Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9855390_1.fastq.gz | Fastqsanger.gz | |||
| SRR9855390_2.fastq.gz | Fastqsanger.gz | |||
| SRR9855400_1.fastq.gz | Fastqsanger.gz | |||
| SRR9855400_2.fastq.gz | Fastqsanger.gz | |||
| SRR9855410_1.fastq.gz | Fastqsanger.gz |
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Project description:To elucidate the pathogenesis of rhabdomyosarcoma (RMS), particularly for different subgroups, we performed a SNP array-based copy number analysis of 54 RMS specimens from primary cases with ERMS (N = 30), ARMS (N = 14), unclassified RMS (N = 1), and RMS of unknown histology (N = 3) together with 7 RMS-derived cell lines. The ERMS subtype was characterized by hyperploidy and was significantly associated with gains of chromosomes 2, 8, and 12, whereas majority of ARMS cases exhibited near-diploid copy number profiles. Recurrent loss of heterozygosity (LOH) of chromosomes 3 (28.6%) and 15q (35.7%) was detected in ARMS. Uniparental disomy/polysomy of 11p was commonly found in both tumor types. Focal gains/amplifications were associated mostly with PAX3-FOXO1 (5/10) or PAX7-FOXO1 (6/6) fusions, but novel amplified regions were also found, including the IRS2 in 2 ARMS. Gain of 13q was significantly associated with good patient outcome in ERMS. These findings not only illustrate genetic differences between ARMS and ERMS but also provide novel insights into the pathogenesis of RMS.
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Project description:Anorectal malformations (ARMs) are among the most common congenital terminal digestive tract malformations. Circular RNAs (circRNAs), a novel type of endogenous non-coding RNAs, play roles in the development of the digestive system; however, their contributions to the pathogenesis of ARMs are not well-established. Many dysregulated circRNAs as the primary factor could play an important role in the development of anorectum. We used high-throughput sequencing to reveal the regulatory mechanism of gene expression underlying the development of anorectal malformations. These results provide original insight into the roles of circRNAs in ARMs and provide a valuable resource for further analyses of molecular mechanisms and signaling networks.
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Project description:In this study, we show that histone variant H3.3 is overexpressed in ARMS patient-derived cell lines and patient tumour specimens. Functionally, knockdown of H3F3A significantly impairs the ability of ARMS cells to undertake migration and invasion and reduces Rho activation in vitro. In addition, a striking reduction in metastatic tumour burden and improved survival is apparent in vivo. Through RNA-sequencing and ChIP-sequencing analyses, we identified Melanoma Cell Adhesion Molecule (MCAM/CD146) as a direct downstream target of H3.3. Therefore, this study identifies a novel H3.3- MCAM axis involved in ARMS metastatic phenotypes, and supports the development of MCAM as a therapeutic target for this disease.
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Project description:Alveolar rhabdomyosarcomas (ARMS) are aggressive soft-tissue sarcomas affecting children and young adults. Most ARMS tumors express the PAX3-FKHR or PAX7-FKHR (PAX-FKHR) fusion genes resulting from the t(2;13) or t(1;13) chromosomal translocations, respectively. However, up to 25% of ARMS tumors are fusion negative, making it unclear whether ARMS represent a single disease or multiple clinical and biological entities with a common phenotype. To test to what extent PAX-FKHR determine class and behavior of ARMS, we used oligonucleotide microarray expression profiling on 139 primary rhabdomyosarcoma tumors and an in vitro model. We found that ARMS tumors expressing either PAX-FKHR gene share a common expression profile distinct from fusion-negative ARMS and from the other rhabdomyosarcoma variants. We also observed that PAX-FKHR expression above a minimum level is necessary for the detection of this expression profile. Using an ectopic PAX3-FKHR and PAX7-FKHR expression model, we identified an expression signature regulated by PAX-FKHR that is specific to PAX-FKHR-positive ARMS tumors. Data mining for functional annotations of signature genes suggested a role for PAX-FKHR in regulating ARMS proliferation and differentiation. Cox regression modeling identified a subset of genes within the PAX-FKHR expression signature that segregated ARMS patients into three risk groups with 5-year overall survival estimates of 7%, 48%, and 93%. These prognostic classes were independent of conventional clinical risk factors. Our results show that PAX-FKHR dictate a specific expression signature that helps define the molecular phenotype of PAX-FKHR-positive ARMS tumors and, because it is linked with disease outcome in ARMS patients, determine tumor behavior. NOTE: Migrated from caArray 1.x, identifier='gov.nih.nci.ncicb.caarray:Experiment:1015897589792480:1'
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Project description:Mapping the Drosophila melanogaster centromeric heterochromatin by CGH analysis of embryos lacking specific chromosomes or chromosome arms.
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Project description:Histone demethylases such as KDM4B play critical roles in oncogenic pathophysiology and, therefore may be effective targets for anticancer therapy. Using a TR-FRET demethylation screen assay, in combination with multiple orthogonal validation approaches, we identified geldanamycin and its analog 17-DMAG as novel KDM4B inhibitors. In addition, we found that these Hsp90 inhibitors effect increased degradation of the alveolar rhabdomyosarcoma (aRMS) driver oncoprotein PAX3-FOXO1 and induce the H3K9me3 and H3K36me3 at genomic loci of PAX3-FOXO1 targets. We found that as monotherapy 17-DMAG significantly inhibits expression of PAX3-FOXO1 target genes and multiple oncogenic pathways, induces a muscle differentiation signature, delays tumor growth and extends survival in aRMS xenograft mouse models. The combination of 17-DMAG with conventional chemotherapy significantly enhances therapeutic efficacy, indicating that targeting KDM4B in combination with chemotherapy may serve as a novel therapy to PAX3-FOXO1-positive aRMS.
2020-12-22 | GSE151493 | GEO