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Gene Expression in Human Rhabdomyosarcoma

ABSTRACT: Gene Expression in Human Rhabdomyosarcoma

PROVIDER: PRJNA1115071 | ENA |

REPOSITORIES: ENA

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Gene Expression in Human Rhabdomyosarcoma

Project description:Gene expression analysis identified unique transcriptional changes in rhabdomyosarcoma when compared with normal muscle. Our studies focused on a gene called VANGL2 that regulated growth and self-renewal in embryonal rhabdomyosarcoma.

2018-03-06 | GSE108022 | GEO

Expression Profiling of human Fusion-Positive and Fusion-Negative Rhabdomyosarcoma

Project description:Genome-wide gene expression in 33 fusion-positive and 25 fusion-negative rhabdomyosarcoma cases was studied using GeneChip Human Genome U133 Plus2 (Affymetrix) Fusion-positive versus fusion-negative rhabdomyosarcoma tumors

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Gene Expression Profiling of Fusion Negative Rhabdomyosarcoma Cell Lines

Project description:We analyzed the expression of two fusion-negative established Rhabdomyosarcoma cell lines. Together with Chip-seq, we were able to identify transcribed loci bound by myogenic regulatory transcription factors (MYF5 and MYOD) that pertain to embryonic muscle development and cell cycle regulation pathways. Keywords: rhabdomyosarcoma, gene expression profiling, RD, Rh18

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Expression Profiling of Rhabdomyosarcoma patients and normal muscle samples

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Exon level expression analysis from rhabdomyosarcoma patient tumors.

Project description:Rhabdomyosarcoma is a childhood tumor with features of aberrant muscle differentiation. We studied samples from 101 rhabdomyosarcoma patients to determine core gene expression signatures relevant in the disease.

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Aberrant DNA methylation in rhabdomyosarcoma

Project description:Many pediatric malignancies are embryonal in nature, and one hypothesis for the origin of embryonal tumors is that they arise from a defect in differentiation, either by an inability to terminally differentiate or a reversion to a pluripotent state. There is emerging evidence that epigenetic regulation plays an important role in the transition from embryonic stem cell to a more committed cell fate, utilizing both de novo DNA methylation and poised M-bM-^@M-^XbivalentM-bM-^@M-^Y chromatin domains (H3K27me3 and H3K4me3) to abolish pluripotency and gain lineage- and cell-type-specific characteristics as a cell differentiates. Thus inappropriate epigenetic silencing by aberrant DNA methylation of bivalent genes required for differentiation could lead to the uncontrolled cell growth observed in cancer. Our broad hypothesis is that aberrant DNA methylation in cancer is targeted to a non-random subset of critical pathways used in normal development. This dysregulation of the normal epigenetic program used in development promotes cellular proliferation and provides a mechanism to block differentiation in pediatric cancers, such as rhabdomyosarcoma. Examination of DNA methylation in fourteen human rhabdomyosarcoma patient samples using RRBS. In addition, RRBS was used to examine DNA methylation in one human rhabdomyosarcoma cell line (RD) forced to terminally differentiate by expression of the forced heterodimer MyoD~E12 (MDE). Lastly, RRBS was used to examine DNA methylation changes during normal differentiation in one primary human normal myoblast cell line

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Gene expression analaysis of the lateral spreading tumor

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Clinical Application of Prognostic Gene Expression Signature in Fusion Gene-Negative Rhabdomyosarcoma

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