DNA methylation profiling of rhabdomyosarcoma tumor samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE67201 | GEO | 2016/09/01
SECONDARY ACCESSION(S): PRJNA279257
REPOSITORIES: GEO
Similar Datasets
Project description:In order to identify the specific DNA methylation pattern of different rhabdomyosarcoma (RMS) samples we performed a genome-wide study using Human DNA methylation platform (Agilent). DNA methylation profiling was carried out in 15 RMS tumor samples using the Human DNA methylation microarray (Agilent) consisting of about 244,000 (60-mer) probes design to interrogate about 27,000 known CpG islands. Enriched-methylated dsDNA for each sample was labeled with Cy5 dye and the control genomic DNA for each sample was labeled with Cy3 dye using Agilent Genomic DNA labeling kit PLUS (Agilent).
2016-09-01 | E-GEOD-67201 | biostudies-arrayexpress
Project description:Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from fresh frozen tissues. To obtain a profile of copy number alterations in RMS, we studied 65 samples in 60 RMS cases. Other data of 38 samples are deposited in GSE41263: GSM1528059 GSM1528057 GSM1528061 GSM1528058 GSM1528054 GSM1528060 GSM1012723 GSM1012722 GSM1012746 GSM1528055 GSM1528056 GSM1530028 GSM1012751 GSM1012724 GSM1012726 GSM1012747 GSM1012725 GSM1012716 GSM1012735 GSM1012713 GSM1012736 GSM1012737 GSM1012738 GSM1012730 GSM1012739 GSM1012740 GSM1012750 GSM1012717 GSM1012718 GSM1012719 GSM1012741 GSM1012732 GSM1012715 GSM1012720 GSM1012742 GSM1012721 GSM1012743 GSM1012744 Copy number analysis of Affymetrix 250K or Cytoscan_HD SNP arrays was performed for 27 rhabdomyosarcoma samples.
2015-06-30 | E-GEOD-63891 | biostudies-arrayexpress
Project description:The methylation enrichment was determined by MIRA-sequencing after MBD2-capture using the MethylCollector™ Ultra Kit (Active Motif) performed on DNA samples derived from rhabdomyosarcoma cells (RMS) TE671 cells. The cells expressing shRNA targeting ZNF555 (shZNF555) were compared to the control cells expressing non-targeting shRNA (shCtl). The signals of methylation-enriched DNA (ENR) were normalised to non-enriched input DNA (INP).
2022-07-28 | E-MTAB-10825 | biostudies-arrayexpress
Project description:Rhabdomyosarcomas (RMS) represent a family of aggressive soft tissue sarcomas that present in both the pediatric and adult setting. Pathologic risk stratification for RMS has been based on histologic subtype, with poor outcomes observed in alveolar rhabdomyosarcoma (ARMS) and adult-type pleomorphic rhabdomyosarcoma (PRMS) compared to embryonal rhabdomyosarcoma (ERMS). Recent genomic sequencing studies have expanded the spectrum of RMS, with several new molecularly defined entities, including fusion-driven spindle cell/sclerosing rhabdomyosarcoma (SC/SRMS) and MYOD1-mutant SC/SRMS. Comprehensive genomic analysis has previously defined the mutational and copy number spectrum for the more common ERMS and ARMS, as well as revealed corresponding methylation signatures. In contrast, genetic and epigenetic correlates have not been defined for the rare SC/SRMS or PRMS histologic subtypes. Herein, we present genomic sequencing, copy number analysis, and methylation profiling of the largest cohort of molecularly characterized RMS samples to date. We identified two novel methylation subtypes, one having SC/SRMS histology and defined by MYOD1 p. L122R mutations and the other matching adult type PRMS. Selected tumors from adolescent patients grouped with the PRMS methylation class, expanding the age range of these rare tumors. Pediatric patients in the MYOD1-mutant group, as well as those clustering with PRMS, appear to have poor overall survival.
2021-11-24 | GSE167059 | GEO
Project description:We measured the expression profiles of a series of 30 Rhabdomyosarcoma biopsy samples (15 embryonal RMS, 10 translocation-positive alveolar RMS and 5 translocation-negative alveolar RMS). Expression data was used for unsupervised hierarchical clustering as well as supervised analysis to find gene expression signatures characteristic for the different histological RMS subgroups.
2004-06-30 | E-MEXP-121 | biostudies-arrayexpress
Project description:Rhabdomyosarcoma (RMS) is the most common childhood sarcoma and is identified as either the embryonal or alveolar (ARMS) subtype. In approximately 75% of cases, ARMSs are characterized by specific chromosomal translocations that involve PAX and FKHR genes. ARMS gene expression signatures vary, depending on the presence or absence of the translocations. Insulin-like growth factor-binding protein 2 (IGFBP2) is strongly overexpressed in translocation-negative RMS. Because IGFBP2 is associated with tumorigenesis, we investigated its functional role in RMS. An analysis of IGFBP2 distribution in RMS cell lines revealed a strong accumulation in the Golgi complex, in which morphological characteristics appeared peculiarly modified. After silencing IGFBP2 expression, our microarray analysis revealed mostly cell cycle and actin cytoskeleton gene modulations. In parallel, IGFBP2-silenced cells showed reduced cell cycle and rates of invasion and decreased seeding in the lungs after tail vein injections in immunodeficient mice. An analysis of IGFBP2 mRNA and protein localization in human tumors showed abnormal protein accumulation in the Golgi complex, mostly in PAX/FKHR-negative RMS. Moreover, an analysis of patients with RMS revealed the presence of conspicuous circulating levels of IGFBP2 proteins in children with highly aggressive RMS tumors. Taken together, our data provide evidence that IGFBP2 contributes to tumor progression and that it could be used as a marker to better classify clinical and biological risks in RMS. Three independent silencing experiments on RH36, an embryonal rhabdomyosarcoma cell line, were performed to study the role of IGFBP2 oncogene in this childhood tumor. Each of 3 biological replicates has its own control which is represented by cell culture treated with a non-targeting siRNA (siCONTROL). 3 controls were used to produce a M-bM-^@M-^\control poolM-bM-^@M-^] that has been used as reference in all microarray experiments. Each microarray experiment consists of a competitive hybridization between test and reference RNA (e.g. silenced cells vs. control), labelled with Cy3 or Cy5. Two microarray experiments were performed for each of three silencing experiment (technical replicate). Each slide was scanned and the data was normalized and analyzed.
2011-12-05 | E-GEOD-23196 | biostudies-arrayexpress
Project description:Frozen skeletal muscle, tumor adjacent skeletal muscle, Endothelial Rhabdomyosarcoma (ERMS) and Alveolar Rhabdomyosarcoma (ARMS) samples were profiled on Illumina bead array. Total RNA from primary resected samples were profiled to allow comparison of 1) normal skeletal muscle tissue with RMS samples and 2) ARMS with ERMS tumors.
2013-12-31 | E-GEOD-28511 | biostudies-arrayexpress
Project description:DNA methylation of rhabdomyosarcoma
| PRJNA604272 | ENA
Project description:DNA methylation of rhabdomyosarcoma
| PRJNA604271 | ENA
Project description:Rhabdomyosarcoma (RMS) is a frequent non-epithelial tumor of soft tissue that originates from a myogenic differentiation defect. Expression of SNAIL transcription factor is elevated in the alveolar subtype of RMS, characterized by a low myogenic differentiation status and high aggressiveness. SNAIL affects RMS metastasis by reorganization of actin cytoskeleton, regulation of ezrin expression and chemotaxis to HGF and SDF-1. The differentiation of human RMS diminishes SNAIL level. SNAIL silencing completely abolishes the growth of human RMS xenotransplants. SNAIL inhibits myogenic differentiation of RMS by binding to the MYF5 promoter, suppressing its expression, displacing MYOD from canonical to alternative E-box sequences and regulating myomiRs expression. SNAIL silencing allows the re-expression of MYF5 and canonical MYOD binding, promoting RMS cell myogenic differentiation. These novel results open potential avenues for the development of innovative therapeutic strategies based on SNAIL silencing.
2020-07-14 | PXD006711 | Pride