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Set 'Sox2 targets': genes upregulated and identified by ChIP on chip as SOX2 [GeneID=6657] transcription factor targets in human embryonic stem cells.

PAG Title Set 'Sox2 targets': genes upregulated and identified by ChIP on chip as SOX2 [GeneID=6657] transcription factor targets in human embryonic stem cells.
PAG ID MAX000154
Type A
Source Link MSigDB
Publication Reference NA
PAG Description Cancer cells possess traits reminiscent of those ascribed to normal stem cells. It is unclear, however, whether these phenotypic similarities reflect the activity of common molecular pathways. Here, we analyze the enrichment patterns of gene sets associated with embryonic stem (ES) cell identity in the expression profiles of various human tumor types. We find that histologically poorly differentiated tumors show preferential overexpression of genes normally enriched in ES cells, combined with preferential repression of Polycomb-regulated genes. Moreover, activation targets of Nanog, Oct4, Sox2 and c-Myc are more frequently overexpressed in poorly differentiated tumors than in well-differentiated tumors. In breast cancers, this ES-like signature is associated with high-grade estrogen receptor (ER)-negative tumors, often of the basal-like subtype, and with poor clinical outcome. The ES signature is also present in poorly differentiated glioblastomas and bladder carcinomas. We identify a subset of ES cell-associated transcription regulators that are highly expressed in poorly differentiated tumors. Our results reveal a previously unknown link between genes associated with ES cell identity and the histopathological traits of tumors and support the possibility that these genes contribute to stem cell-like phenotypes shown by many tumors.
Species Homo sapiens
Quality Metric Scores nCoCo Score: 80
Information Content Rich
Other IDs M3835
Base PAG ID MAX000154
Human Phenotyte Annotation
Curator PAGER curation team
Curator Contact PAGER-contact@googlegroups.com
Gene ID Gene symbol Gene name RP_score
Gene A Gene B Source SCORE

Gene A Gene B Mechanism Source
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