| Literature DB >> 20569696 |
Aviva Presser Aiden1, Miguel N Rivera, Esther Rheinbay, Manching Ku, Erik J Coffman, Thanh T Truong, Sara O Vargas, Eric S Lander, Daniel A Haber, Bradley E Bernstein.
Abstract
Wilms tumor is the most common pediatric kidney cancer. To identify transcriptional and epigenetic mechanisms that drive this disease, we compared genome-wide chromatin profiles of Wilms tumors, embryonic stem cells (ESCs), and normal kidney. Wilms tumors prominently exhibit large active chromatin domains previously observed in ESCs. In the cancer, these domains frequently correspond to genes that are critical for kidney development and expressed in the renal stem cell compartment. Wilms cells also express "embryonic" chromatin regulators and maintain stem cell-like p16 silencing. Finally, Wilms and ESCs both exhibit "bivalent" chromatin modifications at silent promoters that may be poised for activation. In Wilms tumor, bivalent promoters correlate to genes expressed in specific kidney compartments and point to a kidney-specific differentiation program arrested at an early-progenitor stage. We suggest that Wilms cells share a transcriptional and epigenetic landscape with a normal renal stem cell, which is inherently susceptible to transformation and may represent a cell of origin for this disease. Copyright 2010 Elsevier Inc. All rights reserved.Entities:
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Year: 2010 PMID： 20569696 PMCID： PMC2897075 DOI： 10.1016/j.stem.2010.03.016
Source DB: PubMed Journal: Cell Stem Cell ISSN： 1875-9777 Impact factor: 24.633