Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human aggressive fibromatosis tumors

ABSTRACT: This study examines the expression profile of cells from human aggressive fibromatosis tumors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE23356 | GEO | 2014/12/22

SECONDARY ACCESSION(S): PRJNA131469

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

human aggressive fibromatosis tumors

Project description:This study examines the expression profile of cells from human aggressive fibromatosis tumors. Cells from human aggressive fibromatosis tumors were manually minced, and visible clumps were removed. Enzymatic digestion using 10 mg/mL of collagenase IV, 2.4 units/mL Dispase, 0.05% trypsin, was used for 45 min at 37Â°C. Cells were then centrifuged at 1400 rpm for 5 min and washed thrice in PBS. RNA was extracted using RNA was extracted using Trisol as per the manufacturer's instructions, and used for gene profiling studies.

2014-12-22 | E-GEOD-23356 | biostudies-arrayexpress

Homo sapiens

Project description:human aggressive fibromatosis tumors

| PRJNA131469 | ENA

Driver Gene and Potential Biomarker Investigation of Desmoid-type Fibromatosis Through RNA-seq Analysis

Project description:Desmoid type fibromatosis(DTF), a locally aggressive fibromatosis, lacks clear pathogenesis. RNA-seq analysis of 29 DTF cases identified hub genes like ZNF536, TWIST2, and SHOX2, indicating involvement in fibroblastic proliferation. These genes were validated in other fibrotic diseases. Immunohistochemistry revealed TWIST2 as a promising diagnostic biomarker, emphasizing its potential clinical utility.

2025-09-09 | GSE266101 | GEO

Gene expression analysis of gingival fibromatosis gingiva

Project description:Gingival fibromatosis (GF) is a rare oral condition characterized by proliferative fibrous overgrowth of both the attached and marginal gingiva, and the interdental papilla. But there were no papers about gene expression of gingival fibromatosis. The aim of this study was to identify the differential expression of genes in GF using cDNA microarray analysis.

2017-02-14 | GSE58481 | GEO

Role of transglutaminase 2 in promoting biglycan synthesis in idiopathic gingival fibromatosis

Project description:The mechanism of idiopathic gingival fibromatosis is still unclear. To provide new insights into the molecular and cellular differences between idiopathic gingival fibromatosis and periodontitis, we first identified the gene TGM2, which is differentially expressed between the two. We found that the expression of TGM2 is predominantly lower in idiopathic gingival fibromatosis than in periodontitis, and that the activity of SP1 due to the decreased expression of TGM2 promotes the generation of extracellular matrix-related genes in idiopathic gingival fibromatosis. We have identified biglycan, an extracellular matrix that is specifically upregulated in idiopathic gingival fibromatosis, and highlight the effects of SP1 and TGM2 on biglycan expression.

2024-09-24 | GSE277572 | GEO

PDGFRβ signaling cooperates with β-catenin to modulate c-Abl and biologic behavior of desmoid-type fibromatosis [microarray]

Project description:Unsupervised clustering of desmoid tumors and normal mesenchymal tissues was performed using henes associated with HIF1 activity. This accurately distiguished neoplastic tissues from normal controls The study sought to identify genes differentially expressed in desmoid-type fibromatosis as opposed to normal mesenchymal tissues. We noted that beta-catenin, the central driver in desmoid-type fibromatosis, appeared to regulate HIF1 signaling in in vitro studies. Genes associated with HIF1 and angiogenesis pathways were then used to perform unsupervised clustering on desmoid tumors and normal mesenchymal tissues. The genes accurately differentiated neoplastic and normal samples.

2023-10-31 | GSE237692 | GEO

Expression Profile of Relapsed/Refractory Aggressive B-cell Non Hodgkin Lymphoma Tumors

Project description:Expression Profile of Relapsed/Refractory Aggressive B-cell Non Hodgkin Lymphoma Tumors

| PRJNA720938 | ENA

NHGRI-Mayo Clinic Whole Genome Sequencing of Aggressive Prostate Tumors

Project description:NHGRI-Mayo Clinic Whole Genome Sequencing of Aggressive Prostate Tumors

| PRJNA317702 | ENA

Pathogenesis of enamel-renal syndrome associated gingival fibromatosis: a proteomic approach

Project description:The enamel renal syndrome (ERS) is a rare disorder featured by amelogenesis imperfecta, gingival fibromatosis and nephrocalcinosis. Gingival fibromatosis is a hallmark of the disease; it is characterized by the accumulation of a collagen-rich, dense connective tissue and of mineral deposits throughout the gingiva. ERS is caused by biallelic mutations in the FAM20A gene encoding a pseudokinase, likely acting as an allosteric activator of FAM20C, the Golgi casein kinase. How mutations in FAM20A may modify the gingival connective tissue homeostasis and cause fibromatosis is currently unknown. Conditioned media of gingival fibroblasts (GF) obtained from four unrelated ERS patients carrying distinct mutations and three control subjects were used. Secretomic analysis identified 109 dysregulated proteins whose abundance had increased (69 proteins) or decreased (40 proteins) at least 1.5-fold compared to control GF. Gene Ontology (GO) analysis revealed biological processes significantly over-represented or under-represented in the ERS GF. Proteins over-represented were mainly involved in extracellular matrix organization, collagen fibril assembly, and biomineralization whereas those under-represented were extracellular matrix-associated proteins. Accordingly, GO disease analysis indicated un significant enrichment of tumoral angiogenesis and fibrosis.

2022-02-17 | PXD028003 | Pride