comparative molecular characterization of desmoid tumors and nodular fasciitis and suggest that selected tyrosine kinases, transcription factors and members of the Wnt, TGF-beta, IFN and TNF signaling pathways may be implicated in influencing and distinguishing their fate. Keywords: comparative genomic hybridization
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Project description:Secondary hyperparathyroidism is well known complication manifested in end-stage renal disease (ESRD). Both nodular and diffuse parathyreoid hyperplasia occur in ESRD patients. Distinct molecular mechanisms involved in parathyreoid hyperplasia remain poorly understood. Microarray screening proved homogeneity of gene transcripts in hemodialysis patients as compared to transplant cohort and primary hyperparathyreoidism, therefore further studies were performed in hemodialysis patints only. Enrichment analysis conducted on 485 differentially expressed genes between nodular and diffuse parathyreoid hyperplasia revealed highly significant differences in GO terms and KEGG database in ribosome structure (p=3.70-18). Next, RT-qPCR validation of microarray analysis proved higher expression of RAN guanine nucleotide release factor (RANGRF, p<0.001), calcyclin binding protein (CACYBP, p<0.05) and exocyst complex component 8 (EXOC8, p<0.05) and lower expression of peptidylprolyl cis/trans isomerase, NIMA-interacting 1 (PIN1, p<0.01) mRNA in nodular hyperplasia. Multivariate analysis revealed RANGRF and PIN1 expression along with parathyroid weight to be associated with nodular hyperplasia. Higher expression of genes associated with ribosomal structure and function underline extended translation mechanisms involved in parathyreoid nodular formation in long-term hemodialysis treated patients. Parathyroid tissue obtained from ESRD hyperparathyroidism patients who had undergone parathyroidectomy were used for transcriptome screening (Illumina HumanHT-12 v4.0 Expression BeadChips) and subsequently for discriminatory gene analysis, pathway mapping and gene-annotation enrichment analyses. Results were verified on enlarged group of hemodialysis patients with nodular (n=20) and diffuse (n=20) hyperplasia using RT-qPCR method.
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Project description:Secondary hyperparathyroidism is well known complication manifested in end-stage renal disease (ESRD). Both nodular and diffuse parathyreoid hyperplasia occur in ESRD patients. Distinct molecular mechanisms involved in parathyreoid hyperplasia remain poorly understood. Microarray screening proved homogeneity of gene transcripts in hemodialysis patients as compared to transplant cohort and primary hyperparathyreoidism, therefore further studies were performed in hemodialysis patints only. Enrichment analysis conducted on 485 differentially expressed genes between nodular and diffuse parathyreoid hyperplasia revealed highly significant differences in GO terms and KEGG database in ribosome structure (p=3.70-18). Next, RT-qPCR validation of microarray analysis proved higher expression of RAN guanine nucleotide release factor (RANGRF, p<0.001), calcyclin binding protein (CACYBP, p<0.05) and exocyst complex component 8 (EXOC8, p<0.05) and lower expression of peptidylprolyl cis/trans isomerase, NIMA-interacting 1 (PIN1, p<0.01) mRNA in nodular hyperplasia. Multivariate analysis revealed RANGRF and PIN1 expression along with parathyroid weight to be associated with nodular hyperplasia. Higher expression of genes associated with ribosomal structure and function underline extended translation mechanisms involved in parathyreoid nodular formation in long-term hemodialysis treated patients.
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Project description:Splenic masses are common in older dogs and may be malignant, benign, or non-neoplastic; yet diagnosis preceding splenectomy and histopathology remains elusive. MicroRNAs (miRNAs) are 18-25 nucleotide, single stranded, non-coding RNAs that play a role in post-transcriptional regulation. MicroRNAs in tumor samples have been used to diagnose tumors, provide prognostic information, and aid in targeted treatments in human medicine, but have not been extensively evaluated in veterinary medicine. The objective of this study was to determine differential expression of microRNAs (miRNAs) between canine splenic hemangiosarcoma, canine splenic nodular hyperplasia, and normal canine spleens by use of RNA-sequencing. Eighteen miRNAs were found to be significantly differentially expressed between hemangiosarcoma and nodular hyperplasia only. The five of these with the largest fold change were mir-193a, mir-450a, mir-503, mir-542, and mir-876. Four miRNA were significantly differentially expressed between hemangiosarcoma and nodular hyperplasia and also hemangiosarcoma and normal spleen (mir-126, mir-150, mir-203, and mir-452). Findings of this study show that miRNA expression profiles are different between canine splenic hemangiosarcoma, nodular hyperplasia, and normal spleens. This is a preliminary study with findings of clinical relevance, as masses of the spleen cannot be diagnosed pre-operatively in most cases. Canine splenic masses are relatively common, and validation these findings is warranted for potential use as a diagnostic test.
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