DNA methylation of rhabdomyosarcoma
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ABSTRACT:
PROVIDER: PRJNA604272 | ENA |
REPOSITORIES: ENA
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Project description:DNA methylation of rhabdomyosarcoma
| PRJNA604271 | ENA
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
2014-10-22 | E-GEOD-61150 | biostudies-arrayexpress
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).
2016-09-01 | GSE67201 | GEO
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: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 ‘bivalent’ 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.
2014-10-22 | GSE61150 | GEO
Project description:DNA methylation in rhabdomyosarcoma PDX and PDX-derived primary cells
| PRJNA641458 | ENA
Project description:DNA methylation in rhabdomyosarcoma PDX and PDX-derived primary cells
| PRJNA641459 | ENA
Project description:Genome wide DNA methylation profiling of rhabdomuyosarcoma tumors derived from genetically engineered mouse models. The Illumina MouseMethylation285 BeadChip was used to obtain DNA methylation profiles across approximately 285,000 methylation sites in 31 freshly-frozen rhabdomyosarcoma tumors.
2024-11-26 | GSE260806 | GEO
Project description:DNA methylation is a key epigenetic modification regulating genome organization, stability, and gene expression. Stable DNA methylation critically relies on methyl groups provided through folate-mediated one-carbon (C1) metabolism, yet the origin and regulation of C1 supply remain elusive. Here we demonstrate that photorespiration serves as a major C1 source for DNA methylation in Arabidopsis. We show that C1 from formate, a photorespiratory byproduct, is incorporated into 5-methyl-cytosine via the reductive cytosolic folate pathway. This occurs predominantly during the day, negatively regulating serine utilization as alternative C1 source. Consequently, suppression of photorespiration under elevated CO₂ levels alters the DNA methylation landscape, an effect exacerbated when regulation of C1 metabolism by the formate-dependent pathway is impaired. Thus, our findings link the fundamental metabolic process of photorespiration to epigenetic stability, highlighting how rising atmospheric CO₂ levels can induce DNA methylation changes.
2026-01-06 | MTBLS13444 | MetaboLights
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