Aberrant DNA methylation in rhabdomyosarcoma

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Scott Diede 

PROVIDER: E-GEOD-61150 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress