MRI-no-lytic-lesion
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE753 | GEO | 2004/01/01
SECONDARY ACCESSION(S): PRJNA87699
REPOSITORIES: GEO
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Project description:This series represents samples of multiple myeloma patients with bone lytic lesion by MRI. Keywords = multiple myeloma Keywords = osteolytic lesions Keywords = MRI Keywords = osteoblast Keywords = mesenchymal stem cell Keywords = Wnt signaling Keywords = DKK1 Keywords: other
2004-01-01 | GSE754 | GEO
Project description:This series represents samples of multiple myeloma patients with and without bone lytic lesion by MRI. Keywords = multiple myeloma Keywords = osteolytic lesions Keywords = MRI Keywords = osteoblast Keywords = mesenchymal stem cell Keywords = Wnt signaling Keywords = DKK1 Keywords: other
2004-01-01 | GSE755 | GEO
Project description:This series represents samples of multiple myeloma patients with and without bone lytic lesion by MRI.
2007-09-25 | E-GEOD-755 | biostudies-arrayexpress
Project description:Facioscapulohumeral muscular dystrophy (FSHD) is a common, dominantly inherited disease caused by the epigenetic de-repression of the DUX4 gene, a transcription factor normally repressed in somatic cells. As targeted therapies are now possible in FSHD, a better understanding of the relationship between DUX4 activity, muscle pathology and muscle MRI changes are crucial both to understand disease mechanisms and for the design of future clinical trials. Here, we performed MRIs of the lower extremities in 36 individuals with FSHD, followed by needle muscle biopsies in safely accessible muscles. We examined the correlation between MRI characteristics, muscle pathology, and expression of DUX4 target genes. Results show that the presence of elevated MRI STIR signal has substantial predictive value in identifying muscles with active disease and DUX4 target gene expression. In addition, DUX4 target gene expression was detected only in FSHD-affected muscles and not in control muscles, and higher levels of DUX4 target expression was associated with more advanced muscle pathology. These results support the use of MRI to identify FSHD muscles with active disease as measured by histopathology and DUX4 target gene expression and might be useful for the design of studies of disease progression and response to intervention.
2018-09-04 | GSE115650 | GEO
Project description:Osteolytic destruction is a hallmark of multiple myeloma, resulting from activation of osteoclast mediated bone resorption and reduction of osteoblast-mediated bone formation. However, the molecular mechanism underlying the differentiation and activity of osteoclasts and osteoblasts within a myelomatous microenvironment remains unclear. Here, we demonstrate that the osteocyte-expressed major histocompatibility complex class II transactivator (CIITA) contributes to myeloma-induced bone lesions. CIITA upregulates the secretion of osteolytic cytokines from osteocytes through acetylation at histone 3 lysine 14 in the promoter of TNFSF11 (encoding RANKL) and SOST (encoding sclerostin), leading to enhanced osteoclastogenesis and decreased osteoblastogenesis. In turn, myeloma cell–secreted 2-deoxy-D-ribose, the product of thymidine catalyzed by the function of thymidine phosphorylase, upregulates CIITA expression in osteocytes through the STAT1/IRF1 signaling pathway. Our work thus broadens the understanding of myeloma-induced osteolysis and indicates a potential strategy for disrupting tumor-osteocyte interaction to prevent, or treat patients with, myeloma bone disease.
2022-04-23 | GSE200987 | GEO
Project description:Lytic activation from latency is a key transition point in the life cycle of herpesviruses. Epstein-Barr virus (EBV) is a human herpesvirus that can cause lymphomas, epithelial cancers, and other diseases, most of which require the lytic cycle. While the lytic cycle of EBV can be triggered by chemicals and immunologic ligands, the lytic cascade is only activated when expression of the EBV latency-to-lytic switch protein ZEBRA is turned on. ZEBRA then transcriptionally activates other EBV genes and together with some of those gene products ensures completion of the lytic cycle. However, not every latently-infected cell exposed to a lytic trigger turns expression of ZEBRA on, resulting in responsive and refractory subpopulations. What governs this dichotomy? By examining the nascent transcriptome following exposure to a lytic trigger, we find that several cellular genes are transcriptionally upregulated temporally upstream of ZEBRA. These genes regulate lytic susceptibility to variable degrees in latently-infected cells that respond to mechanistically distinct lytic triggers. While increased expression of these cellular genes defines a pro-lytic state, such upregulation also runs counter to the well-known mechanism of viral nuclease-mediated host shut-off that is activated downstream of ZEBRA. Furthermore, a subset of upregulated cellular genes is transcriptionally repressed downstream of ZEBRA, indicating an additional mode of virus-mediated host shut-off through transcriptional repression. Thus, increased transcription of a set of host genes contributes to a pro-lytic state that allows a subpopulation of cells to support the EBV lytic cycle.
2020-01-13 | GSE141220 | GEO
Project description:Canonical Wnt signaling controls proliferation and differentiation of osteogenic progenitor cells, and tumor-derived secretion of the Wnt antagonist Dickkopf-1 (Dkk1) is correlated with osteolyses and metastasis in many bone malignancies. However, the role of Dkk1 in the oncogenesis of primary osteosarcoma (OS) remains unexplored. Here, we over-expressed Dkk1 in the OS cell line MOS-J. Contrary to expectations, Dkk1 had autocrine effects on MOSJ cells in that it increased proliferation and resistance to metabolic stress in vitro. In vivo, Dkk1 expressing MOS-J cells formed larger and more destructive tumors than controls. These effects were attributed in part to up-regulation of the stress response enzyme and cancer stem cell marker aldehyde-dehydrogenase-1 (ALDH1) through Jun-N-terminal kinase signaling. This is the first report linking Dkk1 to tumor stress resistance, further supporting the targeting of Dkk1 not only to prevent and treat osteolytic bone lesions but also to reduce numbers of stress-resistant tumor cells. Two samples were analyzed, one human DKK1 transfected MOS-J cell sample and one control vector transfected MOS-J cell sample.
2012-12-22 | E-GEOD-43112 | biostudies-arrayexpress